Heart disease

Pulmonary valve stenosis

2007-01-11T21:13:00.000-08:00

Pulmonary valve stenosis is a medical condition in which outflow of blood from the right ventricle of the heart is obstructed at the level of the pulmonic valve. This results in the reduction of flow of blood to the lungs. Symptoms include jugular venous distention, cyanosis (usually visible in the nailbeds), and general symptoms of lowered oxygenation of the blood. When the stenosis is mild, it can go unnoticed for many years. If stenosis is severe, you may see sudden fainting or dizziness if exercised too much. Valve replacement or surgical repair (depending upon whether the stenosis is in the valve or vessel) may be indicated. Stenosis can occur in dogs as well as in humans.
Contents

1 Causes
2 See also

Causes
The most common cause is congenital. If severe, it can lead to blue baby syndrome. It can also be secondary to other conditions such as endocarditis.
See also
Aortic valve stenosis Mitral regurgitation
Health disesae,Health disesae,Health disesae,
Health disesae,Health disesae,Health disesae,

Mitral valve prolapse

2007-01-11T21:11:00.000-08:00

From Wikipedia, the free encyclopedia
Mitral valve prolapse (MVP) is a heart valve condition marked by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. In its nonclassic form, MVP carries a low risk of complications. In severe cases of classic MVP, complications include mitral regurgitation, infective endocarditis, and — in rare circumstances — cardiac arrest usually resulting in sudden death.
see also: Mitral valve prolapse dysautonomia
Contents

1 Overview
2 History
3 Subtypes
3.1 Classic versus nonclassic
3.2 Symmetric versus asymmetric
3.3 Flail versus non-flail
4 Signs and symptoms
4.1 Auscultation
5 Complications
5.1 Mitral regurgitation
5.2 Sudden death
6 Prognosis
7 Diagnosis
8 Treatment
8.1 IE prevention
9 Prevalence
10 References

//
Overview
The mitral valve, so named because of its resemblance to a bishop's miter, is the heart valve that prevents the backflow of blood from the left ventricle into the left atrium. It is composed of two leaflets (one anterior, one posterior) that close when the left ventricle contracts.
Each leaflet is composed of three layers of tissue: the atrialis, fibrosa, and spongiosa. Patients with classic mitral valve prolapse have excess connective tissue that thickens the spongiosa and separates collagen bundles in the fibrosa. This is due to an excess of dermatan sulfate, a glycosaminoglycan. This weakens the leaflets and adjacent tissue, resulting in increased leaflet area and elongation of the chordae tendineae. Elongation of the chordae often causes rupture, and is commonly found in the chordae tendineae attached to the posterior leaflet. Advanced lesions — also commonly involving the posterior leaflet — lead to leaflet folding, inversion, and displacement toward the left atrium.
History
The term mitral valve prolapse was coined by J. Michael Criley in 1966 and gained acceptance over the other descriptor of "billowing" of the mitral valve (as described by Dr. Barlow).
For many years, mitral valve prolapse was a poorly understood anomaly associated with a wide variety of both related and seemingly unrelated signs and symptoms, including late systolic murmurs, inexplicable panic attacks, and polythelia (extra nipples). Recent studies suggest that these symptoms were incorrectly linked to MVP because the disorder was simply over-diagnosed at the time. Continuously-evolving criteria for diagnosis of MVP with echocardiography made proper diagnosis difficult, and hence many subjects without MVP were included in studies of the disorder and its prevalence. In fact, some modern studies report that as many as 55% of the population would be diagnosed with MVP if older, less reliable methods of MVP diagnosis—notably M-mode echocardiography—were used today.
In recent years, new criteria have been proposed as an objective measure for diagnosis of MVP using more reliable two- and three-dimensional echocardiography. The disorder has also been classified into a number of subtypes with respect to these criteria.
Subtypes

Diagnosis of mitral valve prolapse is based on modern echocardiographic techniques which can pinpoint abnormal leaflet thickening and other related pathology.
Prolapsed mitral valves are classified into several subtypes, based on leaflet thickness, concavity, and type of connection to the mitral annulus. Subtypes can be described as classic, nonclassic, symmetric, asymmetric, flail, or non-flail.
Note: all measurements below refer to adult patients and applying them to children may be misleading.
Classic versus nonclassic
Prolapse occurs when the mitral valve leaflets are displaced more than 2 mm above the mitral annulus high points. The condition can be further divided into classic and nonclassic subtypes based on the thickness of the mitral valve leaflets: up to 5 mm is considered nonclassic, while anything beyond 5 mm is considered classic MVP.
Symmetric versus asymmetric
Classical prolapse may be subdivided into symmetric and asymmetric, referring to the point at which leaflet tips join the mitral annulus. In symmetric coaptation, leaflet tips meet at a common point on the annulus. Asymmetric coaptation is marked by one leaflet displaced toward the atrium with respect to the other. Patients with asymmetric prolapse are prone to severe deterioration of the mitral valve, with the possible rupture of the chordae tendineae and the development of a flail leaflet.
Flail versus non-flail
Asymmetric prolapse is further subdivided into flail and non-flail. Flail prolapse occurs when a leaflet tip turns outward, becoming concave toward the left atrium, causing the deterioration of the mitral valve. The severity of flail leaflet varies, ranging from tip eversion to chordal rupture. Dissociation of leaflet and chordae tendineae provides for unrestricted motion of the leaflet (hence "flail leaflet"). Thus patients with flail leaflets have a higher prevalence of mitral regurgitation than those with the non-flail subtype.
] Signs and symptoms
Some patients with MVP experience heart palpitations, atrial fibrillation, or syncope, though the prevalence of these symptoms does not differ significantly from the general population. Between 11 and 15% of patients experience moderate chest pain and shortness of breath. These symptoms are most likely not caused directly by the prolapsing mitral valve, but rather by the mitral regurgitation that often results from prolapse.
For unknown reasons, MVP patients tend to have a low body mass index (BMI) and are typically leaner than individuals without MVP. Other features associated with MVP include Pectus excavatum, scoliosis, greater armspan than height, fatigue, and unusual joint flexibility.[1]
Auscultation
Upon auscultation of an individual with mitral valve prolapse, a mid-systolic click, followed by a late systolic murmur heard best at the apex is common.
Complications
Mitral regurgitation
Most cases of mitral valve prolapse are associated with mild mitral regurgitation, where blood aberrantly flows from the left ventricle into the left atrium during systole. Approximately 7% of classic MVP patients experience severe regurgitation, often due to chordae tendineae rupture.
Sudden death
Severe mitral valve prolapse is associated with arrhythmias and atrial fibrillation that may progress and lead to sudden death. As there is no evidence that a prolapsed valve itself contributes to such arrythmias, these complications are more likely due to mitral regurgitation and congestive heart failure.
] Prognosis
The major predictors of mortality are the severity of mitral regurgitation and the ejection fraction. Patients with moderate to severe mitral regurgitation have a relative risk for mortality that is three times that of the general population. Similarly, a left ventricular ejection fraction at or below 50% carries a relative risk of 3.8.

Transthoracic and transesophageal echocardiograms of mitral valve prolapseLeft. A transthoracic echocardiogram displaying prolapse of both the anterior leaflet (AL) and posterior leaflet (PL) of the mitral valve. Right. A transesophageal echocardiogram displaying the heart in the same individual as in the figure to the left. Both figures are during ventricular systole, with the mitral valve closed. AL=Anterior leaflet; PL=Posterior leaflet; LA=Left atrium; LV=Left ventricle; AO=Aorta; Blue line represents the plane of the mitral valve annulus.

DiagnosisEchocardiography, a noninvasive method of visualizing the heart, is the most useful method of diagnosing a prolapsed mitral valve. Two- and three-dimensional echocardiography are particularly valuable as they allow visualization of the mitral leaflets relative to the mitral annulus. This allows measurement of the leaflet thickness and their displacement relative to the annulus. Thickening of the mitral leaflets >5 mm and leaflet displacement >2 mm indicates classic mitral valve prolapse.
Treatment
Mitral valve prolapse can be treated with surgical replacement of the mitral valve. This may be necessary in as many as 11% of patients with classic MVP, and is indicated for patients with an ejection fraction below 60% and progressive left ventricular dysfunction.
IE prevention
People with mitral valve prolapse are at higher risk of infective endocarditis (that is, bacterial infection of the heart tissue), as a result of surgical operations. Therefore they need preventive antibiotic treatment, before any operation that involves massive bleeding. Minor skin wounds (and plastic surgeries, etc), are not a problem, but dental operations such as pulpectomy ("root canal") are. Thus, as a risk lowering measure, people with Mitral valve prolapse should take extra care of their dental hygiene.
Prevalence
Figures vary widely, but most recent studies of mitral valve prolapse indicate a prevalence of 1.3% for classic and 1.1% for nonclassic MVP. MVP occurs less frequently in children, and does not vary significantly with sex. Though the reasons are not understood, patients with mitral valve prolapse tend to be leaner with a relatively low body mass index.
References
^ http://www.nursing.wright.edu/practice/mvp/, Understanding the Mitral Valve Prolapse Syndrome
Playford D, Weyman AE (2001). "Mitral valve prolapse: time for a fresh look". Rev Cardiovasc Med 2 (2): 73-81. PMID 12439384.

Mitral stenosis

2007-01-11T21:06:00.000-08:00

From Wikipedia, the free encyclopedia
Mitral stenosis is a narrowing of the orifice of the mitral valve of the heart.
Contents
1 Overview
2 Etiology
3 Pathophysiology
4 Physical examination
5 Diagnosis
6 Natural history
7 Treatment
8 See also
9 External links
10 References

Overview
Mitral stenosis with marked thickening of the leaflets and left atrial hypertrophy. Superior view. Autopsy preparation.
In normal cardiac physiology, the mitral valve opens during left ventricular diastole, to allow blood to flow from the left atrium to the left ventricle. The reason the blood flows in the proper direction is that, during this phase of the cardiac cycle, the pressure in the left ventricle is less than the pressure in the left atrium, and the blood flows down the pressure gradient. In the case of mitral stenosis, the valve does not open completely, so the left atrium has to have a higher pressure than normal to have the blood overcome the increased gradient caused by the mitral valve stenosis.
Etiology
Most cases of mitral stenosis are due to disease in the heart secondary to rheumatic fever and the consequent rheumatic heart disease. Less common causes of mitral stenosis are calcification of the mitral valve leaflets, and as a form of congenital heart disease.
Pathophysiology
The normal area of the mitral valve orifice is about 4 to 6 cm2. Under normal conditions, a normal mitral valve will not impede the flow of blood from the left atrium to the left ventricle during (ventricular) diastole, and the pressures in the left atrium and the left ventricle during diastole will be equal. The result is that the left ventricle gets filled with blood during early diastole, with only a small portion of extra blood contributed by contraction of the left atrium (the "atrial kick") during late ventricular diastole.

When the mitral valve area goes below 2 cm2, the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve. This gradient may be increased by increases in the heart rate or cardiac output. As the gradient across the mitral valve increases, the amount of time necessary to fill the left ventricle with blood increases. Eventually, the left ventricle requires the atrial kick to fill with blood. As the heart rate increases, the amount of time that the ventricle is in diastole and can fill up with blood (called the diastolic filling period) decreases. When the heart rate goes above a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the left atrium, leading to pulmonary congestion.
When the mitral valve area goes less than 1 cm2, there will be an increase in the left atrial pressures (required to push blood through the stenotic valve). Since the normal left ventricular diastolic pressures is about 5 mmHg, a pressure gradient across the mitral valve of 20 mmHg due to severe mitral stenosis will cause a left atrial pressure of about 25 mmHg. This left atrial pressure is transmitted to the pulmonary vasculature and causes pulmonary hypertension. Pulmonary capillary pressures in this level cause an imbalance between the hydrostatic pressure and the oncotic pressure, leading to extravasation of fluid from the vascular tree and pooling of fluid in the lungs (congestive heart failure causing pulmonary edema).
Increases in the heart rate will allow less time for the left ventricle to fill, also causing an increase in left atrial pressure and pulmonary congestion.
The constant pressure overload of the left atrium will cause the left atrium to increase in size. As the left atrium increases in size, it becomes more prone to develop atrial fibrillation. When atrial fibrillation develops, the atrial kick is lost (since it is due to the normal atrial contraction).
In individuals with severe mitral stenosis, the left ventricular filling is dependent on the atrial kick. The loss of the atrial kick due to atrial fibrillation can cause a precipitous decrease in cardiac output and sudden congestive heart failure.
Physical examination
Upon auscultation of an individual with mitral stenosis, the first heart sound is unusually loud and may be palpable (tapping apex beat) because of increased force in closing the mitral valve.
If pulmonary hypertension secondary to mitral stenosis is severe, the P2 (pulmonic) component of the second heart sound (S2) will become loud.
An opening snap maybe heard after the A2 (aortic) component of the second heart sound (S2), which correlates to the forceful opening of the mitral valve. The mitral valve opens when the pressure in the left atrium is greater than the pressure in the left ventricle. This happens in ventricular diastole (after closure of the aortic valve), when the pressure in the ventricle precipitously drops. In individuals with mitral stenosis, the pressure in the left atrium correlates with the severity of the mitral stenosis. As the severity of the mitral stenosis increases, the pressure in the left atrium increases, and the mitral valve opens earlier in ventricular diastole.
A mid-diastolic rumbling murmur will be heard after the opening snap. The murmur is best heard at the apical region and is not radiated. Since it is low-pitched it should be picked up by the bell of the stethoscope. Rolling the patient towards left, as well as isometric exercise will accentuate the murmur. A thrill might be present when palpating at the apical region of the praecordium.
Peripheral signs include:
Malar flush - pulmonary hypertension is prominent in patients with mitral stenosis
Ankle/sacral oedema when there is right heart failure
Atrial fibrillation - irregularly irregular pulse and loss of 'a' wave in jugular venous pressure
Left parasternal heave - presence of right ventricular hypertrophy due to pulmonary hypertension
Tapping apex beat which is not displaced
Diagnosis
Severity of mitral stenosis
Degree of mitral stenosis
Mean gradient
Mitral valve area
Mild mitral stenosis
<5>1.5 cm2
Moderate mitral stenosis
5 - 10
1.0 - 1.5 cm2
Severe mitral stenosis
> 10
< title="Echocardiography" href="http://en.wikipedia.org/wiki/Echocardiography">echocardiography, which shows decreased opening of the mitral valve leaflets, and blunted flow of blood in early diastole.
The trans-mitral gradient as measured by doppler echocardiography is the gold standard in the evaluation of the severity of mitral stenosis.
Another method of measuring the severity of mitral stenosis is the simultaneous left heart catheterization and right heart catheterization. The right heart catheterization (commonly known as Swan-Ganz catheterization) gives the physician the mean pulmonary capillary wedge pressure, which is a reflection of the left atrial pressure. The left heart catheterization, on the other hand, gives the pressure in the left ventricle. By simultaneously taking these pressures, it is possible to determine the gradient between the left atrium and right atrium during ventricular diastole, which is a marker for the severity of mitral stenosis. This method of evaluating mitral stenosis tend to over-estimate the degree of mitral stenosis, however, because of the time lag in the pressure tracings seen on the right heart catheterization and the slow Y descent seen on the wedge tracings. If a trans-septal puncture is made during right heart catheterization, however, the pressure gradient can accurately quantify the severity of mitral stenosis.
Natural history
The natural history of mitral stenosis secondary to rheumatic fever (the most common cause) is an asymptomatic latent phase following the initial episode of rheumatic fever. This latent period lasts an average of 16.3 ± 5.2 years. Once symptoms of mitral stenosis begin to develop, progression to severe disability takes 9.2 ± 4.3 years.
In individuals who were offered mitral valve surgery but refused, survival with medical therapy alone was 44 ± 6% at 5 years, and 32 ± 8% at 10 years after they were offered correction.
Treatment
The treatment options for mitral stenosis include medical management, surgical replacement of the valve, and percutaneous balloon valvuloplasty.
Mitral stenosis typically progresses slowly (over decades) from the initial signs of mitral stenosis to NYHA functional class II symptoms to the development of atrial fibrillation to the development of NYHA functional class III or IV symptoms. Once an individual develops NYHA class III or IV symptoms, the progression of the disease accelerates and the patient's condition deteriorates.
The indication for invasive treatment with either a mitral valve replacement or valvuloplasty is NYHA functional class III or IV symptoms.
To determine which patients would benefit from percutaneous balloon mitral valvuloplasty, a scoring system has been developed.2 Scoring is based on 4 echocardiographic criteria: leaflet mobility, leaflet thickening, subvalvar thickening, and calcification. Individuals with a score of ≥ 8 tended to have suboptimal results.3 Superb results with valvotomy are seen in individuals with a crisp opening snap, score < title="Echocardiography" href="http://en.wikipedia.org/wiki/Echocardiography">Echocardiography
Mitral valve
Health disesae,Health disesae,Health disesae,
Health disesae,Health disesae,Health disesae,
Health disesae,Health disesae,Health disesae,
Health disesae,Health disesae,Health disesae,
Health disesae,Health disesae,Health disesae,

Mitral regurgitation

2007-01-11T21:01:00.002-08:00

From Wikipedia, the free encyclopedia
Mitral regurgitation (MR), also known as mitral insufficiency, is the abnormal leaking of blood through the mitral valve, from the left ventricle into the left atrium of the heart.
Contents

1 Etiology
2 Pathophysiology
2.1 Acute phase
2.2 Chronic compensated phase
2.3 Chronic decompensated phase
3 Symptoms
4 Diagnostic studies
4.1 Chest x-ray
4.2 Echocardiography
5 Quantification of mitral regurgitation
6 Treatment
6.1 Indication for surgery
7 References
8 See also

Etiology
The mitral valve is composed of the valve leaflets, the mitral valve annulus (which forms a ring around the valve leaflets), the papillary muscles (which tether the valve leaflets to the left ventricle, preventing them from prolapsing into the left atrium), and the chordae tendineae (which connect the valve leaflets to the papillary muscles). A dysfunction of any of these portions of the mitral valve apparatus can cause mitral regurgitation.
Primary mitral regurgitation is due to any disease process that affects the mitral valve apparatus itself. The causes of primary mitral regurgitation include:
Myxomatous degeneration of the mitral valve
Ischemic heart disease / Coronary artery disease
Infective endocarditis
Collagen vascular diseases (ie: SLE, Marfan's syndrome)
Rheumatic heart disease
Trauma
Balloon valvulotomy of the mitral valve
Certain forms of medication (e.g. fenfluramine)
The most common cause of primary mitral regurgitation in the United States (causing about 50% of primary mitral regurgitation) is myxomatous degeneration of the valve. Myxomatous degeneration of the mitral valve is more common in males, and is more common in advancing age. It is due to a genetic abnormality that results in a defect in the collagen that makes up the mitral valve. This causes a stretching out of the leaflets of the valve and the chordae tendineae. The elongation of the valve leaflets and the chordae tendineae prevent the valve leaflets from fully coapting when the valve is closed, causing the valve leaflets to prolapse into the left atrium, thereby causing mitral regurgitation.
Ischemic heart disease causes mitral regurgitation by the combination of ischemic dysfunction of the papillary muscles, and the dilatation of the left ventricle that is present in ischemic heart disease, with the subsequent displacement of the papillary muscles and the dilatation of the mitral valve annulus.
Secondary mitral regurgitation is due to the dilatation of the left ventricle, causing stretching of the mitral valve annulus and displacement of the papillary muscles. This dilatation of the left ventricle can be due to any cause of dilated cardiomyopathy, including aortic insufficiency and nonischemic dilated cardiomyopathy.
Pathophysiology
Comparison of acute and chronic mitral regurgitation

Acute mitral regurgitation
Chronic mitral regurgitation
Electrocardiogram
Normal
P mitrale, atrial fibrillation, left ventricular hypertrophy
Heart size
Normal
Cardiomegaly, left atrial enlargement
Systolic murmur
Heard at the base, radiates to the neck, spine, or top of head
Heard at the apex, radiates to the axilla
Apical thrill
May be absent
Present
Jugular venous distension
Present
Absent
The pathophysiology of mitral regurgitation can be broken into three phases of the disease process: the acute phase, the chronic compensated phase, and the chronic decompensated phase.
Acute phase
Acute mitral regurgitation (as may occur due to the sudden rupture of a chordae tendineae or papillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle. The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta (the forward cardiac output or forward stroke volume), but also the blood that regurgitates into the left atrium (the regurgitant volume). The combination of the forward stroke volume and the regurgitant volume is known as the total stroke volume of the left ventricle.
In the acute setting, the stroke volume of the left ventricle is increased (increased ejection fraction), but the forward cardiac output is decreased. The mechanism by which the total stroke volume is increased is known as the Frank-Starling mechanism.
The regurgitant volume causes a volume overload and a pressure overload of the left atrium. The increased pressures in the left atrium inhibit drainage of blood from the lungs via the pulmonary veins. This causes pulmonary congestion.
Chronic compensated phase
If the mitral regurgitation develops slowly over months to years or if the acute phase can be managed with medical therapy, the individual will enter the chronic compensated phase of the disease. In this phase, the left ventricle develops eccentric hypertrophy in order to better manage the larger than normal stroke volume. The eccentric hypertrophy and the increased diastolic volume combine to increase the stroke volume (to levels well above normal) so that the forward stroke volume (forward cardiac output) approaches the normal levels.
In the left atrium, the volume overload causes enlargement of the chamber of the left atrium, allowing the filling pressure in the left atrium to decrease. This improves the drainage from the pulmonary veins, and signs and symptoms of pulmonary congestion will decrease.
These changes in the left ventricle and left atrium improve the low forward cardiac output state and the pulmonary congestion that occur in the acute phase of the disease. Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerances.
Chronic decompensated phase
An individual may be in the compensated phase of mitral regurgitation for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mitral regurgitation. It is currently unclear what causes an individual to enter the decompensated phase of this disease. However, the decompensated phase is characterized by calcium overload within the cardiac myocytes.
In this phase, the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of mitral regurgitation, and the stroke volume of the left ventricle will decrease. The decreased stroke volume causes a decreased forward cardiac output and an increase in the end-systolic volume. The increased end-systolic volume translates to increased filling pressures of the ventricular and increased pulmonary venous congestion. The individual may again have symptoms of congestive heart failure.
The left ventricle begins to dilate during this phase. This causes a dilatation of the mitral valve annulus, which may worsen the degree of mitral regurgitation. The dilated left ventricle causes an increase in the wall stress of the cardiac chamber as well.
While the ejection fraction is less in the chronic decompensated phase than in the acute phase or the chronic compensated phase of mitral regurgitation, it may still be in the normal range (ie: > 50 percent), and may not decrease until late in the disease course. A decreased ejection fraction in an individual with mitral regurgitation and no other cardiac abnormality should alert the physician that the disease may be in its decompensated phase.
Symptoms
The symptoms associated with mitral regurgitation are dependent on which phase of the disease process the individual is in. Individuals with acute mitral regurgitation will have the signs and symptoms of decompensated congestive heart failure (ie: shortness of breath, pulmonary edema, orthopnea, paroxysmal nocturnal dyspnea), as well as symptoms suggestive of a low cardiac output state (ie: decreased exercise tolerance). Cardiovascular collapse with shock (cardiogenic shock) may be seen in individuals with acute mitral regurgitation due to papillary muscle rupture or rupture of a chordae tendineae.
Individuals with chronic compensated mitral regurgitation may be asymptomatic, with a normal exercise tolerance and no evidence of heart failure. These individuals may be sensitive to small shifts in their intravascular volume status, and are prone to develop volume overload (congestive heart failure).
Diagnostic studies
There are many diagnostic tests that have abnormal results in the presence of mitral regurgitation. These tests suggest the diagnosis of mitral regurgitation and may indicate to the physician that further testing is warranted. For instance, the electrocardiogram (ECG) in long standing mitral regurgitation may show evidence of left atrial enlargement and left ventricular hypertrophy. Atrial fibrillation may also be noted on the ECG in individuals with chronic mitral regurgitation. The ECG may not show any of these finding in the setting of acute mitral regurgitation.
The quantification of mitral regurgitation usually employs imaging studies such as echocardiography or magnetic resonance angiography of the heart.
Chest x-ray
The chest x-ray in individuals with chronic mitral regurgitation is characterized by enlargement of the left atrium and the left ventricle. The pulmonary vascular markings are typically normal, since pulmonary venous pressures are usually not significantly elevated.

Echocardiography

transesophageal echocardiogram of mitral valve prolapse
The echocardiogram is commonly used to confirm the diagnosis of mitral regurgitation. Color doppler flow on the transthoracic echocardiogram (TTE) will reveal a jet of blood flowing from the left ventricle into the left atrium during ventricular systole.
Because of the inability in getting accurate images of the left atrium and the pulmonary veins on the transthoracic echocardiogram, a transesophageal echocardiogram may be necessary to determine the severity of the mitral regurgitation in some cases.
Factors that suggest severe mitral regurgitation on echocardiography include systolic reversal of flow in the pulmonary veins and filling of the entire left atrial cavity by the regurgitant jet of MR.
Quantification of mitral regurgitation

Determination of the degree of mitral regurgitation
Degree of mitral regurgitation
Regurgitant fraction
Regurgitant Orifice area
Mild mitral regurgitation
<> 60 percent
> 0.3 cm2

The degree of severity of mitral regurgitation can be quantified by the percentage of the left ventricular stroke volume that regurgitates into the left atrium (the regurgitant fraction).
Methods that have been used to assess the regurgitant fraction in mitral regurgitation include echocardiography, cardiac catheterization, fast CT scan, and cardiac MRI.
The echocardiographic technique to measure the regurgitant fraction is to determine the forward flow through the mitral valve (from the left atrium to the left ventricle) during ventricular diastole, and comparing it with the flow out of the left ventricle through the aortic valve in ventricular systole. This method assumes that the aortic valve does not suffer from aortic insufficiency. The regurgitant fraction would be described as:
Another way to quantify the degree of mitral regurgitation is to determine the area of the regurgitant flow at the level of the valve. This is known as the regurgitant orifice area, and correlates with the size of the defect in the mitral valve. One particular echocardiographic technique used to measure the orifice area is measurement of the proximal isovelocity surface area (PISA). The flaw of using PISA to determine the mitral valve regurgitant orifice area is that it measures the flow at one moment in time in the cardiac cycle, which may not reflect the average performance of the regurgitant jet.
Treatment
The treatment of mitral regurgitation depends on the acuteness of the disease and whether there are associated signs of hemodynamic compromise.
In acute mitral regurgitation secondary to a mechanical defect in the heart (ie: rupture of a papillary muscle or chrordae tendineae), the treatment of choice is urgent mitral valve replacement. If the patient is hypotensive prior to the surgical procedure, an intra-aortic balloon pump may be placed in order to improve perfusion of the organs and to decrease the degree of mitral regurgitation.
If the individual with acute mitral regurgitation is normotensive, vasodilators may be of use to decrease the afterload seen by the left ventricle and thereby decrease the regurgitant fraction. The vasodilator most commonly used is nitroprusside.
Individuals with chronic mitral regurgitation can be treated with vasodilators as well. In the chronic state, the most commonly used agents are ACE inhibitors and hydralazine. Studies have shown that the use of ACE inhibitors and hydralazine can delay surgical treatment of mitral regurgitation1,2. The current guidelines for treatment of mitral regurgitation limit the use of vasodilators to individuals with hypertension, however.
There are two surgical options for the treatment of mitral regurgitation: mitral valve replacement and mitral valve repair.
Indication for surgery
Indications for surgery for chronic mitral regurgitation3
Symptoms
LV EF
LVESD
NYHA II - IV
> 60 percent
< title="Pulmonary artery" href="http://en.wikipedia.org/wiki/Pulmonary_artery">Pulmonary artery systolic pressure ≥ 50 mmHg
Indications for surgery for chronic mitral regurgitation include signs of left ventricular dysfunction. These include an ejection fraction of less than 60 percent and a left ventricular end systolic dimension (LVESD) of greater than 45 mm.
References
1. Greenberg BH, Massie BM, Brundage BH, Botvinick EH, Parmley WW, Chatterjee K. Beneficial effects of hydralazine in severe mitral regurgitation. Circulation. 1978 Aug;58(2):273-9. (Medline abstract)
2. Hoit BD. Medical treatment of valvular heart disease. Curr Opin Cardiol. 1991 Apr;6(2):207-11. (Medline abstract)
3. Bono w et al. ACC/AHA Guidelines for the Management of Patients With Valvular Heart Disease. ACC/AHA Task Force Report. JACC Vol. 32, No. 5, November 1998:1486-1588 (Full article)
See also
Mitral valve
Left ventricle
Left atrium
Systole (medicine)
Diastole
Cardiac output
Mitral valve prolapse

Libman-Sacks endocarditis

2007-01-11T21:01:00.001-08:00

From Wikipedia, the free encyclopedia
Libman-Sacks endocarditis is a form of nonbacterial endocarditis that is seen in systemic lupus erythematosus. It was named after American physicians Emanuel Libman and Benjamin Sacks. It is the most common cardiac manifestation of lupus. The vegetations are formed from strands of fibrin, neutrophils, lymphocytes, and histiocytes. The mitral valve is typically affected, and the vegetations occur on the ventricular surface of the valve. Libman-Sacks lesions rarely produce significant valve dysfunction and the lesions only rarely embolize. The pathology is the same as nonbacterial thrombotic endocarditis except focal necrosis (hematoxylin bodies) can be found only in Libman-sacks endocarditis.
Retrieved from "http://en.wikipedia.org/wiki/Libman-Sacks_endocarditis"

Heart valve dysplasia

2007-01-11T21:00:00.000-08:00

Heart valve dysplasia is a congenital heart defect which in dogs and cats affects the aortic, pulmonary, mitral, and tricuspid heart valves. Pulmonary valve stenosis and aortic valve stenosis are discussed separately. Dysplasia of the mitral and tricuspid valves can cause leakage of blood or stenosis.
Dysplasia of the mitral and tricuspid valves - also known as the atrioventricular (AV) valves - can appear as thickened, shortened, or notched valves. The chordae tendinae can be fused or thickened. The papillary muscles can be enlarged or atrophied. The cause is unknown, but genetics play a large role. Dogs and cats with tricuspid valve dysplasia often also have an open foramen ovale, an atrial septal defect, or inflammation of the right atrial epicardium.[1] In dogs, tricuspid valve dysplasia can be similar to Ebstein's anomaly in humans.[2]
Mitral valve stenosis is one of the most common congenital heart defects in cats. In dogs, it is most commonly found in Great Danes, German Shepherd Dogs, Bull Terriers, Golden Retrievers, Newfoundlands, and Mastiffs. Tricuspid valve dysplasia is most common in the Old English Sheepdog, German Shepherd Dog, Weimaraner, Labrador Retriever, and Great Pyrenees.[1] It is inherited in the Labrador Retriever.[3]
The disease and symptoms are similar to progression of acquired valve disease in older dogs. Valve leakage leads to heart enlargement, arrhythmias, and congestive heart failure. Heart valve dysplasia can be tolerated for years or progress to heart failure in the first year of life. Diagnosis is with an echocardiogram. There is a poor prognosis with significant heart enlargement.
References
a b Ettinger, Stephen J.;Feldman, Edward C. (1995). Textbook of Veterinary Internal Medicine, 4th ed., W.B. Saunders Company. ISBN 0-7216-6795-3.
Abbott, Jonathan A. (2000). Small Animal Cardiology Secrets, 1st ed., Hanley & Belfus, Inc.. ISBN 1-56053-352-8.
Famula, Thomas R.; Siemens, Lori M.; Davidson, Autumn P.; Packard, Martin (2002). "Evaluation of the genetic basis of tricuspid valve dysplasia in Labrador Retrievers". American Journal of Veterinary Research 63 (6): 816-820. Retrieved on 2006-08-26.

Endocarditis

2007-01-11T20:53:00.000-08:00

Endocarditis

EndocarditisClassifications and external resources

Bartonella henselae bacilli in cardiac valve of a patient with blood culture-negative endocarditis. The bacilli appear as black granulations.

Endocarditis is an inflammation of the inner layer of the heart, the endocardium. The most common structures involved are the heart valves.
Endocarditis can be classified by etiology as either infective or non-infective, depending on whether a microorganism is the source of the problem.
Contents

1 Infective endocarditis
1.1 Classification
1.2 Etiology and pathogenesis
1.3 Clinical and pathological features
1.4 Diagnosis
1.5 Micro-organisms responsible
1.6 Treatment
2 Non-infective endocarditis
3 References
4 External links
//
] Infective endocarditis
As the valves of the heart do not actually receive any blood supply of their own, which may be surprising given their location, defense mechanisms (such as white blood cells) cannot enter. So if an organism (such as bacteria) establish hold on the valves, the body cannot get rid of them.
Normally, blood flows smoothly through these valves. If they have been damaged (for instance in rheumatic fever) bacteria have a chance to take hold.
Classification
Traditionally, infective endocarditis has been clinically divided into acute and subacute (between acute and chronic) endocarditis. This classifies both the tempo of progression and severity of disease. Thus subacute bacterial endocarditis (SBE) is often due to streptococci of low virulence and mild to moderate illness which progresses slowly over weeks and months, while acute bacterial endocarditis (ABE) is a fulminant illness over days to weeks, and is more likely due to Staphylococcus aureus which has much greater virulence, or disease-producing capacity.
This terminology is now discouraged. The terms short incubation (meaning less than about six weeks), and long incubation (greater than about six weeks) are preferred despite the lack of advantage in meaning.
Infective endocarditis may also be classified as culture-positive or culture-negative. Culture-negative endocarditis is due to micro-organisms that require a longer period of time to be identified in the laboratory. Such organisms are said to be fastidious because they have demanding growth requirements. Some pathogens responsible for culture-negative endocarditis include Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria.
Finally, the distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important.
The Russian classification includes "endocarditis in narcotic abusers" in addition to above given classification, as this disease is very common in narcotic drug users who inject with non-sterile injections/syringes.
Etiology and pathogenesis
As previously mentioned, altered blood flow around the valves is a risk factor in obtaining endocarditis. The valves may be damaged congenitally, from surgery, by auto-immune mechanisms, or simply as a consequence of old age. The damaged part of a heart valve becomes covered with a blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE).
In a healthy individual, a bacteraemia (where bacteria get into the blood stream through a minor cut or wound) would normally be cleared quickly with no adverse consequences. If a heart valve is damaged and covered with a piece of a blood clot, the valve provides a place for the bacteria to attach themselves and an infection can be established.
The bacteraemia is often caused by minor dental procedures, such as a tooth removal. It is important that a dentist is told of any heart problems before commencing.
Another group of causes result from a high number of bacteria getting into the bloodstream. Colorectal cancer, serious urinary tract infections, and IV drug use can all introduce large numbers of bacteria. With a large number of bacteria, even a normal heart valve may be infected. A more virulent organism (such as Staphylococcus aureus) is usually responsible for infecting a normal valve.
Intravenous drug users tend to get their right heart valves infected because the veins that are injected enter the right side of the heart. The injured valve is most commonly affected when there is a pre-existing disease. (In rheumatic heart disease this is the aortic and the mitral valves, on the left side of the heart.)
Clinical and pathological features
Fever (often spiking)
Continuous presence of micro-organisms in the bloodstream determined by serial collection of blood cultures
Vegetations on valves on echocardiography
Septic emboli, causing circulatory problems (stroke, gangrene of fingers)
Chronic renal failure
Osler's nodes (painful subcutaneous lesions in the distal fingers)
Janeway lesions (painless hemorrhagic cutaneous lesions on the palms and soles)
Roth spots on the retina
Conjunctival petechiae
A new or changing heart murmur, particularly murmurs suggestive of valvular incompetence
Splinter hemorrhages
Diagnosis
In general, a patient should fulfill the Duke Criteria [1] in order to establish the diagnosis of endocarditis.
As the Duke Criteria relies heavily on the results of echocardiography, research has addressed when to order an echocardiogram by using signs and symptoms to predict occult endocarditis among patients with intravenous drug abuse[2][3][4] and among non drug abusing patients [5][6]. Unfortunately, this research is over 20 years old and it is possible that changes in the epidemiology of endocarditis and bacteria such as staphylococcus make the following estimates incorrectly low.
Among patients who do not use illicit drugs and have a fever in the emergency room, there is a less than 5% chance of occult endocarditis. Mellors [6] in 1987 found no cases of endocarditis nor of staphylococcal bacteremia among 135 febrile patients in the emergency room. The upper confidence interval for 0% of 135 is 5%, so for statistical reasons alone, there is up to a 5% chance of endocarditis among these patients. In contrast, Leibovici [5] found that among 113 non-selected adults admitted to the hospital because of fever there were two cases (1.8% with 95%CI: 0% to 7%) of endocarditis.
Among patients who do use illicit drugs and have a fever in the emergency room, there is about a 10% to 15% prevalence of endocarditis. This estimate is not substantially changed by whether the doctor believes the patient has a trivial explanation for their fever[4]. Weisse[2] found that 13% of 121 patients had endocarditis. Marantz [4] also found a prevalence of endocarditis of 13% among such patients in the emergency room with fever. Samet [3] found a 6% incidence among 283 such patients, but after excluding patients with initially apparent major illness to explain the fever (including 11 cases of manifest endocarditis), there was a 7% prevalence of endocarditis.
Among patients with staphylococcal bacteremia (SAB), one study found a prevalence of 29% in community-acquired SAB versus 5% in nosocomial SAB[7]. However, only 2% of strains were resistant to methicillen and so these numbers may be low in areas of higher resistance.
EchocardiographyThe transthoracic echocardiogram has a sensitivity and specificity of approximately 65% and 95% if the echocardiographer believes there is 'probabable' or 'almost certain' evidence of endocarditis[8][9].
[Discussion is needed here, including transthoracic versus transesophageal]
Micro-organisms responsible
Many types of organism can cause infective endocarditis. These are generally isolated by blood culture, where the patient's blood is removed, and any growth is noted and identified.
Alpha-haemolytic streptococci, that are present in the mouth will often be the organism isolated if a dental procedure caused the bacteraemia.
If the bacteraemia was introduced through the skin, such as contamination in surgery, during catheterisation, or in an IV drug user, Staphylococcus aureus is common.
A third important cause of endocarditis is Enterococci. These bacteria enter the bloodstream as a consequence of abnormalities in the gastrointestinal or urinary tracts. Enterococci are increasingly recognized as causes of nosocomial or hospital-acquired endocarditis. This contrasts with alpha-haemolytic streptococci and Staphylococcus aureus which are causes of community-acquired endocarditis.
Some organisms, when isolated, give valuable clues to the cause, as they tend to be specific.
Candida albicans, a yeast, is associated with IV drug users and the immunocompromised.
Pseudomonas species, which are very resilient organisms that thrive in water, may contaminate street drugs that have been contaminated with drinking water.
Streptococcus bovis, which is part of the natural flora of the bowel, tends to present when the patient has bowel cancer.
HACEK organisms are a group of bacteria that live on the dental gums, and are associated with IV drug users who contaminate their needles with saliva.
Treatment
High dose antibiotics are administered by the intravenous route to maximize diffusion of antibiotic molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because neither the heart valves nor the vegetations adherent to them are supplied by blood vessels. Antibiotics are continued for a long time, typically two to six weeks. Surgical removal of the valve is necessary in patients who fail to clear micro-organisms from their blood in response to antibiotic therapy, or in patients who develop cardiac failure resulting from destruction of a valve by infection. A removed valve is usually replaced with an artificial valve which may either be mechanical (metallic) or obtained from an animal such as a pig; the latter are termed bioprosthetic valves. Infective endocarditis is associated with a 25% mortality.
Non-infective endocarditis
Non-infective or marantic endocarditis is rare. A form of sterile endocarditis is termed Libman-Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and the antiphospholipid syndrome. Non-infective endocarditis may also occur in patients with cancers, particularly mucinous adenocarcinoma.
References
^ Durack D, Lukes A, Bright D (1994). "New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service.". Am J Med 96 (3): 200-9. PMID 8154507.
^ a b Weisse A, Heller D, Schimenti R, Montgomery R, Kapila R (1993). "The febrile parenteral drug user: a prospective study in 121 patients.". Am J Med 94 (3): 274-80. PMID 8452151.
^ a b Samet J, Shevitz A, Fowle J, Singer D (1990). "Hospitalization decision in febrile intravenous drug users.". Am J Med 89 (1): 53-7. PMID 2368794.
^ a b c Marantz P, Linzer M, Feiner C, Feinstein S, Kozin A, Friedland G (1987). "Inability to predict diagnosis in febrile intravenous drug abusers.". Ann Intern Med 106 (6): 823-8. PMID 3579068.
^ a b Leibovici L, Cohen O, Wysenbeek A (1990). "Occult bacterial infection in adults with unexplained fever. Validation of a diagnostic index.". Arch Intern Med 150 (6): 1270-2. PMID 2353860.
^ a b Mellors J, Horwitz R, Harvey M, Horwitz S (1987). "A simple index to identify occult bacterial infection in adults with acute unexplained fever.". Arch Intern Med 147 (4): 666-71. PMID 3827454.
^ Kaech C, Elzi L, Sendi P, Frei R, Laifer G, Bassetti S, Fluckiger U (2006). "Course and outcome of Staphylococcus aureus bacteraemia: a retrospective analysis of 308 episodes in a Swiss tertiary-care centre.". Clin Microbiol Infect 12 (4): 345-52. PMID 16524411.
^ Shively B, Gurule F, Roldan C, Leggett J, Schiller N (1991). "Diagnostic value of transesophageal compared with transthoracic echocardiography in infective endocarditis.". J Am Coll Cardiol 18 (2): 391-7. PMID 1856406. ^ Erbel R, Rohmann S, Drexler M, Mohr-Kahaly S, Gerharz C, Iversen S, Oelert H, Meyer J (1988). "Improved diagnostic value of echocardiography in patients with infective endocarditis by transoesophageal approach. A prospective study.". Eur Heart J 9 (1): 43-53. PMID 3345769

Aortic valve stenosis

2007-01-11T20:46:00.000-08:00

Aortic valve stenosis
Aortic valve stenosis (AS) is a heart condition caused by the incomplete opening of the aortic valve.
The aortic valve controls the direction of blood flow from the left ventricle to the aorta. When in good working order, the aortic valve does not impede the flow of blood between these two spaces. Under some circumstances, the aortic valve becomes narrower than normal, impeding the flow of blood. This is known as aortic valve stenosis, or aortic stenosis, often abbreviated as AS.
Contents

1 Pathophysiology
2 Etiology
3 Prevalence
4 Physical examination
5 The electrocardiogram (ECG) in aortic stenosis
6 Major complications of aortic stenosis
6.1 Congestive heart failure
6.2 Syncope
6.3 Angina
7 Associated symptoms
8 Cautions
9 Calculation of valve area
9.1 Planimetry
9.2 The continuity equation
9.3 The Gorlin equation
9.4 The Hakki equation
10 References

Frank-Starling law of the heart

2007-01-11T20:45:00.000-08:00

Frank-Starling law of the heart
The Frank-Starling law of the heart (also known as Starling's law or the Frank-Starling mechanism) states that the more the ventricle is filled with blood during diastole (end-diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume).
Effectively, this means that the force of contraction will increase as the heart is filled with more blood and is a direct consequence of the effect of an increasing load on a single muscle fibre. The force that any single muscle fibre generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibres is related to the end-diastolic volume of the ventricle. In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometres, a length which is rarely exceeded in the normal heart.
This can be seen most dramatically in the case of a premature ventricular contraction. The premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction will come at its regular time, the filling time for the LV increases, causing an increased LV end diastolic volume. Because of the Frank-Starling law, the next ventricular contraction will be more forceful, causing the ejection of the larger than normal volume of blood, and bringing the LV end-systolic volume back to baseline.
For example, during venoconstriction the end diastolic volume increases, increasing preload, this will increase stroke volume. The heart will pump what it receives.
The above is true of healthy myocardium. In the failing heart, the more the myocardium is dilated, the weaker it can pump, as it then reverts to Laplace's law.
History
The law is named after the two physiologists, Otto Frank and Ernest Starling who first described it.
Long before the development of the sliding filament hypothesis and our understanding that active tension depends on the sarcomere's length, in 1914 Ernest Starling hypothesized that "the mechanical energy set free in the passage from the resting to the active state is a function of the length of the fiber." Therefore, the initial length of myocardial fibers determines the work done during the cardiac cycle.
See also
Starling equation

Cardiac output

2007-01-11T20:44:00.000-08:00

Cardiac output
From Wikipedia, the free encyclopedia
Cardiac output is the volume of blood being pumped by the heart, in particular a ventricle in a minute. It is equal to the heart rate multiplied by the stroke volume.
Therefore, if there are 70 beats per minute, and 70 ml blood is ejected with each beat of the heart, the cardiac output is 4900 ml/minute. This value is typical for an average adult at rest, although cardiac output may reach up to 30 liters/minute during extreme exercise.
When cardiac output increases in a healthy but untrained individual, most of the increase can be attributed to increase in heart rate. Change of posture, increased sympathetic nervous system activity, and decreased parasympathetic nervous system activity can also increase cardiac output. Heart rate can vary by a factor of approximately 3, between 60 and 180 beats per minute, whilst stroke volume can vary between 70 and 120 ml, a factor of only 1.7.
Contents

1 Measuring Cardiac Output
1.1 The Fick Principle
1.2 Dilution methods
1.3 Doppler method
1.4 Pulmonary Artery Thermodilution (Trans-right-heart Thermodilution)
1.5 PulseCO and PiCCO Technology
1.6 FloTrac technology
1.7 Impedance plethysmography
2 Equations

//
Measuring Cardiac Output
There are many invasive and several non-invasive methods for measuring cardiac output in mammals.
A non-invasive method, often used in teaching students of physiology, reasons as follows:
The pressure in the heart rises as blood is forced into the aorta
The more stretched the aorta, the greater the pulse pressure
In healthy young subjects, each additional 2ml of blood results in a 1 mmHg rise in pressure
Therefore Stroke volume = 2ml x Pulse pressure
Cardiac Output is therefore 2ml x Pulse Pressure x Heart Rate
The Fick Principle
Fick principle involves measuring:
VO2 consumption per minute using a spirometer (with the subject re-breathing air) and a CO2 absorber
the oxygen content of blood taken from the pulmonary artery (representing venous blood)
the oxygen content of blood from a cannula in a peripheral artery (representing arterial blood)
From these values, we know that:
where CO = Cardiac Output, CA = Oxygen concentration of arterial blood and CV = Oxygen concentration of venous blood.
This allows us to say
and therefore calculate cardiac output.
Dilution methods
This method measures how fast flowing blood can dilute an indicator substance introduced to the circulatory system, usually using a pulmonary artery catheter. Early methods used a dye, the cardiac output being inversely proportional to the concentration of dye sampled downstream. More specifically, the cardiac output is equal to the quantity of indicator dye injected divided by the area under the dilution curve measured downstream (the Stewart-Hamilton equation):
The trapezoid rule is often used as an approximation of this integral. A more modern technique is to use cold saline as the indicator, and then measure the change in temperature downstream. Cardiac output can be affected by the phase of respiration, especially under mechanical ventilation, and should therefore be measured at a defined phase of the respiratory cycle (typically end-expiratory).
Doppler method
This technique uses ultrasound and the Doppler effect to measure cardiac output. The blood velocity through the aorta cause a 'Doppler shift' in the frequency of the returning ultrasound waves. Echocardiographic measurement of the aortic root cross-sectional area (or, alternatively, the descending aorta area) multiplied by the measured velocity time integral of flow through that area and heart rate, yields the cardiac output.
Pulmonary Artery Thermodilution (Trans-right-heart Thermodilution)
The pulmonary artery catheter (PAC) also known as the Swan-Ganz thermodilution catheter provides right heart blood pressures. Using the PAC thermodilution cardiac output can be measured. Modern catheters are fitted with a distal heated filament, which allows automatic thermodilution measurement via heating the blood and measuring the resultant thermodilution trace. This provides near continuous cardiac output monitoring. The PAC is used in assessment of haemodynamic status and direct intracardiac and pulmonary artery pressures. The distal (pulmonary artery) port allows sampling of mixed venous blood for the assessment of oxygen transport and the calculation of derived parameters such as oxygen consumption, oxygen utilization coefficient, and intrapulmonary shunt fraction.
The PAC is balloon tipped which can be inflated to occlude the pulmonary artery, the subsequence back pressure is a reflection of the left atrial filling pressure and until recently was considered a good indicator of preload.
The pulmonary artery wedge pressure (PAWP) has been superseded by more reliable techniques such as intrathoracic blood volume or stroke volume variation as indicators of volume status. The PAC also allows sampling of mixed venous blood, the oxygen content of which can be used to indicate the adequacy of overall oxygen delivery. The PAC has fallen out of common use as clinicians favour less invasive, less hazardous technologies for monitoring haemodynamic status. Considerable controversy exists over whether the PAC increases mortality; recent studies suggest it neither increases nor improves mortality. Complications such as cardiac tamponade, pulmonary artery rupture and air emboli are a danger.
PulseCO and PiCCO Technology
PiCCO (PULSION Medical Systems AG, Munich, Germany) and PulseCO (LiDCO Ltd, London, England) generate continuous cardiac output by analysis of the arterial blood pressure waveform. In both cases, an independent technique is required to provide initial calibration of the continuous cardiac output analysis, as arterial waveform analysis cannot account for unmeasured variables such as compliance of the vascular tree.
In the case of PiCCO, transpulmonary thermodilution is used as the independent technique. This uses the Stewart-Hamilton principle outlined above, but measured from central venous line to a central (i.e. femoral or axillary) arterial line. The cardiac output derived from this cold-saline thermodilution is used to calibrate the arterial pulse contour analysis, which can then provide continuous cardiac output monitoring. The PiCCO algorithm is dependent on blood pressure waveform morphology (i.e. mathematical analysis of the pulse contour waveform) and calculates continuous cardiac output as described by Wesseling and co-workers. Transpulmonary thermodilution spans right heart, pulmonary circulation and left heart; this allows further mathematical analysis of the thermodilution curve, giving measurements of cardiac filling volumes (GEDV), intrathoracic blood volume, and extravascular lung water.
In the case of LiDCO, the independent calibration technique is lithium dilution, again using the Stewart-Hamilton principle. Lithium dilution has the advantage of being usable from a peripheral vein to a peripheral arterial line; however, it does not provide information on cardiac filling volumes and extravascular lung water. Dilution measurements cannot be performed too frequently, and can be subject to error in the presence of certain muscle relaxants. The PulseCO algorithm used by LiDCO is based on pulse power derivation and is not dependent on waveform morphology.
FloTrac technology
A more recent development is the FloTrac system which can derive cardiac output from the arterial waveform without the need for an independent method of calibration. Hence continuous cardiac output can be measured directly from a conventional arterial line. This method has yet to be extensively evaluated, but early studies suggest that it is accurate. Another similar system that uses the arterial pulse is the pressure recording analytical method (PRAM). Neither the FloTrac nor the PRAM require external calibration.
Impedance plethysmography
This advanced technique was developed by NASA, it measures changing impedance in the chest as the heart beats to calculate cardiac output. This technique has progressed clinically (often called BioZ, i.e. biologic impedance, as promoted by the leading manufacturer in the US) and allows low cost, non-invasive estimations of cardiac output and total peripheral resistance, using only 4 skin electrodes, with minimal removal of clothing in physician offices having the needed equipment.
Equations
By simplifying D'arcy's Law, we get the equation that
When applied to the circulatory system, we get:
Where ABP = Aortic (or Arterial) Blood Pressure, RAP = Right Atrial Pressure and TPR = Total Peripheral Resistance.
However, as ABP>>RAP, and RAP is approximately 0, this can be simplified to:
Physiologists will often re-arrange this equation, making ABP the subject, to study the body's responses.
As has already been stated, Cardiac Output is also the product of the heart rate and the stroke volume, which allows us to say:

Afterload

2007-01-11T20:43:00.000-08:00

Ventricular systole. (Red arrow is path from left ventricle to aorta. Afterload is largely dependent upon aortic pressure.
In cardiac physiology, afterload is the tension produced by a chamber of the heart in order to contract. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
Afterload can also be described as the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber. Everything else held equal, as afterload increases, cardiac output decreases.
In the case of the left ventricle, the afterload is a consequence of the blood pressure, since the pressure in the ventricle must be greater than the blood pressure in order to open the aortic valve.
Pathology
Disease processes that increase the left ventricular afterload include increased blood pressure and aortic valve disease.
Hypertension (Increased blood pressure) increases the left ventricular afterload because the left ventricle has to work harder to eject blood into the aorta. This is because the aortic valve won't open until the pressure generated in the left ventricle is higher than the elevated blood pressure.
Aortic stenosis increases the afterload because the left ventricle has to overcome the pressure gradient caused by the stenotic aortic valve in addition to the blood pressure in order to eject blood into the aorta. For instance, if the blood pressure is 120/80, and the aortic valve stenosis creates a trans-valvular gradient of 30 mmHg, the left ventricle has to generate a pressure of 150 mmHg in order to open the aortic valve and eject blood into the aorta.
Aortic insufficiency increases afterload because a percentage of the blood that is ejected forward regurgitates back through the diseased aortic valve. This leads to elevated systolic blood pressure.
Mitral regurgitation decreases the afterload. During ventricular systole, the blood can regurgitate through the diseased mitral valve as well as be ejected through the aortic valve. This means that the left ventricle has to work less to eject blood, causing a decreased afterload.
See also
Preload Cardiac output

Afterload

Preload (cardiology)

2007-01-11T20:30:00.000-08:00

Heart during ventricular diastole.
In cardiac physiology, preload is the volume of blood present in a ventricle of the heart, after passive filling and atrial contraction. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
Preload is theoretically most accurately described as the initial stretching of cardiac myocytes prior to contraction. This cannot be measured in vivo and therefore other measurements are used as estimates. Estimation is inaccurate, for example in a chronically dilated ventricle new sarcomeres may have formed in the heart muscle allowing the relaxed ventricle to appear enlarged.
Preload is affected by venous blood pressure and the rate of venous return. These are affected by venous tone and volume of circulating blood.
Preload is the ventricular End-diastolic volume. Preload increases with exercise (slightly), increasing blood volume (overtransfusion) and excitement (sympathetics).
See also
Afterload
Cardiac output Frank-Starling law of the heart

Aortic valve replacement

2007-01-11T20:23:00.000-08:00

Aortic valve replacement is a surgical procedure in which a patient's aortic valve is replaced by a different valve. The aortic valve can be affected by a range of diseases and require aortic valve replacement. The valve can either become leaky (regurgitant or insufficient) or stuck partially shut (stenotic). Aortic valve replacement currently requires open heart surgery. As of 2006, percutaneous aortic valve replacement is being researched, which allows the implantion of valves using a catheter without open heart surgery.
Contents

• 1 Types of Heart Valves
o 1.1 Mechanical, Tissue and Homograft Valves
o 1.2 Durability
• 2 Surgical Procedure
• 3 Hospital Stay and Recovery Time
• 4 Surgical Outcome and Risk of Procedure
• 5 See also

Types of Heart Valves
Mechanical, Tissue and Homograft Valves
There are two basic types of artificial heart valve, mechanical valves and tissue valves. Tissue heart valves are usually made from animal tissues, either animal heart valve tissue or animal pericardial tissue. The tissue is treated to prevent rejection and to prevent calcification.
There are alternatives to animal tissue valves. In some cases a human aortic valve can be implanted. These are called homografts. Homograft valves are donated by patients and harvested after the patient expires. The durability of homograft valves is probably the same for porcine tissue valves. Another procedure for aortic valve replacement is the Ross procedure or pulmonary autograft. The Ross procedure, named after Dr. Donald Ross - one of the pioneers in cardiac surgery in the U.K., is surgery where the aortic valve is removed and replaced with the patient's own pulmonary valve. A pulmonary homograft (pulmonary valve taken from a cadaver) is then used to replace the patients own pulmonary valve. This procedure was first used in 1967.
Although mechanical valves are long-lasting and generally only one surgery is needed, there is an increased risk of blood clots forming with mechanical valves. As a result, mechanical valve recipients must generally take anti-coagulant drugs such as warfarin for the rest of their lives, which effectively makes them borderline hemophiliacs.
Durability
Mechanical valves are designed to outlast the patient, and have typically been stress-tested to last several hundred years. Tissue valves will typically last between 10-15 years. In younger patients, tissue valves will wear out faster. For this reason, older patients are often recommended tissue valves.
Surgical Procedure
Aortic valve replacement is most frequently done through a median sternotomy, meaning the chestbone is sawed through. Once the pericardium has been opened, the patient is placed on cardiopulmonary bypass machine, also referred to as the heart-lung machine. This machine takes over the task of breathing for the patient and pumping his blood around while the surgeon replaces the heart valve.
Once the patient is on bypass, an incision is made in the aorta. The surgeon then removes the patient's diseased aortic valve and a mechanical or tissue valve is put in its place. Once the valve is in place and the aorta has been closed, the patient is taken off the heart-lung machine. Transesophageal echocardiogram (or TEE, an ultra-sound of the heart done through the esophagus) can be used to verify that the new valve is functioning properly. Pacing wires are usually put in place, so that the heart can be manually paced should any complications arise after surgery. Drainage tubes are also inserted to drain fluids from the chest and pericardium following surgery. These are usually removed within 36 hours while the pacing wires are generally left in place until right before the patient is discharged from the hospital.
Hospital Stay and Recovery Time
Immediately after aortic valve replacement, the patient will frequently stay in a Cardiothoracic Intensive Care Unit for 12-36 hours. After this, the patient is often moved to a lower-dependency unit and then to a cardiac surgery ward. Total time spent in hospital following surgery is usually between 4 and 10 days, unless complications arise.
Recovery from aortic valve replacement will take 1-3 months if the patient is in good health. Patients are advised not to do any heavy lifting for 6-8 weeks following surgery to avoid damaging the sternum (breast bone) while it heals.
Surgical Outcome and Risk of Procedure
The risk of death or serious complications from aortic valve replacement is typically quoted as being between 1-5%, depending on the health and age of the patient, as well as the skill of the surgeon. Older patients, as well as more fragile ones, are sometimes inelegible for surgery because of elevated risks.
See also
• Aortic valve repair
• Mitral valve repair
Mitral valve repair
From Wikipedia, the free encyclopedia
Mitral valve repair is an open heart procedure performed by cardiothoracic surgeons to treat stenosis (narrowing) or regurgitation (leakage) of the mitral valve. The mitral valve is the "inflow valve" for the left side of the heart. Blood flows from the lungs, where it picks up oxygen, and into the heart through the mitral valve. When it opens, the mitral valve allows blood to flow into the heart's main pumping chamber called the left ventricle. It then closes to keep blood from leaking back into the lungs when the ventricle contracts (squeezes) to push blood out to the body. It has two flaps, or leaflets.
The techniques of mitral valve repair include inserting a cloth-covered ring around the valve to bring the leaflets into contact with each other (annuloplasty), removal of redundant/loose segments of the leaflets (quadrangular resection), re-suspension of the leaflets with artificial (Gore-Tex) cords, and more recently the "bow-tie" procedure where a single stitch allows to repair the valve non-surgically.
Occasionally, the mitral valve is abnormal from birth (congenital). More often the mitral valve becomes abnormal with age (degenerative) or as a result of rheumatic fever. In rare instances the mitral valve can be destroyed by infection or a bacterial endocarditis. Mitral regurgitation may also occur as a result of ischemic heart disease (coronary artery disease).
A history of mitral valve repair
The development of the heart-lung machine in the 1950s paved the way for replacement of the mitral valve with an artificial valve in the 1960s. For decades, mitral valve replacement was the standard operation for a patient with a diseased mitral valve.
There are significant downsides to an artificial mitral valve. Infection of the prosthetic valve can occur, which is very dangerous. Patients with mechanical heart valves are required to take blood thinners for the rest of their lives and are at risk for bleeding complications. Artificial tissue valves will last between 10 and 15 years, placing the patient at risk of a second operation to replace the valve. The risk of stroke with an artificial mitral valve is significant (approximately 1 % per year).
In the last two decades, some surgeons have embraced surgical techniques to repair, rather than replace, the mitral valve. These techniques were pioneered by a French heart surgeon, Dr. Alain F. Carpentier, who published a landmark paper in the mid 1980s entitled The French Correction.
See also
• Aortic valve repair
• Cardiac surgery

Aortic insufficiency

2007-01-11T20:21:00.000-08:00

Aortic insufficiency
Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle.
Aortic insufficiency can be due to abnormalities of either the aortic valve or the aortic root (the beginning of the aorta).
Contents

1 Etiology
2 Physiology
3 Pathophysiology
4 Hemodynamics
4.1 Acute aortic insufficiency
4.2 Chronic aortic insufficiency
5 Physical examination
6 Diagnostic evaluation
7 Prognosis
8 Treatment
8.1 Medical treatment
8.2 Surgical treatment
9 References
10 See also
//
Etiology
About half of the cases of aortic insufficiency are due to the aortic root dilatation (annuloaortic ectasia), which is idiopathic in over 80% of cases, but otherwise occurs with aging and hypertension, Marfan syndrome, aortic dissection, and syphilis. In about 15% the cause is innate bicuspidal aortic valve, while another 15% cases are due to retraction of the cusps as part of postinflammatory processes of endocarditis in rheumatic fever and various collagen vascular diseases.
Physiology
In individuals with a normally functioning aortic valve, the valve is only open when the pressure in the left ventricle is higher than the pressure in the aorta. This allows the blood to be ejected from the left ventricle into the aorta during ventricular systole. After ventricular systole, the pressure in the ventricle decreases, as the ventricle relaxes and gets ready to fill up with blood from the left atrium. This relaxation of the left ventricle (early ventricular diastole) causes a fall in the pressure in the left ventricle. When the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve will close, preventing blood from going from the aorta back into the left ventricle. The amount of blood that is ejected by the heart is known as the stroke volume or stroke work. Under normal conditions, the entire stroke volume delivers oxygenated blood to the body.
Pathophysiology
In aortic insufficiency, when the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve is not able to completely close. This causes a leaking of blood from the aorta into the left ventricle. This means that some of the blood that was already ejected from the heart is regurgitating back into the heart. The percentage of blood that regurgitates back through the aortic valve due to AI is known as the regurgitant fraction. For instance, if an individual with AI has a stroke volume of 100 ml and during ventricular diastole 25 ml regurgitates back through the aortic valve, the regurgitant fraction is 25%. This regurgitant flow causes a decrease in the diastolic blood pressure in the aorta, and therefore an increase in the pulse pressure (systolic pressure - diastolic pressure)- not to be confounded with hypertension.
Since some of the blood that is ejected during systole regurgitates back during diastole, there is decreased effective forward flow in AI.
AI causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart.
The pressure overload (due to elevated pulse pressure and hypertension) causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI. The concentric hypertrophy is due to the hypertension associated with AI, while the eccentric hypertrophy is due to volume overload caused by the regurgitant fraction.
Hemodynamics
The hemodynamic sequelae of AI are dependent on the rate of onset of AI. Acute AI and chronic AI will have different hemodynamics and individuals will have different signs and symptoms.
[edit] Acute aortic insufficiency
In acute AI, as may be seen with acute perforation of the aortic valve due to endocarditis, there will be a sudden increase in the volume of blood in the left ventricle. The ventricle, unable to deal with the sudden change in volume, decompensates. The filling pressure of the left ventricle will increase. This causes pressure in the left atrium to rise, and the individual will develop congestive heart failure.
Severe acute aortic insufficiency is considered a medical emergency. There is a high mortality rate if the individual does not undergo immediate surgery for aortic valve replacement. If the acute AI is due to aortic valve endocarditis, there is a risk that the new valve may become seeded with bacteria. However, this risk is small.1
Acute AI may be difficult to diagnose clinically, since the left ventricle had not yet developed the eccentric hypertrophy and dilatation that allow an increased stroke volume and bounding peripheral pulses that are common in chronic AI. On auscultation, there may be a short diastolic murmur and a soft S1. S1 is soft because the elevated filling pressures close the mitral valve in diastole (rather than the mitral valve being closed at the beginning of systole).
Chronic aortic insufficiency
If the individual survives the initial hemodynamic derailment that acute AI presents as, the left ventricle adapts by eccentric hypertrophy and dilatation of the left ventricle, and the volume overload is compensated for. The left ventricular filling pressures will revert to normal and the individual will no longer have overt heart failure.
In this compensated phase, the individual may be totally asymptomatic and may have normal exercise tolerance.
Eventually (typically after a latency period) the left ventricle will become decompensated, and filling pressures will increase. While most individuals would complain of symptoms of congestive heart failure to their physicians, some enter this decompensated phase asymptomatically. Proper treatment for AI involves aortic valve replacement prior to this decompensation phase.
Physical examination
The physical examination of an individual with aortic insufficiency involves auscultation of the heart to listen for the murmur of aortic insufficiency and related heart sounds. The murmur of chronic aortic insufficiency is typically desribed as early diastolic and decresendo, which is best heard at aortic area when the patient is sitted and leans forward with breath held in expiration. The murmur is usually soft and seldom causes thrill. If there is radiation to the right parasternal region, ascending aortic aneurysm has to be excluded.
There is there increased stroke volume of the left ventricle due to volume overload, an ejection systolic 'flow' murmur may also be present when auscultating the same aortic area. Unless there is cocomittant aortic valve stenosis, the murmur should not start with an ejection click.
There may also be an Austin Flint murmur, a soft mid-diastolic rumble heard at the apical area. It appears when regurgitant jet from the severe aortic insufficiency renders partial closure of the anterior mitral leaflet.
Peripheral physical signs of aortic insufficiency are related to the high pulse pressure and the rapid decrease in blood pressure during diastole due to the AI:
large-volume, 'collapsing' pulse
bounding peripheral pulses; also known as Watson's water hammer pulse
low diastolic and increased pulse pressure
Corrigan's pulse (rapid upstroke and collapse of the carotid artery pulse)
de Musset's sign (head nodding in time with the heart beat)
Quincke's sign (pulsation of the capillary bed in the nail)
Duroziez's sign (systolic and diastolic murmurs described as 'pistol shots' heard over the femoral artery when it is gradually compressed)
Traube's sign (a double sound heard over the femoral artery when it is compressed distally)
Rarer signs include:
Lighthouse sign (blanching & flushing of forehead)
Ladolfi's sign (alternating constriction & dilatation of pupil)
Becker's sign (pulsations of retinal vessels)
Müller's sign (pulsations of uvula)
Mayen's sign (diastolic drop of BP>15 mm Hg with arm raised)
Rosenbach's sign (pulsatile liver)
Gerhardt's sign (enlarged spleen)
Hill's sign (A ≥ 20 mmHg difference in popliteal and brachial systolic cuff pressures, seen in chronic severe AI)
[[Lincoln sign (pulsatile popliteal)
Sherman sign (dorsalis pedis pulse is quickly located & unexpectedly prominent in age>75 yr)
Diagnostic evaluation
The most common test used for the evaluation of the severity of aortic insufficiency is the echocardiogram, which can provide two-dimensional views of the regurgitant jet, and allow measurement of the velocity and volume of the jet.
The echocardiographic findings in severe aortic regurgitation include:
An AI color jet dimension > 60 percent of the left ventricular outflow tract (LVOT) diameter (may not be true if the jet is eccentric)
The pressure half-time of the regurgitant jet is < title="Millisecond" href="http://en.wikipedia.org/wiki/Millisecond">mserly termination of the mitral inflow (due to increase in LV pressure due to the AI.)
Early diastolic flow reversal in the descending aorta.
Regurgitant volume > 60 ml
Regurgitant fraction > 55 percent
Prognosis
The risk of death in individuals with aortic insufficiency, dilated ventricle, normal ejection fraction who are asymptomatic is about 0.2 percent per year. Risk increases if the ejection fraction decreases or if the individual develops symptoms.
Treatment
Indications for surgery for chronic severe aortic insufficiency2
Symptoms
Ejection fraction
Other information
NYHA class III - IV
≥ 50 %

NYHA class II
≥ 50 %
Progression of symptoms or worsoning parameters on echocardiography
CHA class ≥ II angina
≥ 50 %

Regardless of symptoms
25 - 49 %

Cardiac surgery for other cause (ie: CAD, other valvular disease, ascending aortic aneurysm)
Aortic insufficiency can be treated either medically or surgically, depending on the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction.
Surgical treatment is typically warranted prior to the ejection fraction falling below 55% or the left ventricular end-systolic dimension falling below 55mm, regardless of symptoms. If either of these thresholds is passed, the prognosis worsens.
Medical treatment
Medical therapy of chronic aortic insufficiency involves the use of vasodilators. Small trials have shown a short term benefit in the use of ACE inhibitors, nifedipine, and hydralazine in improving left ventricular wall stress, ejection fraction, and mass. The use of these vasodilators is only indicated in individuals who suffer from hypertension in addition to AI. The goal in using the use of these pharmacologic agents is to decrease the afterload so that the left ventricle is spared somewhat. The regurgitant fraction may not change significantly, since the gradient between the aortic and left ventricular pressures is usually fairly low at the initiation of treatment.
Surgical treatment
The surgical treatment of choice at this time is an aortic valve replacement. This is currently an open-heart procedure, requiring the individual to be placed on cardiopulmonary bypass.
In the case of severe acute aortic insufficiency, all individuals should undergo surgery if there are no absolute contraindications for surgery. Individuals with bacteremia with aortic valve endocarditis should not wait for treatment with antibiotics to take effect, given the high mortality associated with the acute AI. In stead, replacement with an aortic valve homograft should be performed if feasible.
In the future, it is believed that a percutaneous approach to aortic valve replacement will be feasible.
References
1. al Jubair K, al Fagih MR, Ashmeg A, Belhaj M, Sawyer W. Cardiac operations during active endocarditis. J Thorac Cardiovasc Surg. 1992 Aug;104(2):487-90. (Medline abstract)
2. Bonow et al., ACC/AHA Task Force Report. ACC/AHA Guidelines for the Management of Patients With Valvular Heart Disease. JACC Vol. 32, No. 5, November 1998:1486-1588 (Full article)
See also
Aortic valve replacement
Preload
Afterload

Ventricular hypertrophy

2007-01-11T20:10:00.000-08:00

Although ventricular hypertrophy may occur in either the left or right or both ventricles of the heart, left ventricular hypertrophy (LVH) is more commonly encountered.
Contents

1 Physiology
2 LVH
3 RVH
4 See also

Physiology
The ventricles are the chambers in the heart responsible for pumping blood either to the lungs (right ventricle) or the rest of the body (left ventricle). Increased ventricular mass is an adaptation by the ventricle(s) of the heart to increased stress, such as chronically increased volume load (preload) or increased pressure load (afterload).
It is a physiological response that enables the heart to adapt to increased stress; however, the response can become pathological and ultimately lead to a deterioration in function. For example, hypertrophy is a normal physiological adaptation to exercise that enables the ventricle to enhance its pumping capacity. Aerobic training results in the heart being able to pump a larger volume of blood through an increase in the size of the ventricles. Anaerobic training results in the thickening of the myocardial wall to push blood through arteries compressed by muscular contraction. This type of physiologic hypertrophy is reversible and non-pathological, increasing the heart's ability to circulate blood. Chronic hypertension causes pathological ventricular hypertrophy. This response enables the heart to maintain a normal stroke volume despite the increase in afterload. However, over time, pathological changes occur in the heart that lead to a functional degradation and heart failure.
If the precipitating stress is volume overload (as through aerobic exercise, which increases blood return to the heart through the action of the skeletal-muscle pump), the ventricle responds by adding new sarcomeres in-series with existing sarcomeres (i.e. the sarcomeres lengthen rather than thicken). This results in ventricular dilation while maintaining normal sarcomere lengths - the heart can expand to receive a greater volume of blood. The wall thickness normally increases in proportion to the increase in chamber radius. This type of hypertrophy is termed eccentric hypertrophy.
In the case of chronic pressure overload (as through anaerobic exercise, which increases resistance to blood flow by compressing arteries), the chamber radius may not change; however, the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres. This is termed concentric hypertrophy. This type of ventricle is capable of generating greater forces and higher pressures, while the increased wall thickness maintains normal wall stress. This type of ventricle becomes "stiff" (i.e., compliance is reduced) which can impair filling and lead to diastolic dysfunction.
LVH
See main article, Left ventricular hypertrophy The most common cause is high blood pressure. Other causes are exercise (athletic hypertrophy) and congenital bases (hypertrophic cardiomyopathy or HCM).
The diagnosis of LVH is usually made by echocardiography. Also, ECG, electrocardiogram is used in the detection of Left ventricular hypertrophy. The walls of the ventricle can be measured and a thickness of greater than 1.5 cm is considered enlarged. Athletic hypertrophy is usually less than this thickness and will return to normal size with cessation of the activity. HOCM may be diagnosed in the absence of other causes of LVH and with the presence of a family history.
RVH
The common causes of right ventricular hypertrophy (RVH) are:
Pulmonary hypertension
Fallot tetralogy
Pulmonary valve stenosis
Ventricular septal defect (VSD)
See also
cardiology
cardiovascular disease
cardiomegaly

Cardiac stress test

2007-01-11T20:08:00.000-08:00

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This article or section may be confusing or unclear for some readers.Please improve the article or discuss this issue on the talk page. This article has been tagged since December 2006.

An elderly man takes a spin on a stress test treadmill to check his heart's functioning.
A cardiac stress test is a medical test performed to evaluate the ability for arterial blood flow to the myocardium (heart muscle) to increase during the stress of physical exercise, compared to blood flow while at rest. As an exercise test, results also reflect overall physical fitness. These tests do not assess emotional stress, or other connotations of the term stress.
Stress test abnormalities reflect marked imbalances of relative blood flow to different portions of the left ventricular muscle tissue. This is important, because the left ventricle portion of the heart performs the greatest amount of work involved in pumping blood around the body. Blood flow imbalances within the heart muscle of the other three heart chambers are not detected.
Usually, only high grade stenoses of the larger surface heart arteries can be detected. Severe stenoses, e.g. stenoses greater than 75% lumen narrowing, are one possible result of advanced arterial disease and are the usual basis for both "stable" or reproducible exercise-related angina (chest pain) and for "positive" stress tests. Less severe stenoses are automatically compensated for by dilation of the ventricular arterioles during exercise and do not usually produce enough imbalance of relative blood flow to be detectable by stress test methods.
Severe stenoses, as detected by stress tests, essentially always reflect advanced arterial disease. However, stress tests do not detect atheromata present throughout the heart or other body arteries, nor do they reveal the vulnerable plaques, which are the cause of most heart attacks. Recent (late 1990s) clinical studies have demonstrated that the vulnerable plaques which produce most myocardial infarctions are commonly present within multiple regions of the heart arteries, yet are typically relatively flat, i.e. not protruding into the artery lumen sufficiently to produce enough stenosis (usually less than 50%), to be detected by stress test methods.
Contents
[hide]
1 Test overview
2 Purpose
3 Variations
4 Diagnostic value
5 Risks
6 Further research
7 See also
8 References

//
Test overview
The patient either walks on a treadmill or is given IV medication which simulates exercise while connected to an ECG machine, usually the standard 10 connections used to record a 12-lead ECG. Patient symptoms and blood pressure response are repeatedly checked. Using ECG and blood pressure monitoring alone, the test is variously called a cardiac stress test, exercise stress test, exercise treadmill test, exercise tolerance test, stress test or exercise ECG test.
If radioactive isotopes are also used (commonly, Technetium Tc99m Sestamibi and rarely, Thallium-201), then it is usually called a nuclear stress test. Given the ability to visualize the relative amounts of radioisotope within different regions of the heart muscle, nuclear stress tests are more accurate in detecting regional relatively normal versus decreased blood flow to cardiac cells. However, balanced global reductions may still not be recognized because absolute blood flow is not quantitatively measurable, only regional comparative variations.
Purpose
The American Heart Association recommends EKG treadmill testing as the first choice for patients with medium risks of coronary heart disease based on the risk factors of smoking, family history of coronary stenosis, hypertension, diabetes and high cholesterol.
Perfusion (Cardiolite®) stress testing is appropriate for select patients, especially those with an abnormal resting EKG. More severe stenosis (probably greater than 70% occlusion) can produce abnormalities in both EKG waveforms and cardiac wall motion at rest or under stress echocardiographic testing. Such high grade narrowings are typically the primary culprit responsible for those angina episodes which reproducibly occur at a given level of exercise. However, most heart attacks result from rupture of atheroma lesions associated with only mild narrowing (20% on average by intravascular ultrasound (IVUS) clinical studies), thus stress tests do not work well for detecting the vulnerable plaques which are responsible for most heart attacks. Like all tests, stress testing has problems with both falsely positive and falsely negative results compared with other clinical tests.
Angiogram and/or intracoronary ultrasound (preferably in a hospital capable of Percutaneous Coronary Intervention [PCI] with stenting) can provide even greater information, but at the risk of complications associated with cardiac catheterization.
Variations
Some patients with abnormal resting EKGs, or those who are unable to walk safely, can be "exercised" pharmacologically instead of walking on a treadmill. The patient will typically receive a pharmaceutical such as dypridamole or adenosine (both vasodilators) while a cardiologist or physician's assistant reviews the electrocardiogram (EKG) tracing and checks blood pressure periodically.
A radiotracer (typically Tc99m Sestamibi although Thallium is possible) is injected during the simulated exercise portion. After a suitable waiting period, pictures are taken with a gamma camera. The pictures are then compared with the patient's resting images in order to assess the status of the patient's coronary arteries.
Diagnostic value
The American Heart Association journal, Circulation, describes:Treadmill test: sensitivity of 67%, specificity of 70%Nuclear test: sensitivity of 81%, specificity of 99%
However, these numbers reference detection of advanced artery luminal narrowing as assessed by stress methods compared with angiography as the "gold standard". As a predictor of future heart attack, both methods suffer in that they only detect lumen stenosis, a common symptom of some very advanced atheroma, but not the vulnerable plaques which produce most heart attacks. Because of this, most clinical cardiology experience demonstrates that the actual sensitivity and specificity values for detecting likelihood of future heart attack, as opposed to lumen narrowing, are much lower than stated above.
Whatever the actual numbers, the value of stress tests has increasingly been recognized as limited, especially for people without symptoms. Yet, according to United States data from 2004, for about 65% of men and 47% of women, the first symptom of cardiovascular disease is heart attack or sudden death (death within one hour of symptom onset).
Over the last couple of decades, other methods have been increasingly developed as ways to better detect atherosclerotic disease before it becomes symptomatic. These have included both (a) anatomic detection methods and (b) physiologic measurement methods.
Examples of anatomic methods include: (1) coronary calcium scoring by CT, (2) carotid IMT (intimal medial thickness) measurement by ultrasound, e.g. IntiMaTe, and (3) IVUS.
Examples of physiologic methods include: (1) lipoprotein subclass analysis, (2) HbA1c, (3) hs-CRP, (4) homocysteine, and (5) the metabolic syndrome.
Advantages: The anatomic methods directly measure some aspect of the actual atherosclerotic disease process itself, thus offer potential for earlier detection, including before symptoms start, disease staging and tracking of disease progression. The physiologic methods are often less expensive and safer and changing them for the better may slow disease progression, in some cases with marked improvement.
Disadvantages: The anatomic methods are generally more expensive and several are invasive, such as IVUS. The physiologic methods do not quantify the current state of the disease or directly track progression. For both, clinicians and third party payers have been slow to accept the usefulness of these newer approaches.
Risks
Absolute contraindications to cardiac stress testing include acute myocardial infarction [MI] (heart attack) within 48 hrs, unstable angina not yet stabilized with medical therapy, uncontrolled arrhythmia which may have significant hemodynamic responses (for example ventricular tachycardia), symptomatic severe aortic stenosis, aortic dissection, pulmonary embolism, pericarditis.
Major side effects from cardiac stress testing can include palpitation, chest pain, shortness of breath, headache, nausea, or fatigue. Adenosine and dipyridamole can cause mild drug-induced hypotension. However, hypotension caused by exercise stress testing or dobutamine is almost always abnormal and concerning for severe coronary disease.
Stress tests using radiological agents confer a definite (albeit low) long term risk of cancer, but patients undergoing such examinations often receive little or inaccurate information about these risks. For comparison, the annual background radiation per annum a person receives is approximately 3 mSv. A chest xray is approximately 0.1 mSv. A coronary angiogram (cardiac catheterization) has an effective dose of 3-20 mSv (depending on operator skill, type of intervention, etc). A routine chest helical MDCT is around 5-7 mSv. A cardiac CT (with retrospective EKG gating) is around 8-13 mSv (Morin). A sestamibi scan is approximately 12 mSv. A thallium scan is approximately 25 mSv. A thallium scan corresponds the dose of 250 chest x rays, or an extra cancer risk of about 1 in 16000 exposed patients (A. de González). The lifetime risk of fatal cancer development is 4%/Sv or 0.004%/mSv or about 0.1% for a thallium scan. Therefore, frequent usage of these tests has to balance the benefits against the risks of radiation.
Another major risk of stress testing, whether by exercise or pharmacological agents, is the possibility of inducing an MI, especially in patients with severe multi-vessel coronary artery disease. This risk, however, is substantially lower than the risk (about 1%) of major complications (such as inducing a heart attack, stroke, peripheral artery clot and embolism) from cardiac catheterization.
The choice of pharmacologic stress agent to be used (dobutamine, adenosine, dipyridamole) depends on factors such as concurrent medications and diseases. Dobutamine is usually used when a patient has asthma or severe COPD, takes the medication theophylline or has ingested coffee or chocolate (anything with caffeine), or has 2nd or 3rd degree AV block (a type of heart block). Adenosine or dipyridamole is generally used when a patient has poorly controlled hypertension, glaucoma, or has left bundle branch block (LBBB, another type of heart block). It is well known that patients with LBBB can have false positive septal ischemia if dobutamine is used as a pharmacologic agent in nuclear stress test.
Conclusion Most physicians support the population-wide reduction of risk factors which cause heart attack. These risk factors are contained in the well-known cardiac Framingham Risk Score. Physicians typically take a history; perform a physical and then obtain baseline bloodwork and a resting EKG. Stress testing is the established method of investigating moderate-risk patients for coronary artery disease as well as obtaining prognostic information for the patient.
Further research
Magnetic resonance imaging (MRI) has expanded the choice of modalities available for cardiac stress testing. MRI has superior spatial resolution (on the order of around 1.5 mm for cine imaging and 2.5 mm for perfusion imaging), and temporal resolution (around 40 ms for cine imaging), compared with that of a nuclear or PET stress test (spatial resolution of around 9mm for nuclear and 6mm for PET). The increased spatial resolution allows for more sensitive detection of ischemia, which initially starts at the thin subendocardial layer, due to stenotic epicardial supply vessels. First-pass stress perfusion cardiac MR imaging is performed using a rapid bolus injection of gadolinium based contrast and rapidly obtaining T1 weighted images of the myocardium at every R-R interval after pharmacologic stress induced with adenosine. The stress and resting first-pass perfusion MRI data can then be analyzed using a convolution model (such as the Marquard-Levenberg least-squares algorithm) to determine the quantitative global myocardial perfusion reserve (Michael Jerosch-Herold). Delayed hyper-enhancement imaging can be done after 10-15 minutes of contrast injection to evaluate for regions of infarction or fibrosis which has increased signal due to the slower washout of contrast from these areas (Thomson LE). Stress cardiac MRI perfusion testing thus is sensitive enough to detect subtle ischemia and myocardial infarctions even if they are limited only to the subendocardial level. The major problem again is that they still do not detect the "vulnerable plaques" which is the major cause of most heart attacks.
Stress testing, even if done in time, will detect only some of these people before symptoms, debility or death. Stress testing methods, though more effective than a resting EKG, only detect medium to high grade flow limitations; this assuming the testing is fully and aggressively performed. However, most acute artery flow disrupting events leading to heart attacks are due to rupture of "vulnerable plaques". Most of the "vulnerable plaques" cause less than 40% lumen narrowing, a degree of stenosis too small for most stress testing methods to detect.
Historically, through the mid-1980s, it was believed that detecting these high grade stenoses was the key to recognizing people who would have heart attacks in the future. However, there was also long-standing experience that some people could exercise all the way to maximum predicted heart rate, have no abnormal symptoms and completely normal stress test results, only to die of a massive heart attack within a few days to weeks. From the 1960s to 1990s, despite the success of stress testing identifying many who were at high risk for heart attack, its failure to correctly identify many others was a conundrum, discussed in medical circles but unexplained.
The high grade stenoses which are detected by stress test methods are often, though not always, responsible for recurring symptoms of angina. Cardiac stress tests do detect some individuals who already have with very advanced coronary arterial disease and stenosis, some of whom did not recognize that they had advanced disease. However, stress test results (especially stress perfusion cardiac MRI which can detected subtle diffuse subendocardial decreased perfusion due to microvascular disease) are also sometimes abnormal in some people who do not have high grade narrowings of their coronary arteries as visualized by coronary angiography, which provides more accurate information and partial visualization of the coronary artery lumens. This was long viewed as a false positive result, with some of these individuals diagnosed as having Syndrome X, i.e meaning clear recurring signs of angina, though with smooth open coronary artery lumens on coronary angiography. The actual underlying issues responsible for this apparent conundrum are now better understood, see atheroma and microvascular disease.
In the 1950s, heart attacks were commonly attributed to coronary thrombosis, a clot closure of a coronary artery, based on post mortem examination findings. In the late 1950s to early 1960s, this concept became replaced by the concept of stenosis based on the angiographic view of the lumens of the coronary arteries. In turn the angiographic view led to promotion of cardiac stress testing to detect stenoses, i.e. the severe ones more commonly present in people experiencing recurrent angina with physical exertion.
By the early to mid-1990s, it became more widely recognized that rupture of more rapidly evolving and unstable atheroma, hidden within the walls of the coronary arteries, called "vulnerable plaques", even though they often produce little or no stenosis of the coronary lumen, is the primary event which produces most heart attacks; thus back to the coronary thrombosis view, though with more sophistication of understanding some of the complexities. Two clinical trials published in the late 1990's, focusing on the relation between plaque structure, lumen stenosis and myocardial infarction, in which each individuals coronary anatomy was tracked with both angiography and IVUS found that 75% or greater stenotic areas were responsible for only about 14% of heart attacks. The typical heart attack occurred at an artery location with extensive, eccentric plaque within the wall but a luminal stenosis of only 20%. This finding added further evidence to the importance of the concept of vulnerable plaques. The detection of these vulnerable plaques using high resolution CT, MRI, IVUS, OCT (Optical Coherence Tomography), and molecular imaging is currently hotly researched. For CT, as of 2005, 64-slice multidetector machines are providing the best artery and lumen images, yet still do not clearly reveal which plaques are vulnerable. It is hope that perhaps with better resolution and ability to characterize the content of the plaques that an imaging modality may in the future be able to indicate which plaques is "vulnerable" as it is clear that detecting stenosis itself, however subtle, is not enough.
Unfortunately, cardiac stress tests are only capable of detecting medium to high grade limitations of blood flow to the left ventricular heart muscle which may produce recurring angina, not the atheroma which produce heart attacks. Stress test methods do not evaluate blood flow to non-left-ventricle heart muscle. Thus stress test results are often falsely negative for many people, in terms of predicting who is at high risk for myocardial infarction due to atheroma or ruptured "vulnerable plaques".
It has become clear that stress testing recognizes most people at risk for heart attacks too late, unfortunately only after the disease and symptoms of the disease have developed. By the time, a majority of people would already have at least medium stenosis of coronary vessels with development of atheroma or have already had heart attacks or died. It is hoped that research in higher resolution imaging techniques will allow for earlier detection and characterization of subtle atheroma and to initiate lifestyle changes and optimal medical therapy in "vulnerable patients" before they develop symptoms.
See also
Atherosclerosis
Atheroma
Cardiac arrhythmia
Coronary circulation
Cardiology diagnostic tests and procedures
References
Circulation, Fletcher et al. AHA Exercise Standards for Testing. 201:104:1694.
National Guideline Clearinghouse. Cardiac Stress Test Supplement. ICSI:2003Nov.26p.87.
Michael Jerosch-Herold (2004). "Analysis of myocardial perfusion MRI". Journal of Magnetic Resonance Imaging 19 (6): 758-770..
Thomson LE (2004). "Magnetic resonance imaging for the assessment of myocardial viability". Journal of Magnetic Resonance Imaging 19 (6): 771-788..
A. de González (2004). "Risk of cancer from diagnostic X-rays: estimates for the UK and 14 other countries". The Lancet 363 (9406): 345-351..
Morin (2003). "Radiation Dose in Computed Tomography of the Heart". Circulation 107: 917-922..

Aorta

2007-01-11T20:05:00.000-08:00

The aorta (generally pronounced /eɪ.oʊɹ.tə/ or "ay-orta") is the largest artery in the human body, originating from the left ventricle of the heart and bringing oxygenated blood to all parts of the body in the systemic circulation.
Contents

1 The course of the aorta
2 Features
3 Diseases/pathology
4 In popular culture
5 References
6 External links
//
The course of the aorta
The aorta is usually divided into three segments/sections [1] [2] :
Ascending aorta — the section between the heart and the arch of aorta
Arch of aorta — the peak part that looks somewhat like an inverted "U"
Descending aorta — the section from the arch of aorta to the point where it divides into the common iliac arteries
Thoracic aorta — the half of the descending aorta above the diaphragm
Abdominal aorta — the half of the descending aorta below the diaphragm
Features
The aorta is an elastic artery, and as such is quite distensible. When the left ventricle contracts to force blood into the aorta, the aorta expands. This stretching gives the potential energy that will help maintain blood pressure during diastole, as during this time the aorta contracts passively.
Diseases/pathology
Aneurysm of sinus of Valsalva
Aortic aneurysm - myotic, bacterial (e.g. syphilis), senile, genetic, associated with valvular heart disease
Dissecting aortic aneurysm
Aortic coarctation - pre-ductal, post-ductal
Atherosclerosis
Marfan syndrome
Trauma, most often thoracic and distal to the left subclavian artery[3] and frequently quickly fatal[4]
In popular culture
One of the Twin Peaks baddie, Windom Earle's better known lines is "I haven't felt this excited since I punctured Caroline's aorta".
References
^ Tortora, Gerard J: "Principles of Human W. & Karen A. Koos: "Human Anatomy, second edition", page 479. Wm. C. Brown Publishing, 1994 (ISBN 0-697-12252-2)
^ De Graaff, Van: "Human Anatomy, fifth edition", pages 548-549. WCB McGraw-Hill, 1998 (ISBN 0-697-28413-1)
^ Samett EJ. Aorta, Trauma. eMedicine.com. URL: http://www.emedicine.com/radio/topic44.htm. Accessed on: August 9, 2006. ^ "Aortic Trauma in Scotland - A Population Based Study.". Eur J Vasc Endovasc Surg. PMID 16750920

Ventricle (heart)

2007-01-11T20:04:00.000-08:00

From Wikipedia, the free encyclopedia
In the heart, a ventricle is a heart chamber which collects blood from an atrium (another heart chamber that is smaller than a ventricle) and pumps it out of the heart.
In a four-chambered heart, such as that in humans, there are two ventricles: the right ventricle pumps blood into the pulmonary circulation for the lungs, and the left ventricle pumps blood into the systemic circulation for the rest of the body. (See Double circulatory system for details.)
Ventricles have thicker walls than the atria, and thus can create the higher blood pressure. Comparing the left and right ventricle, the left ventricle have thicker walls because it needs to pump blood to the whole body.

Pulse

2007-01-08T20:03:00.000-08:00

From Wikipedia, the free encyclopedia
For other uses, see Pulse (disambiguation).
In medicine, a person's pulse is the throbbing of their arteries as an effect of the heart beat. It can be felt at the neck, at the wrist and other places.
Pressure waves move through the blood vessels, which are pliable; these waves are not caused by the forward movement of the blood. When the heart contracts, blood is ejected into the aorta and the aorta stretches. At this point the wave of distention (pulse wave) is most pronounced, but relatively slow-moving (3 to 6 m/s). As it travels towards the peripheral blood vessels, it gradually diminishes and becomes faster. In the large arterial branches, its velocity is 7 to 10 m/s; in the small arteries, it is 15 to 35 m/s. The pressure pulse is transmitted 15 or more times more rapidly than the blood flow.
The term pulse is also used, although incorrectly, to denote the frequency of the heart beat, usually measured in beats per minute. In most people, the pulse is an accurate measure of heart rate. Under certain circumstances, including arrhythmias, some of the heart beats are ineffective and the aorta is not stretched enough to create a palpable pressure wave. The pulse is irregular and the heart rate can be (much) higher than the pulse rate. In this case, the heart rate should be determined by auscultation of the heart apex, in which case it is not the pulse. The pulse deficit (difference between heart beats and pulsations at the periphery) should be determined by simultaneous palpation at the radial artery and auscultation at the heart apex.
A normal pulse rate for a healthy adult, while resting, can range from 60 to 100 beats per minute (BPM). During sleep, this can drop to as low as 40 BPM; during strenuous exercise, it can rise as high as 200–220 BPM. Generally, pulse rates are higher in younger persons. A resting heart rate for an infant is as high as or higher than an adult's pulse rate during strenuous exercise.
Besides its rate, the pulse has other qualities which reflect the state of the cardiovascular system, such as its rhythm, fullness and the shape of the pulse wave. Certain diseases cause characteristic changes in these qualities. The absence of a pulse at the temple of the skull can be a sign of giant cell arteritis; absent or decreased pulses in the limbs may indicate peripheral artery occlusive disease.
Pulses are manually palpated with fingers or thumb. When palpating the carotid artery, the femoral artery or the brachial artery, the thumb may be used. However, the thumb has its own pulse which can interfere with detecting the patient's pulse at other points, where two or three fingers should be used. Fingers or thumb must be placed near an artery and pressed gently against a firm structure, usually a bone, in order to feel the pulse.
An alternative way of finding pulse rate is by listening to the heartbeat. This is most commonly done with a stethoscope but can also be done using anything that will transmit sound to the ears, or by pressing the ear directly to the chest.
Attributes of pulse measurement include the rate or frequency of the pulse and its rhythm including its regularity and quality expressed as volume or strength.
Checking the radial pulse.

Common pulse points
radial pulse - located on the thumb side of the wrist (radial artery)
ulnar pulse - located on the little finger side of the wrist (ulnar artery)
carotid pulse - located in the neck (carotid artery). The carotid artery should be palpated gently. Stimulating its baroreceptors with vigorous palpitation can provoke severe bradycardia or even stop the heart in some sensitive persons. Also, a person's two carotid arteries should not be palpated at the same time, to avoid a risk of fainting or brain ischemia.
brachial pulse - located between the biceps and triceps, on the medial side of the elbow cavity; frequently used in place of carotid pulse in infants (brachial artery)
femoral pulse - located in the thigh (femoral artery)
popliteal pulse - located behind the knee in the popliteal fossa, found by holding the bent knee. The patient bends the knee at approximately 120°, and the physician holds it in both hands to find the popliteal artery in the pit behind the knee.
dorsalis pedis pulse - located on top of the foot (dorsalis pedis artery)
tibialis posterior pulse - located in the back of the ankle behind the medial malleolus (posterior tibial artery).
temporal pulse - located on the temple directly in front of the ear (temporal artery)
The ease of palpability of a pulse is dictated by the patient's blood pressure. If his or her systolic blood pressure is below 90 mmHg, the radial pulse will not be palpable. Below 80 mmHg, the brachial pulse will not be palpable. Below 60 mmHg, the carotid pulse will not be palpable. Since systolic blood pressure rarely drops that low, the lack of a carotid pulse usually indicates death. It is not unheard of, however, for patients with certain injuries, illnesses or other medical problems to be conscious and aware with no palpable pulse.

Heart transplantation

2007-01-08T19:56:00.000-08:00

Diagram illustrating the placement of a donor heart in an orthotopic procedure. Notice how the back of the patient's left atrium and great vessels are left in place.
Heart transplantation or cardiac transplantation, is a surgical transplant procedure performed on patients with end-stage heart failure or severe coronary artery disease. The most common procedure is to take a working heart from a recently deceased organ donor (allograft) and implant it into the patient. The patient's own heart may either be removed (orthotopic procedure) or, less commonly, left in to support the donor heart (heterotopic procedure). It is also possible to take a heart from another species (xenograft), or implant a man-made artificial one, although the success of these two procedures has been less successful in comparison to the far more commonly performed allografts.
Contents

1 History
2 Indications
3 Contraindications
4 Procedures
4.1 Pre-Operative
4.2 Operative
4.2.1 Orthotopic procedure
4.2.2 Heterotopic procedure
4.3 Post-Operative
5 'Living Organ' transplant
6 Prognosis
7 References
8 External links
//
History
The first heart transplant was performed by Professor Christiaan Barnard at Groote Schuur Hospital in December 1967. The patient was a Louis Washkansky of Cape Town, South Africa, who lived for 18 days after the procedure before dying of pneumonia.The donor was Denise Darvall, who had recently been critically injured in a car accident.
Indications
In order for a patient to be recommended for a heart transplant they will generally have advanced, irreversible heart failure with a severely limited life expectancy. Other possible treatments, including medication, for their condition should have been considered or attempted prior to recommendation. Generally, the following causes of heart failure can be treated with a heart transplant:
Cardiomyopathy
Congenital heart disease
Coronary artery disease
Heart valve disease
Life-threatening arrhythmias.
Contraindications
Some patients are less suitable for a heart transplant, especially if they suffer from other circulatory conditions unrelated to the heart. The following conditions in a patient would increase the chances of complications occurring during the operation:
Kidney, lung, or liver disease
Insulin-dependent diabetes with other organ dysfunction
Life-threatening diseases unrelated to heart failure
Vascular disease of the neck and leg arteries.
Procedures
Pre-Operative
A typical heart transplantation begins with a suitable donor heart being located from a recently deceased or brain dead donor. The transplant patient is contacted by a nurse coordinator, and instructed to attend the hospital in order to be evaluated for the operation and given pre-surgical medication. At the same time, the heart is removed from the donor and inspected by a team of surgeons to see if it is in a suitable condition to be transplanted. Occasionally it will be deemed unsuitable. This can often be a very distressing experience for an already emotionally unstable patient, and they will usually require emotional support before being sent home.
Operative
Once the donor heart has passed its inspection, the patient is taken into the operating theatre and given a general anesthetic. Either an orthotopic or a heterotopic procedure is followed, depending on the condition of the patient and the donor heart.
Orthotopic procedure
The orthotopic procedure begins with the surgeons removing the patient's faulty heart. This involves making a vertical incision through the center of the ribcage in order to expose the chest cavity. The patient is attached to a heart-lung machine, in order for the surgeons to open the pericardium and remove the heart by dissecting the great vessels leading from it. The rear section of the left atrium and the pulmonary vein are the only parts of the patient's original heart left in place. The donor heart is then trimmed, in order for it to fit onto the patients remaining left atrium and vessels. It can then be sutured in place. The newly implanted heart is restarted and the patient's chest cavity is closed.
Heterotopic procedure
In the heterotopic procedure, the patient's own heart is not removed before implanting the donor heart. The new heart is positioned so that the chambers and blood vessels of both hearts can be connected to form what is effectively a 'double heart'. The procedure can give the patients original heart a chance to recover, and if the donor's heart happens to fail (eg. through rejection), it may be removed, allowing the patients original heart to start working again. Heterotropic procedures are only used in cases where the donor heart is not strong enough to function by itself (due to either the patients body being considerably larger than the donor's, the donor having a weak heart, or the patient suffering from pulmonary hypertension).
Post-Operative
The patient is taken into ICU to recover. When they wake up, they will be transferred to a special recovery unit in order to be rehabilitated. How long they remain in hospital post-transplant depends on the patient's general health, how well the new heart is working, and their ability to look after their new heart. Once the patient is released, they will have to return to the hospital for regular check-ups and rehabilitation sessions. They may also require emotional support. The number of visits to the hospital will decrease over time, as the patient adjusts to their transplant. The patient will have to remain on lifetime immunosuppressant medication to avoid the possibility of rejection. Since the vagus nerve is severed during the operation, the new heart will beat at around 100 bpm until nerve regrowth occurs.
'Living Organ' transplant
Doctors made medical history in May 2006, at Papworth Hospital in Cambridgeshire, England, when they successfuly transplanted a 'beating heart' into a patient. Normally a donor's heart is injected with potassium chloride in order to stop it beating, before being removed from the donor's body and packed in ice in order to preserve it. The ice can usually keep the heart fresh for a maximum of four to six hours, depending on its condition to start with. Rather than freezing the heart, this new procedure involves keeping it at body temperature and hooking it up to a special machine called an Organ Care System that allows it to continue beating with warm, oxygenated blood flowing through it. This can maintain the heart in a suitable condition for much longer than the traditional method.
Prognosis
The prognosis for heart transplant patients following the orthotopic procedure has greatly increased over the past 20 years, and as of July 15, 2005, the survival rates were as follows:[citation needed]1 year survival rate: 86.4% (males) and 84.6% (females)3 year survival rate: 78.9% (males) and 76.1% (females)5 year survival rate: 72% (males) and 68.5 (females).
References
http://www.capegateway.gov.za/eng/pubs/public_info/C/99478#
http://news.bbc.co.uk/1/hi/health/5041054.stm
http://www.americanheart.org/presenter.jhtml?identifier=4588
http://www.cts.usc.edu/ht-pg-hearttransplantprocedure.html
http://health.yahoo.com/ency/healthwise/tx4074abc
http://health.allrefer.com/health/heart-transplant-indications.html http://www.harthosp.org/transplant/heart.htm#indications

Congenital heart defect

2007-01-08T19:53:00.000-08:00

From Wikipedia, the free encyclopedia
(Redirected from Heart defects)

A congenital heart defect (CHD) is a defect in the structure of the heart
and great vessels of the newborn. Most heart defects either obstruct blood flow in the heart or vessels near it or cause blood to flow through the heart in an abnormal pattern, although other defects affecting heart rhythm (such as long QT syndrome) can also occur. Heart defects are among the most common birth defects, and are the leading cause of birth defect-related deaths.
Contents

1 Overview
2 Epidemiology
3 Aetiology
4 Major categories
4.1 Patent ductus arteriosus
4.2 Hypoplasia
4.3 Obstruction defects
4.4 Septal defects
4.5 Cyanotic defects
4.6 Other defects
5 Signs and Symptoms
6 Treatment
7 Defects
8 References
//

Congenital heart defects can be broadly categorised into two groups, acyanotic heart defects ('pink' babies) and cyanotic heart defects ('blue' babies).
Epidemiology
Slightly less than 1% of all newborn infants have congenital heart disease. Eight defects are more common than all others and make up 80% of all congenital heart diseases, whereas the remaining 20% consist of many independently infrequent conditions or combinations of several defects. Ventricular septal defect (VSD) is generally considered to be the most common type of malformation, accounting for about 1/3 of all congenital heart defects.
The incidence is higher when a parent or a sibling has a heart defect (4-5%), in stillborns (3-4%), abortuses (10-25%), and premature infants (2%).
The number of adults with problems connected to a congenital heart defect is rising and is passing the number of children with congenital heart defects in most western countries. This group is called GUCH patients.
Aetiology
The cause of most congenital heart defects is unknown.
Where a cause is known, it may be of a multifactorial origin and/or a result of genetic predisposition and environmental factors.
Known genetic causes of heart disease includes chromosomal abnormalities such as trisomies 21, 13, and 18, as well as a range of newly recognised genetic point mutations, point deletions and other genetic abnormalities as seen in syndromes such as CATCH 22, familial ASD with heart block, Alagille syndrome, Noonan syndrome, and many more.
Known antenatal environmental factors include maternal infections (Rubella), drugs (alcohol, hydantoin, lithium and thalidomide) and maternal illness (diabetes mellitus, phenylketonuria, and systemic lupus erythematosus).
Major categories
Patent ductus arteriosus
Main article: Patent ductus arteriosus
The ductus arteriosus is a temporary pathway in the foetal heart between the pulmonary artery and aorta, which allows blood to bypass the fetus' nonfunctioning lungs until birth. Normally, the ductus closes within a few hours or days of birth; when it does not, the result is patent ductus arteriosus. This defect is common in premature infants but rare in full-term infants.
Hypoplasia
Main article: Hypoplastic left heart syndrome
Hypoplasia can affect the heart, which typically results in the failure of either the right ventricle or the left ventricle to adequately develop, leaving only one side of the heart capable of pumping blood to the body and lungs. Hypoplasia of the heart is rare but is the most serious form of CHD; it is called hypoplastic left heart syndrome when it affects the left side of the heart and hypoplastic right heart syndrome when it affects the right side of the heart. In both conditions, the presence of a patent ductus arteriosus (and, when hypoplasia affects the right side of the heart, a patent foramen ovale) is vital to the infant's ability to survive until emergency heart surgery can be performed, since without these pathways blood cannot circulate to the body (or lungs, depending on which side of the heart is defective). Hypoplasia of the heart is generally a cyanotic heart defect Obstruction defects
Obstruction defects occur when heart valves, arteries, or veins are abnormally narrow or blocked. Common obstruction defects include pulmonary valve stenosis, aortic valve stenosis, and coarctation of the aorta, with other types such as bicuspid aortic valve stenosis and subaortic stenosis being comparatively rare. Any narrowing or blockage can cause heart enlargement or hypertension.
Septal defects
The septum is a wall of tissue which separates the left heart from the right heart. It is comparatively common for defects to exist in the interatrial septum or the interventricular septum, allowing blood to flow from the left side of the heart to the right, reducing the heart's efficiency. Ventricular septal defects are collectively the most common type of CHD, although approximately 30% of adults have a type of atrial septal defect called patent foramen ovale. Septal defects may or may not cause cyanosis depending on the severity of the defect.
Cyanotic defects
Cyanotic heart defects are called such because they result in cyanosis, a bluish-grey discoloration of the skin due to a lack of oxygen in the body. Such defects include persistent truncus arteriosus, total anomalous pulmonary venous connection, tetralogy of Fallot, transposition of the great vessels, and tricuspid atresia.
Other defects
Ebstein's anomaly
Brugada syndrome
Marfan syndrome
DiGeorge Syndrome
Signs and Symptoms
Symptoms and signs are related to the type and severity of the heart defects. Some children have no signs while others may exhibit shortness of breath, cyanosis, chest pain, syncope, sweating, heart murmur, respiratory infections, underdeveloping of limbs and muscles, poor feeding, or poor growth. Most defects cause a whispering sound, or murmur, as blood moves through the heart causing some of these symptoms. All of these symptoms occur at a young age of a child or infant which is typically found during a physical examination.
Treatment
Sometimes CHD improves with no treatment necessary. At other times the defect is so small and does not require any treatment. Most of the time CHD is serious and requires surgery and/or medications. Medications include diuretics which aid the baby in eliminating water, salts, and digoxin, which aids in strengthening the contraction of the heart. This slows the heartbeat and removes some fluid from tissues. Some defects require surgical procedures to repair as much as possible to restore circulation back to normal. In some cases, multiple surgeries are needed to be performed to help balance the circulation. Interventional cardiology now offers patients minimally invasive alternatives to surgery. Device closures can now be treated with a standard transcatheter procedure using a closure device mounted on a balloon catheter. Equally stenosis can be treated using a balloon dilation procedure to dilate the obstruction during cardiac catheterization.[1]
Defects
Aortic stenosis
Atrial septal defect (ASD)
Atrioventricular septal defect (AVSD)
Coarctation of the aorta (CoA)
Dextrocardia
Ebstein's anomaly
Hypoplastic left heart syndrome (HLHS)
levo-Transposition of the great arteries (l-TGA)
Partial anomalous pulmonary venous connection (PAPVC)
Patent ductus arteriosus (PDA)
Pulmonary atresia
Pulmonary stenosis
Tetralogy of Fallot (ToF)
Total anomalous pulmonary venous connection (TAPVC)
dextro-Transposition of the great arteries (d-TGA)
Tricuspid atresia
Truncus arteriosus
Ventricular septal defect (VSD)
This is an incomplete list, which may never be able to satisfy certain standards for completeness. Revisions and sourced additions are welcome.

References
^ W. Hellenbrand (2006). Non-surgical Alternatives in the Treatment of Congenital Heart Defects.

Cardiology

2007-01-08T19:46:00.000-08:00

A diagram of a heart with an ECG indicator; diagrams like this are used in Cardiology.
Cardiology is the branch of medicine dealing with disorders of the heart and blood vessels. The field is commonly divided in the branches of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians specializing in this field of medicine are called cardiologists.
The term cardiology is derived from the Greek word καρδιά (transliterated as kardia and meaning heart or inner self).

Atrium (anatomy)

2007-01-08T19:44:00.000-08:00

From Wikipedia, the free encyclopedia

In anatomy, the atrium (plural: atria) refers to a chamber or space. As such it may for example be the atrium of the lateral ventricle in the brain or, popularly, the blood collection chamber of a heart. It has a thin-walled structure that allows blood to return to the heart. There is at least one atrium in an animal with a closed circulatory system. In fish, the circulatory system is very simple: a two-chambered heart including one atrium and one ventricle. In other vertebrate groups, the circulatory system is much more complicated. Their circulatory systems are divided into two types: a three-chambered heart, with two atria and one ventricle, or a four-chambered heart, with two atria and two ventricles. The atrium's function in the circulatory system includes receiving blood as it returns to the heart to complete a circulating cycle, whereas the ventricle's function is to pump blood out of the heart to start a new cycle.
Human heart
Humans have a four chambered heart.
The right atrium receives de-oxygenated blood from the superior vena cava and inferior vena cava. The left atrium receives oxygenated blood from the left and right pulmonary veins.
The atria do not have valves at their inlets. As a result, a venous pulsation is normal and can be detected in the jugular vein (see: jugular venous pressure).
Internally, there is the rough musculae pectinati, crista terminalis which acts as a boundary inside the atrium and the smooth walled part derived from the sinus venosus. There is also a fossa ovalis in the interatrial septum which was used in the fetal period as a means of bypassing the lung.
There are two atria, one on either side of the heart. On the right side is the atrium that holds blood that needs oxygen. It sends blood to the right ventricle which sends it to the lungs for oxygen. After it comes back, it is sent to the left atrium. The blood is pumped from the left atrium and sent to the ventricle where it is sent out of the heart. It is then sent to all the rest of the body.

Artificial heart

2007-01-08T19:27:00.000-08:00

An AbioCor artificial heart

Artificial heart
From Wikipedia, the free encyclopedia

An artificial heart is a prosthetic device that is implanted into the body to replace the original biological heart. It is distinct from a cardiac pump, which is an external device used to provide the functions of both the heart and the lungs. Thus, the cardiac pump need not be connected to both blood circuits. Also, a cardiac pump is only suitable for use not longer than a few hours, while for the artificial heart the current record is 17 months.
This synthetic replacement for an organic mammalian heart (usually human), remains one of the long-sought Holy Grails of modern medicine. Although the heart is conceptually a simple organ (basically a muscle that functions as a pump), it embodies complex subtleties that defy straightforward emulation using synthetic materials and power supplies. The obvious benefit of a functional artificial heart would be to lower the need for heart transplants, because the demand for donor hearts (as it is for all organs) always greatly exceeds supply. A heart-lung machine was used in 1953 during the first successful open heart surgery. Dr. John Heysham Gibbon performed the operation and developed the heart-lung substitute himself. Whether this could be counted as an artificial heart is a subject of debate. In either case, the first official artificial heart that was patented was done so by Paul Winchell in 1963. Winchell subsequently assigned the patent to the University of Utah, where Robert Jarvik ultimately used it as the model for his Jarvik-7. One of the innovations of the Jarvik-7 was the inner coating of rough material, the contribution of a man named David Gernes. This coating helped the blood to clot and coat the inside of the device, enabling a more natural blood flow. Early attempts prior to the Jarvik-7 were disappointing; hosts died within hours or days and/or suffered massive foreign-body rejection problems. Jarvik's human designs were more impressive but his patients succumbed as well; his first Jarvik-7 patient, 61-year-old retired dentist Barney Clark, survived for 112 days after it was implanted at the University of Utah on December 2, 1982. Another problem is that an artificial heart requires an external power supply such as a battery pack worn on the patient's waist; no design so far has been able to use the body's own natural biological energy.
After about 90 people received the Jarvik device, the artificial hearts were banned for permanent use in patients with heart failure, because most of the recipients could not live more than half a year. However, it is used temporarily for some heart transplantation candidates who cannot find a natural heart immediately but urgently need an efficiently working heart.
On July 2, 2001, Robert Tools received the first completely self-contained artificial heart transplant in a surgery done by University of Louisville doctors at Jewish Hospital in Louisville, Kentucky. It is called the AbioCor Implantable Replacement Heart. Tom Christerson survived for 17 months after his artificial heart transplant.
The Syncardia CardioWest total artificial heart (CW-TAH) was developed by University of Arizona researchers and approved for bridge-to-transplant use in 2004. It is the first implantable artificial heart to be approved by the U.S. Food and Drug Administration. The longest CW-TAH implantation went 602 days (approximately 20 months.) (1)
The AbioMed company of Danvers, Massachusetts produced the AbioCor device, which on September 6, 2006 became the first fully implantable artificial heart to be approved, albeit under Humanitarian Use Device rules.
Most doctors are confident that with increased understanding of the heart and continuing improvements in prosthetics engineering, computer science, electronics, battery technology, fuel cells, etc. that the practical artificial heart will be a reality sometime in the 21st century.
In fiction
The earliest example of a fictional artificial heart is the French pulp hero the Nyctalope.
In the fictional Star Trek universe, Captain Jean-Luc Picard had an artificial heart implanted in 2328, which was later replaced twice. Joseph Sisko, father of Benjamin Sisko, had several artificial organs, including a new aorta he received in 2372.
The British science fiction series Space: 1999 had a character, Victor Bergman (portrayed by Barry Morse), with an artificial heart. He was able to modify its rate of operation with a wrist-worn device.
The novels of Philip K. Dick feature the use of 'artiforgs' or artificial organs.
The German heavy metal band Accept wrote about artificial hearts in their album "Metal Heart" (1985).
In the 1987 movie Robocop, there is a commercial for an artificial heart clinic called "The Family Heart Center" where surgeons operate on persons and implant artificial hearts from "the complete line of hearts by Jensen and Yamaha," encouraging its customers "You pick the heart!" These hearts come with extended warranties, financing, and qualify for "health tax credit."
References
(1) N. Gray, Jr, C. Selzman. Current status of the total artificial heart. American Heart Journal, 152, (1):4-10. July 2006. link
FDA Approval Press Release September 5, 2006.
Further Reading
George B. Griffenhagen and Calvin H. Hughes. The history of the mechanical heart. Smithsonian Report for 1955, (Pub. 4241): 339-356, 1956.
Retrieved from "http://en.wikipedia.org/wiki/Artificial_heart"

Heart cancer

2007-01-08T19:25:00.000-08:00

From Wikipedia, the free encyclopedia
Heart cancer is a extremely rare form of cancer of the heart. Heart cancer is divided into primary tumors of the heart and secondary tumors of the heart. Most heart cancers are benign myxomas, fibromas, rhabdomyomas and hamartomas, although malignant sarcomas (such as angiosarcoma or cardiac sarcoma) have been known to occur. In a study of 12,487 autopsies performed in Hong Kong seven cardiac tumors were found, most of which were benign. However, cancer can also spread to heart from other parts of the body. In addition the heart can be affected by treatment for cancer in other parts of the body.[1] [2]
References
1. ^ Heart cancer: Is there such a thing? from the Mayo Clinic website, retrieved on November 11, 2006.
2. ^ Heart Cancer from the U.S. Department of Energy website, retrieved on November 11, 2006.

The heart is a hollow.

2007-01-08T18:55:00.000-08:00

The heart and lungs, from an older edition of Gray's Anatomy.
This article is about the organ. For the symbol of love, see Heart (symbol). For other uses, see Heart (disambiguation).
The heart is a hollow, muscular organ in vertebrates, responsible for pumping blood through the blood vessels by repeated, rhythmic contractions, or a similar structure in annelids, mollusks, and arthropods. The term cardiac (as in cardiology) means "related to the heart" and comes from the Greek καρδιά, kardia, for "heart." The heart is composed of cardiac muscle, an involuntary muscle tissue which is found only within this organ.
Contents
[hide]
• 1 Early development
• 2 Structure
• 3 Physiology
o 3.1 Regulation of the cardiac cycle
o 3.2 Other physiological functions
• 4 First aid
• 5 The hearts of other animals
o 5.1 Vertebrates
o 5.2 Invertebrates
o 5.3 Heartbeat
• 6 Food use
• 7 As a symbol
• 8 References

Early development
Main article: Heart development

At 21 days after conception, the human heart rate begins beating at 75-80 beats per minute and accelerates linearly for the first month of beating.
The human embryonic heart begins beating approximately 21 days after conception, or five weeks after the last normal menstrual period (LMP), which is the date normally used to date pregnancy. The human heart begins beating at a rate near the mother’s, about 75-80 beats per minute (bpm). The embryonic heart rate (EHR) then accelerates linearly for the first month of beating, peaking at 165-185 bpm during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 bpm per day, or about 10 bpm every three days, an increase of 100 bpm in the first month. [1]
After peaking at about 9.2 weeks after the LMP, it decelerates to about 150 bpm (+/-25 bpm) during the 15th week after the LMP. After the 15th week the deceleration slows reaching an average rate of about 145 (+/-25 bpm) bpm at term. The regression formula which describes this acceleration before the embryo reaches 25 mm in crown-rump length or 9.2 LMP weeks is:
Age in days = EHR(0.3)+6
See: Embryonic Heart Rates Compared in Assisted and Non-Assisted Pregnancies
There is no difference in male and female heart rates before birth.[1]] Structure

Anterior (frontal) view of the opened heart. Arrows indicate normal blood flow. Image provided courtesy of www.3dscience.com.
In the human body, the heart is normally situated to the left of the middle of the thorax, underneath the breastbone (see diagrams). The heart is usually felt to be on the left side because the left heart (left ventricle) is stronger (it pumps to all body parts). The left lung is smaller than the right lung because the heart occupies more of the left hemithorax. The heart is enclosed by a sac known as the pericardium and is surrounded by the lungs. The pericardium is a double membrane structure containing a serous fluid to reduce friction during heart contractions. The mediastinum, a subdivision of the thoracic cavity, is the name of the heart cavity.
The apex is the blunt point situated in an inferior (pointing down and left) direction. A stethoscope can be placed directly over the apex so that the beats can be counted. This physical location is between the sixth and seventh rib, just to the left of the sternum [2]. In normal adults, the mass of the heart is 250-350, or about three fourths the size of a clenched fist. g (9-12 oz), but extremely diseased hearts can be up to 1000 g (2 lb) in mass due to hypertrophy. It consists of four chambers, the two upper atria (singular: atrium ) and the two lower ventricles. On the left is a picture of a fresh human heart which was removed from a 64-year-old British male.

The function of the right side of the heart (see right heart) is to collect deoxygenated blood, in the right atrium, from the body and pump it, via the right ventricle, into the lungs (pulmonary circulation) so that carbon dioxide can be dropped off and oxygen picked up (gas exchange). This happens through a passive process called diffusion. The left side (see left heart) collects oxygenated blood from the lungs into the left atrium. From the left atrium the blood moves to the left ventricle which pumps it out to the body. On both sides, the lower ventricles are thicker and stronger than the upper atria. The muscle wall surrounding the left ventricle is thicker than the wall surrounding the right ventricle due to the higher force needed to pump the blood through the systemic circulation.
Physiology
Regulation of the cardiac cycle
Cardiac muscle is myogenic (able to contract and relax on its own). It is a specialized muscle found nowhere else but in the heart because it has its own conducting system. This is in contrast with skeletal muscle, which requires either conscious or reflex nervous stimuli. The heart's rhythmic contractions occur spontaneously, although the waves or nerves can be changed by nervous frequency influences such as exercise or the perception of danger.
The rhythmic sequence of contractions is coordinated by the sinoatrial and atrioventricular nodes. The sinoatrial node, often known as the cardiac pacemaker, is located in the upper wall of the right atrium and is responsible for the wave of electrical stimulation (See action potential) that initiates atria contraction. Once the wave reaches the atrioventricular node, situated in the lower right atrium, it is conducted through the bundles of His and causes contraction of the ventricles. The time taken for the wave to reach this node from the sinoatrial nerve creates a delay between contraction of the two chambers and ensures that each contraction is coordinated simultaneously throughout all of the heart. In the event of severe pathology, the Purkinje fibers can also act as a pacemaker; this is usually not the case because their rate of spontaneous firing is considerably lower than that of the other pacemakers and hence is overridden.
Other physiological functions
The heart also secretes atrial natriuretic factor (ANF), a powerful peptide hormone that affects the blood vessels, the adrenal glands, the kidneys, and the regulatory regions of the brain in order to regulate blood pressure and volume.
First aid
See cardiac arrest for emergencies involving the heart
If a person is encountered in cardiac arrest (no heartbeat), cardiopulmonary resuscitation (CPR) should be started, and help called. If an automated external defibrillator is available, this device may automatically administer defibrillation if this is indicated.
The hearts of other animals
Main article: Circulatory system#Types of circulatory systems
Vertebrates
The hearts of fish have only two chambers: one atrium and one ventricle. In fish, the system has only one circuit. The blood pumps through the gills and on to the bodily tissues before returning to the heart.
Amphibians and most reptiles have a three-chambered heart, in which oxygenated blood from the lungs and de-oxygenated blood from the respiring tissues enter by separate atria, and are directed via a spiral valve to the appropriate vessel—aorta for oxygenated blood and pulmonary artery for deoxygenated blood. The spiral valve is essential to keeping the mixing of the two types of blood to a minimum, enabling the animal to have higher metabolic rates, and be more active than otherwise.
Mammals, birds and crocodiles show complete separation of the heart into two pumps, for a total of four heart chambers; it is thought that the four-chambered heart of birds evolved independently of that of mammals.
Invertebrates
Many invertebrates, such as bivalves and arthropods, exhibit an open circulatory system where blood flows both in vessels and freely in the body cavity. In these animals the blood usually collects in a series of specialised sinuses, or cavities, where it directly comes in contact with tissues. It is then returned to the heart and is again released into the body.
The earthworm has no heart; instead it has five aortic arches that serve the same purpose.
Heartbeat
Smaller animals have faster heartbeats. This is evident within a species as well, as the young beat their hearts faster than the adults. See Early development above for information about the early human heart rates.
The Gray Whale's heart beats 9 times per minute, Harbour Seal 10 when diving, 140 when on land, elephant 25, human 72, sparrow 500, shrew 600, and hummingbird 1,200 when hovering. These heart rates usually vary on the animal's ratio of surface area to body mass; an elephant with relatively less surface area than a mouse loses proportionally less heat and requires comparatively less blood to be pumped throughout its body. An ectothermic animal will usually have a slower, and more variable heartbeat than an endothermic animal of similar size.
Food use
The hearts of cattle, sheep, pigs, chickens and certain fowl are consumed as food in many countries. They are counted among offal, but being a muscle, the taste of heart is much more like regular meat than that of other offal. It resembles venison in structure and taste.
As a symbol
For more details on this topic, see Heart (symbol).
The heart was historically seen by some as the seat of the soul and the organ responsible for human thought. Even though we now know that the heart has nothing to do with thought or love, people still carry on using the term "heart" metaphorically when talking about love. When used in this metaphorical sense, the heart is often illustrated as an icon (♥).
The term "heart" can also refer to the core or center of anything e.g. "The heart of the matter".
References
1. ^ Terry J. DuBose Sex, Heart Rate and Age
See also
• Artificial heart
• Atrium
• Cardiology
• Cardiothoracic Surgery
• Cardiovascular pathology
• Circulatory system
• Echocardiography
• Electrical conduction system of the heart
• Haemodynamics
• Heart cancer
• Heart defects
• Heart rate
• Heart transplant
• Human anatomy
• Pulse
• Ventricle
• Aorta
• Ventricular hypertrophy
• Holiday heart syndrome
• Circle map — simplified mathematical model of the beating heart.
• MUGA scan
• Cardiac stress test

Papillary muscle

2007-01-07T20:36:00.002-08:00

In anatomy, the papillary muscles of the heart serve to limit the movements of the mitral and tricuspid valves and prevent them from being inverted. They do not close or open the valves, which close passively in response to pressure gradients. Instead they brace the valves against the high pressure.
The U wave in an ECG represents papillary muscle repolarization. It usually does not appear unless a patient's electrolytes are imbalanced.

Coronary artery bypass surgery

2007-01-07T20:02:00.000-08:00

Coronary artery bypass surgery, also coronary artery bypass graft surgery, and colloquially heart bypass or bypass surgery is a surgical procedure performed to relieve angina and reduce the risk of death from coronary artery disease. Arteries and /or veins from elsewhere in the patient's body are grafted from the aorta to the coronary arteries to bypass atherosclerotic narrowings and improve the blood supply to the coronary circulation supplying the myocardium (heart muscle).

Early in a coronary artery bypass surgery during vein harvesting from the legs (left of image) and the establishment of bypass (placement of the aortic cannula) (bottom of image). The perfusionist and heart-lung machine (HLM) are on the upper right. The patient's head (not seen) is at the bottom.

Coronary artery bypass surgery during mobilization (freeing) of the right coronary artery from its surrounding tissue, adipose tissue (yellow). The tube visible at the bottom is the aortic cannula (returns blood from the HLM). The tube above it (obscured by the surgeon on the right) is the venous cannula (receives blood from the body). The patient's heart is stopped and the aorta is cross-clamped. The patient's head (not seen) is at the bottom.
Contents
1 History
2 Terminology
2.1 Number of bypasses
3 Prognosis
4 Complications
5 Procedure (Simplified)
6 Conduits used for bypass
6.1 Graft patency
7 Minimally Invasive CABG

//
History
The technique was pioneered by Argentinian René Favaloro and others at the Cleveland Clinic in the late 1960s.[1] Currently, about 500,000 CABGs are performed in the United States each year.
Terminology
There are many variations on terminology, in which one or more of 'artery', 'bypass' or 'graft' is left out. The most frequently used acronym for this type of surgery is CABG (pronounced 'cabbage'),[2] pluralized as CABG's (pronounced 'cabbages'). More recently the term aortocoronary bypass (ACB) has come into popular use. CAGS (Coronary Artery Graft Surgery, pronounced phonetically) has been used (primarily outside the United States) and should not be confused with Coronary Angiography (CAG).
Number of bypasses
The terms single bypass, double bypass, triple bypass and quadruple bypass refer to the number of coronary arteries bypassed in the procedure. In other words, a double bypass means two coronary arteries are bypassed (e.g. the left anterior descending (LAD) coronary artery and right coronary artery (RCA)); a triple bypass means three vessels are bypassed (e.g. LAD, RCA, left circumflex artery (LCX)); a quadruple bypass means four vessels are bypassed (e.g. LAD, RCA, LCX, first diagnonal artery of the LAD). Less commonly more than four coronary arteries may be bypassed.
A greater number of bypasses does not imply a person is "sicker," nor does a lesser number imply a person is "healthier." A person with a large amount of coronary artery disease (CAD) may receive less bypass grafts due to the lack of suitable "target" vessels. A coronary artery may be unsuitable for bypass grafting it if it is small (< title="Stenosis" href="http://en.wikipedia.org/wiki/Stenosis">stenosis ("narrowing") of the left main coronary artery requires only two bypasses (to the LAD and the LCX). However, a left main lesion places a person at the highest risk for death from a cardiac cause.[citation needed]
The surgeon reviews the coronary angiogram prior to surgery and identifies the lesions (or "blockages") in the coronary arteries. The surgeon will estimate of the number of bypass grafts prior to surgery, but the final decision is made in the operating room upon examination of the heart.
Prognosis
Prognosis following CABG depends on a variety of factors, but successful grafts typically last around 10-15 years. In general, CABG improves the chances of survival of patients who are at high risk (meaning those presenting with angina pain shown to be due to ischemic heart disease), but statistically after about 5 years the difference in survival rate between those who have had surgery and those treated by drug therapy diminishes. Age at the time of CABG is critical to the prognosis, younger patients with no complicating diseases have a high probability of greater longevity. The older patient can usually be expected to suffer further blockage of the coronary arteries.
Complications
Infection at incision sites
Deep vein thrombosis (DVT)
Nonunion or malunion of the sternum
Anesthetic complications such as malignant hyperthermia)
Myocardial infarction due to hypoperfusion, early graft occlusion, or graft failure
Acute renal failure due to hypoperfusion
Stroke during reperfusion
Stenosis of the graft, particularly of saphenous vein grafts
Keloid scarring
Chronic pain at incision sites
Postoperative stress-related illnesses such as constipation, chronic bracing, memory loss, trench mouth, and teeth grinding
Death due to myocardial infarction, stroke, renal failure, or sepsis
Most commonly, the sternum is cut down the middle with a bone saw and the chest opened (a procedure known as median sternotomy). Depending on a number of factors, the surgeon may decide to place the patient on cardiopulmonary bypass ("on-pump") or use stabilizing devices to hold the heart still while sewing the anastomoses ("off-pump"). Blood vessels are harvested from elsewhere in the body for grafting. Sometimes artery end branches supplying tissues near the heart are rerouted to create the bypass.
Procedure (Simplified)
1) An artery may be detached from the chest wall and the open end attached to the coronary artery below the blocked area.
2) A piece of a long vein in the leg may be taken. One end is sewn onto the large artery leaving the heart -- the aorta. The other end of the vein is attached or "grafted" to the coronary artery below the blocked area.
Either way, blood can use this new path to flow freely to the heart muscle.
Conduits used for bypass
The choice of conduits is highly surgeon and institution dependent. Typically, the left internal thoracic artery (LITA) (previously referred to as left internal mammary artery or LIMA) is grafted to the Left Anterior Descending artery and a combination of other arteries and veins is used for other coronary arteries. The right internal thoracic artery (RITA), the great saphenous vein from the leg and the radial artery from the forearm are frequently used. The right gastroepiploic artery from the stomach is used infrequently used given the difficult mobilization from the abdomen.
Graft patency
Grafts can become diseased and may occlude in the months to years after bypass surgery is performed. Patency is a term used to describe the chance that a graft remain open. A graft is considered patent if there is flow through the graft without any significant (>70% diameter) stenosis in the graft.
Graft patency is dependent on a number of factors, including the type of graft used (internal thoracic artery, radial artery, or great saphenous vein), the size or the coronary artery that the graft is anastomosed with, and, of course, the skill of the surgeon(s) performing the procedure. Arterial grafts (e.g. LITA, radial) are far more sensitive to rough handling than the saphenous veins and may go into spasm if handled improperly.
Generally the best patency rates are achieved with the in-situ (the proximal end is left connected to the subclavian artery) left internal thoracic artery with the distal end being anastomosed with the coronary artery (typically the left anterior descending artery or a diagonal branch artery). Lesser patency rates can be expected with radial artery grafts and "free" internal thoracic artery grafts (where the proximal end of the thoracic artery is excised from its origin from the subclavian artery and re-anastomosed with the ascending aorta). Saphenous vein grafts have worse patency rates, but are more available, as the patients can have multiple segments of the saphenous vein used to bypass different arteries.
Veins that are used either have their valves removed or are turned around so that the valves in them do not occlude blood flow in the graft. LITA grafts are longer-lasting than vein grafts, both because the artery is more robust than a vein and because, being already connected to the arterial tree, the LITA need only be grafted at one end. The LITA is usually grafted to the left anterior descending coronary artery (LAD) because of its superior long-term patency when compared to saphenous vein grafts.[3][4]
Minimally Invasive CABG
Alternate methods of minimally invasive coronary artery bypass surgery have been developed in recent times. Off-pump coronary artery bypass surgery (OPCAB) is a technique of performing bypass surgery without the use of cardiopulmonary bypass (the heart-lung machine). Futher refinements to OPCAB have resulted in Minimally invasive direct coronary artery bypass surgery (MIDCAB) which is a technique of performing bypass surgery through a 5 to 10 cm incision.

Heart disease

2006-12-21T00:39:00.000-08:00

Heart disease is an umbrella term for a number of different diseases which affect the heart. The most common heart diseases are:
Coronary heart disease, a disease of the heart itself caused by the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium
Ischaemic heart disease, another disease of the heart itself, characterized by reduced blood supply to the organ.
Cardiovascular disease, a sub-umbrella term for a number of diseases that that affect the heart itself and/or the blood vessel system, especially the veins and arteries leading to and from the heart. Research on disease dimorphism suggests that women who suffer with cardiovascular disease usually suffer from forms that affect the blood vessels while men usually suffer from forms that affect the heart muscle itself. Well known causes of cardiovascular disease include diabetes mellitus, hypertension and hypercholesterolemia.

Pulmonary heart disease, a failure of the right side of the heart.
Hereditary heart disease, heart disease caused by unavoidable genetic factors
Hypertensive heart disease, heart disease caused by high blood pressure, especially localised high blood pressure
Inflammatory heart disease, heart disease that involves inflammation of the heart muscle and/or the tissue surrounding it.
Valvular heart disease, heart disease that affects the valves of the heart.
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Key to health

2006-12-20T06:43:00.000-08:00

Are Stem Cells the key to health? by Mike Martinez

We hear much controversy concerning the ethical nature of Stem Cell reasearch. In particular embryonic stem cells. The reason is clear, embryonic stem cells are taken from a developing embryo, thus destroying it. Yet Stem Cell research continues because they have shown to have the potential to develop or transform themselves in almost any cell in the human body. This means a rejuvenation of damaged or injured organs. Many of todays so called degenerative diseases, which we currently have little if any effective therapies, could in fact be alleviated or healed. Advocates of Stem Cell research argue that Stem Cells could hold the key to curing diseases like cancer, AIDS, Alzheimer and multiple sclerosis, just to name a few. Facinating science.
However what most people have not heard about is Adult Stem Cells. These Stem Cells are found in the human body, mainly in the bone marrow. Recent research shows that Adult Stem Cells also have the ability to renew damaged organs and tissue within the body.
In fact, while embryonic Stem Cells have not been used in even one human theraphy, Adult Stem Cells have already been used successfully in numerous patients. Jay Lefkowitz, a former adviser to President Bush on Stem Cell policy says, "Adult Stem cells are really where the real progress is being made."
The key difference with Stem Cells is that they can divide, regenerate and actually become different organ cells. Research has conclusively shown Stem Cells can become liver cells, blood cells, pancrea cells, heart cells, and even brain cells. Almost any cell or tissue in the body.
For decades now Adult Stem Cells have been used very successfully in bone marrow transplants to treat certain cases of blood disorders and leukemia. A massive amount of research, which is still in it's early stage but none the less very promising, shows impressive results for heart damage due to heart attacks, liver disease, bone and cartilage diseases and brain disorders.
In a landmark experiment, Professor Saul J. Sharkis of John Hopkins University was able to convert bone-marrow Adult Stem Cells from animal donors into healthy liver cells. He says, "It is mind blowing stuff. I never would have thought this would be possible."
In another landmark experiment carried out by scientist at Yale University in 2001, Adult Stem Cells taken from the bone marrow of male mice were injected into female mice whose own marrow was destroyed by radiation irradation. Eleven months later, the male stem cells (identified through the Y chromosome) were found not only in the females' bone marrow, but also in their blood, guts, lungs and skin tissue.
While there is still much to learn about the magic of Adult Stem Cells, we can rest assure that a breakthrough in health is right around the corner.
About the Author
Mike Martinez is at the forefront educating people on the benefits of Adult Stem Cell enhancement for optimal health. For more information visit http:www.stemcellmagic.com , hearth.com ,
hearth-disesae.com , coronary.com ,
Cardiac.net, heart-attack.net,heart.net
, coronar.net healthdisesae@hotmail,
coronary@yahoo.com, Cardiac@hotmail.com,
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Heart Disease by Hock

2006-12-19T23:10:00.000-08:00

Beware Of Kids That Have Signs Of Heart Disease! by Ng Peng Hock

Under normal circumstances, we would think that only adults, especially elderly, will have narrowing and hardening of arteries. But, the findings of a study presented at the annual American Heart Association in Chicago last month (Nov 2006) will probably change our views.
A group of researchers in Canada, Finland, Australia, the United States, Norway, Italy, and Netherlands found that children with risk factors for heart disease, including high cholesterol and diabetes, are now showing signs of heart disease, including hardened of blood vessels and arterial wall thickness. The report revealed that in 12 of the 15 studies examined, children with risk factors were more likely to have increased thickness in the arterial walls, which could lead to heart attacks in adulthood. The risk factors include familial hypercholesterolemia where children whose defective genes causes high cholesterol levels in them, diabetes, obesity, and genetic factors.
Some experts and doctors felt that the finding is probably not new as previous postmortem studies of young United States soldiers who died in the Korean War had shown atherosclerotic changes in their arteries. The process must have begun much earlier on in their life. It is evident that deposits of plaque containing cholesterol and lipids takes years to build up and risk factors in childhood hasten the process.
There is indication that the number of young people who died suddenly has been on the rise. While the risk of atherosclerosis or the hardening of arteries can certainly carry over from childhood to adulthood, it is still no concrete evidence to link these sudden deaths of young people with childhood atherosclerosis unless their postmortem findings are made known.
Although there is an increasing number of children suffer from these and other risk factors for cardiovascular disease, testing for future heart conditions is still not standard practice. Currently, there is also no need to routinely screen lipid levels in all children.
If the lipid levels are normal, no specific treatment is needed. Nevertheless, maintaining healthy lifestyle is very important. This includes attention paid to healthy diet, regular exercise, and good weight management.
Selectively those with diabetes and those at risk are screened and statins have been used to treat children with familial hypercholesterolemia. Statins are drugs that lower bad cholesterol levels by limiting the amount of cholesterol the body can make.
America's Most Trusted Doctor Reveals ... How to Prevent and Reverse Heart Disease - Without Drugs or Surgery. Read more about his confession at: http://www.howtopreventheartdiesase.com/heart-disease-prevention-dr-robert-article.html
About the Author
Feel free to use this article on your website or ezine as long as the following information about author/website is included. Heart Disease Prevention - 8 Simple Ways You Can Do Immediately, Go to: http://www.howtoperventheartdisease.com
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Heart Disease by Dustin

2006-12-19T23:07:00.000-08:00

The Hidden Links Between Depression And Heart Disease by Dustin Cannon

While there are tales of people dying of a broken heart, such sayings have long been relegated to the fantasy bin. However, recent research has shown that there are true connections between depression and heart disease.
Depression was once considered to be only a psychological disorder with no physiological underpinnings. However, it is now known that depression often has biochemical origins and can therefore be treated with medication like other types of diseases.
However, the biological origin of some forms of depression means that there could be a fundamental link between the two disorders on a physical level. However, it is also possible that depression may make sufferers less likely to take care of themselves properly which can increase the occurrence of heart disease. Likewise, the discovery that one has heart disease can trigger depression in some who may have had a latent susceptibility to the disorder.
Scientific studies have linked the occurred of coronary heart disease and ischaemic heart diseases, both of which are related to poor blood flow to certain sections of the heart and are one of the biggest killers in the world, have been statistically linked with depressive disorders. It has long been known that there is a stress and heart disease connection and, in this case, it is easy to understand.
Stress releases a number of chemicals, including adrenaline, which cause the body to go into "fight or flight" mode. These chemicals do a number of things, including increasing blood flow to the muscles, increasing the rate of respiration, and increasing heart rate, all of which can possibly damage heart muscle tissue. However, the link with clinical depression is somewhat more vague. It is possible that there is a chemical link between the two diseases; however, many scientists suspect that the relationship is not physical in nature but rather a natural couplet since the prospect of facing heart disease may make some people depressed and some people with depression may not be able to care for themselves as adequately as those who do not suffer from the disease which makes it more likely that they will suffer heart disease from simple neglect. People who suffer from depression are also more likely to abuse tobacco and alcohol and frequently do not exercise regularly.
Those who suffer from both heart disease and depression should make sure that their psychiatrist or psychologist is in close contact with their cardiologist. Since the two disorders are related, the treatment should be coordinated to make sure that the treatment of one of the diseases will not negatively impact the other.
Both heart disease and depression are disorders whose prognosis declines with time. Therefore, it is important that both are detected early in order to have the best possible patient outcomes.
About the Author
Dustin Cannon is owner of JustArticlesVIP.com and writes on a variety of subjects. To learn more about this topic Dustin recommends you visit: Good Medicine RX
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Heart Healthy Diet

2006-12-19T23:04:00.000-08:00

Heart Healthy Diet by Nitin Chhoda

Chances are that someone you know has been a victim of heart disease or high blood pressure, and the frightening part is that it is one of the top 3 causes of death in the country. In fact, my father died due to a sudden, massive heart attack. Diet plays a major role in the development (and treatment) of heart problems. There are several things we can do to improve heart health.
For example, did you know that eating more garlic (in raw or cooked forms) is associated with a lower incidence of heart disease, owing to its anti-oxidant properties? Onions also have a similar effect. Munching on small amounts ( 1 to 2 oz. ) of nuts such as peanuts, almonds, and walnuts is extremely beneficial for the heart. These are rich in fiber and mono-unsaturated fats (the good type).
The health of your heart is a gift that's yours for the taking. It's time for a change of heart. Let's take a look at the do's and don'ts for a healthy heart.
Some diets are bad for your heart. A high sugar, low fiber diet. (pizzas, breads, rice, pasta) A high sodium to potassium ratio. (salted foods, low intake of fresh fruits and vegetables) A diet low in calcium and magnesium. (low intake of dairy products) A diet high in saturated fats and low in essential fats. (high intake of fast foods and red meats, low intake of fish and nuts) Each of these can be corrected in part, by a simple nutrition plan, which is outlined below.
Choosing the right kind of carbohydrates is important. Ask yourself if you find it difficult to get by without the following foods - Cakes, candies, chocolates, cookies, etc. If you do, then it is time to cut down slowly. Eat more whole-wheat cereals, bran, oats, oranges, tomatoes, sprouts, mushrooms, cabbage, cauliflower, and lettuce. Make a fresh bowl of soup each day with these vegetables. Eat lean meats, chicken and fish regularly. Soda is a big culprit in obesity and heart disease. Just try and substitute it with plain old water!
The importance of minerals cannot be overlooked. A lack of calcium, magnesium, and potassium can increase blood pressure. Decrease the intake of sodium, and substitute regular salt with sea salt, which contains an abundance of minerals. Magnesium is strongly correlated with heart health. Non-fat milk, fish and yogurt are great ways to get extra calcium, without the saturated fat. If you take calcium supplements, ask your doctor if you can take a magnesium supplement as well.
Fat plays an important role in heart health, more specifically the type of fat. While we all know the long-term benefits of low fat eating, few realize the immediate repercussions of high fat foods. For example, eating a single high fat meal on Sunday night can increase your risk of having a heart attack on Monday morning!!
In a nutshell, the following foods / factors can prevent heart disease: seafood (omega 3' fats) and olive oil. Nuts like walnuts, almonds (omega 3's and magnesium). Fruits, vegetables. (Anti-oxidants). Grains, legumes. Garlic and onions.
As always, try and minimize stress and avoid smoking. Check your blood pressure and cholesterol levels regularly. Don't forget your annual physical!
About the AuthorFor more information and to register for free and get full-color exercise routines, diet plans and grocery lists, visit http://www.best-weight-loss-program.net/ , for exercises for women, visit http://ww.toningforwomen.com/ and to train with Nitin, visit http://www.phonefitnestrainer.com/
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Ideas:Diseases of the Heart

2006-12-19T22:58:00.000-08:00

Philosophy & Ideas: Diseases of the Heart by David Hulme

The tragedy of human heart disease has motivated many medical researchers. For many years, it has provoked philosophy and ideas as well as opportunities for the advancement of medicine. As early as 1905 the heart of a dog was transplanted into another dog at the University of Chicago. But it wasn't until 1967 that the celebrated South African surgeon Christiaan Barnard performed the transplant of a human heart. Mechanical hearts of various kinds have also met with some success. Notable was Barney Clark, who in 1982 became the first recipient of the Jarvik-7, a permanent-replacement artificial heart. He lived for 112 days attached to a cumbersome console. Another patient, William Schroeder, lived for 620 days after the implanting of a Jarvik-7.
The artificial heart is generally used to bridge patients over the waiting period until a suitable human heart becomes available for transplant. In 1985 Thomas Gaidosh received a Jarvik-7 and four days later a human heart. He lived 11 more years.
There have been many amazing developments in the field. Last summer in Louisville, Kentucky, surgeons implanted a revolutionary self-contained artificial heart into the chest of a terminally ill diabetic man. Though his condition had been grave, the device allowed him relief from other organ malfunctions by canceling the effect of his diseased heart.
These attempts at resolving physical disease demonstrate significant progress. But the heart is more than a muscular pump that is sometimes diseased. We also speak of it as the seat of emotional well-being. That may not be too far from the truth. Some years ago I interviewed a medical doctor, Redford Williams, who had written a book titled The Trusting Heart. His purpose was to show the toxic effect on the body of our own hostile spirit and, conversely, the physical benefits of a positive frame of mind. From his studies of the endocrine system and the effects of stress and emotion, he had discovered something that the ancients knew: Our emotions can keep us well or make us sick. Take these words of advice from the wisdom literature of Solomon: "A sound heart is life to the body, but envy is rottenness to the bones" (Proverbs 14:30). Further he wrote, "A merry heart does good, like medicine, but a broken spirit dries the bones" (Proverbs 17:22).
Other wisdom attributed to religion and the Bible, particularly Scriptures, makes clear that the human heart is the center of another kind of sickness. It is diseased in a far more profound way. Jesus said: "What comes out of a man, that defiles a man. For from within, out of the heart of men, proceed evil thoughts, adulteries, fornications, murders, thefts, covetousness, wickedness, deceit, lewdness, an evil eye, blasphemy, pride, foolishness" (Mark 7:20-22). This is the natural way of humans, though we don't like to admit it. Pushed to the limit, under certain circumstances we are all capable of such things.
Just as there is help for diseased heart muscle, there is help for these other diseases of the "heart." The Spirit of God will gradually cure the works of the flesh that Jesus defined. Interfacing with the human spirit, God's Spirit is available to heal us.
Take, for example, some of the works of the flesh mentioned by the apostle Paul in his letter to the Galatian church, and set them against the curative fruit of the Spirit. Murder, anger and hatred are overcome by love or benevolence; variance, strife and fierce indignation are defeated by peace and a tranquil mind; the sexual sins fall to the power of self-control and one's moral values. Paul adds that there are more works of the flesh than he has named, but the lesson is clear: There is help for whichever disease of the heart we have.
About the AuthorAuthor, David Hulme, Publisher for Vision Media Productions and author of "Identity, Ideology And The Future Of Jerusalem," contributes articles on culture, current events and ideology for Vision Media. More information about these and other current events and ideology topics can be found at http://www.vision.org
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Basic Steps to Good Health(health disesae)

2006-12-19T19:04:00.000-08:00

Basic Steps to Good Health ...(health disesae)by Chris Chenoweth

EAT WELL - Eat a well-balanced diet that includes plenty of fruits and vegetables, as well as foods that are high in complex carbohydrates, moderate amounts of protein, and low in fat. Make sure you eat regular meals. Skipping meals or eliminating certain foods can lead to out-of-control hunger, resulting in overeating. Eat in moderation. Most people eat for pleasure as well as nutrition. If your favorite foods are high in fat, salt or sugar, the key is moderation.
DRINK WATER - Drink lots of water. Most people do NOT drink enough water. Dehydration is very subtle. By the time you feel thirsty, you are already dehydrated. Most of us are dehydrated because we do not drink enough water for our body to operate at optimal capacity. Insufficient water consumption (dehydration) makes you tired, gives you headaches, and weakens your immune system. Water is the most important nutrient that our body needs in order to function properly. When the body becomes dehydrated, the organs can become damaged, resulting in various types of degenerative diseases. Every major system in our body depends on water.
EXERCISE REGULARLY - Anyone can benefit from starting a basic aerobic exercise program. If you get little exercise, even walking 10 minutes a day can help your body immensely. Exercise controls blood sugar, helps you lose weight, and helps your body detoxify. Walking is the most easily accessible and beneficial exercise and anyone can do it.
REDUCE STRESS - Avoid excessive amounts of caffeine that can increase your anxiety level and avoid alcohol that can mask symptoms and make them worse. Try deep breathing exercises, massage, guided imagery, and meditation. Learn it is okay to say NO occasionally. Make time for yourself, your number one priority.
GET ENOUGH REST - Most Americans do not get enough sleep. Getting enough sleep is vitally important for physical and emotional health. If you have difficulty sleeping, NEVER read, eat or watch television in bed.
DO NOT SMOKE - The nicotine and other poisonous chemicals in tobacco greatly increase the likelihood of developing certain cancers and heart disease. Every time you light up, you hurt your lungs and heart. The longer you smoke, the worse the damage becomes.
AVOID TOO MUCH SUN EXPOSURE - Skin damage from overexposure to the sun is cumulative over the years and is irreversible. Too much time in the sun can cause sunburn, especially for fair-skinned people, and other potential problems. These problems range from fatal skin cancers to allergic reactions.
FASTEN YOUR SEAT BELT - If worn properly, seat belts absorb the force of a crash impact and hold you securely in place, greatly reducing your risk of injury.
SEE YOUR DOCTOR REGULARLY FOR PREVENTIVE CARE - Doctors do not only treat patients when they are ill. With regular checkups and preventive services, you can help prevent serious health conditions such as heart disease, cancer, high blood pressure, diabetes, etc.
Using the above guidelines will start you on your way to a healthier life. You will feel good about yourself, have more energy, look better, and provide a good role model for your family.
If you would like additional information on healthy ways to lose weight, learn how to burn fat with one of the most effective and healthy fat-burning systems available, the BURN THE FAT program.

About the Author
Chris Chenoweth, author of the DO-IT-YOURSELF HOME, HEALTH & MONEY GUIDE, writes articles pertaining to diet, exercise, health, and business .
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Coronary circulation

2006-12-19T08:28:00.000-08:00

The coronary circulation consists of the blood vessels that supply blood to, and remove blood from, the heart muscle itself. Although blood fills the chambers of the heart, the muscle tissue of the heart, or myocardium, is so thick that it requires coronary blood vessels to deliver blood deep into the myocardium. The vessels that supply blood high in oxygen to the myocardium are known as coronary arteries. The vessels that remove the deoxygenated blood from the heart muscle are known as cardiac veins.
The coronary arteries that run on the surface of the heart are called epicardial coronary arteries. These arteries, when healthy, are capable of autoregulation to maintain coronary blood flow at levels appropriate to the needs of the heart muscle. These relatively narrow vessels are commonly affected by atherosclerosis and can become blocked, causing angina or a heart attack. (See also: circulatory system.)
The coronary arteries are classified as "end circulation", since they represent the only source of blood supply to the myocardium: there is very little redundant blood supply, which is why blockage of these vessels can be so critical.

Contents
1 Coronary anatomy
1.1 Variations
1.2 Coronary artery dominance
2 Blood supply of the papillary muscles
3 Coronary flow

Coronary anatomy
The exact anatomy of the myocardial blood supply varies considerably from person to person. A full evaluation of the coronary arteries requires cardiac catheterization or CT coronary angiography.
In general there are two main coronary arteries, the left and right.
Right coronary artery
Left coronary artery
Both of these arteries originate from the beginning (root) of the aorta, immediately above the aortic valve. As discussed below, the left coronary artery originates from the left aortic sinus, while the right coronary artery originates from the right aortic sinus
Variations
Four percent of people have a third, the posterior coronary artery. In rare cases, a patient will have one coronary artery that runs around the root of the aorta.
Occasionally, a coronary artery will exist as a double structure (ie there are two arteries, parallel to each other, where ordinarily there is one). Dana Carvey has this variation, which led to a mishap during his CABG operation.

Coronary artery dominance
The artery that supplies the posterior descending artery (PDA) and the posterolateral artery (PLA) determines the coronary dominance.
If the right coronary artery (RCA) supplies both these arteries, the circulation can be classified as "right-dominant".
If the left circumflex artery (LCX) supplies both these arteries, the circulation can be classified as "left-dominant".
If the RCA supplies the PDA and the LCX supplies the PLA, the circulation is known as "co-dominant".
Approximately 70% of the general population are right-dominant, 20% are co-dominant, and 10% are left-dominant. [1]

Blood supply of the papillary muscles
The papillary muscles tether the mitral valve (the valve between the left atrium and the left ventricle) and the tricuspid valve (the valve between the right atrium and the right ventricle) to the wall of the heart. If the papillary muscles are not functioning properly, the mitral valve leaks during contraction of the left ventricule. This causes some of the blood to travel "in reverse", from the left ventricle to the left atrium, instead of forward to the aorta and the rest of the body. This leaking of blood to the left atrium is known as mitral regurgitation.
The anterolateral papillary muscle receives two blood supplies: the LAD and LCX, and is therefore somewhat resistant to coronary ischemia. On the other hand, the posteromedial papillary muscle is supplied only by the PDA. This makes the posteromedial papillary muscle significantly more susceptible to ischemia. The clinical significance of this is that a myocardial infarction involving the PDA is more likely to cause mitral regurgitation.

Coronary flow
During contraction of the ventricular myocardium (systole), the subendocardial coronary vessels (the vessels that enter the myocardium) are compressed due to the high intraventricular pressures. However the epicardial coronary vessels (the vessels that run along the outer surface of the heart) remain patent. Because of this, blood flow in the subendocardium stops. As a result most myocardial perfusion occurs during heart relaxation (diastole) when the subendocardial coronary vessels are patent and under low pressure. This contributes to the filling difficulties of the coronary arteries.
The primary determinant of coronary blood flow is the level of myocardial/cardiac oxygen consumption. As the heart beats more vigorously, ATP is consumed at a greater rate due to the increased force and/or frequency of contraction and the depolarization and repolarization of the cardiac membrane potential. The increase in oxygen consumption results in the release of a vasodilator substance, the identity of which remains unknown. The vasodilator reduces vascular resistance and allows more blood to flow through the heart during each diastole. Systolic compression remains the same. Failure of oxygen delivery via increases in blood flow to meet the increased oxygen demand of the heart results in tissue ischemia, a condition of oxygen debt. Brief ischemia is associated with intense chest pain, known as angina. Severe ischemia can cause the heart muscle to die of oxygen starvation, called a myocardial infarction. Chronic moderate ischemia causes contraction of the heart to weaken, known as myocardial hibernation.
In addition to metabolism, the coronary circulation possesses unique pharmacologic characteristics. Prominent among these is its reactivity to adrenergic stimulation. The majority of circulation in the body constrict to norepinephrine, a sympathetic neurotransmitter the body uses to increases blood pressure. In the coronary circulation, norepinephrine elicits vasodilation, due to the predominance of beta-adrenergic receptors in the coronary circulation. Agonists of alpha-receptors, such as phenylephrine, elicit very little constriction in the coronary circulation.

Diet and heart disease

2006-12-19T01:57:00.000-08:00

Diet and heart disease
From Wikipedia, the free encyclopedia
(Redirected from Diet and Heart Disease)
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Diet may play an important role in causing or preventing heart disease. Doctors and nutritionists have studied numerous diets and dietary components in an effort to minimise the risk of heart diseases.
Contents
1 Misconceptions
1.1 Saturated fats & Cholesterol
2 Dietary factors that may increase risk
2.1 Trans fats
2.2 Salt
2.3 Homogenised milk
3 Preventive diets
3.1 Vegetarian diet
3.2 Cretan Mediterranean-style diet
3.3 Alcohol
4 Summary
5 See also
6 References
7 External links
7.1 Government advice
7.2 Science sites
7.3 Other sites

Misconceptions

Saturated fats & Cholesterol
One of the earliest suggestions that saturated fats and cholesterol could be related to heart disease was proposed by Ancel Keys in the late 1950s. While this and other similar studies were eagerly received by commercial beneficiaries such as the processed oil and food industries, other scientific studies have cast doubts on whether saturated fats should be demonised.
An analysis of American statistics covering the sixty year period from 1910 to 1970 found that the proportion of traditional animal fats in the American diet declined from 83% to 62%, and the annual consumption of butter in particular declined from 18 pounds to 4 pounds per person. The study also found that over the past eighty years, the percentage of vegetable oil consumption in the form of margarine, vegetable shortening and other refined oils has increased by around 400%, with the consumption of sugar and processed foods by 60%.[1] This suggests that hydrogenated oils (which contain trans fat, not saturated fat) and sugar should be suspected to be more at fault than saturated fats.
A famous project called the Framingham Heart Study, started in 1948, found after 40 years of testing that while those who weighed more and had abnormally high blood cholesterol levels were slightly more at risk of developing heart disease, weight gain and cholesterol levels had an inverse correlation with saturated fat and cholesterol intake in the diet.[2] It was also found that the subjects with the highest saturated fat consumption weighed the least, but also happened to be the most physically active of the population under study. A director of the Framingham Heart Study, Dr William Castelli, wrote in 1992 [1]

For example, in Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol... In view of this, this study fails to describe a relationship of those traditional dietary constituents, saturated fat and cholesterol, known to have an adverse effect on blood lipids, and thereby, on the subsequent development of coronary disease end points.[3]

One large trial, the Multiple Risk Factor Intervention Trial (MRFIT) produced surprising results. It compared the death rates and eating habits of 12,000 men, and treated certain individuals by controlling high blood pressure with medicines, preventing smoking, and stipulating a low fat, low cholesterol diet. The MRFIT trial found that while those on the low fat diet had a slightly decreased mortality from Coronary heart disease, the overall mortality from all causes for those who were treated and obeyed the suggested diet was higher.[4]
Another study from the 1960s which examined the health of Yemenite Jews found that the diet of the subjects living in Yemen contained no sugar and obtained all its fat from animal sources. The subjects who had moved from Yemen to Israel altered their diets so that 25-30 percent of their carbohydrate intake was derived from sugar, and they obtained their fat from the consumption of margarine and vegetable oils. The Yemenite group was found to have few examples of heart disease and diabetes, whereas incidences of these disorders were far higher in the Israeli group.[5]
Saturated fats have gained an unjust notoriety by being confused with trans fats, both in early studies from the mid 20th century, and also as they were long grouped together in various U.S. databases used by researchers to correlate dietary trends with disease conditions.[6][7][8]

Dietary factors that may increase risk

Trans fats
Main article: Trans fat
While both saturated and trans fats increase levels of LDL cholesterol (so-called "bad" cholesterol), trans fats also lower the levels of HDL cholesterol (so-called "good" cholesterol) [2]; this increases the risk of coronary heart disease (CHD). The NAS is concerned "that dietary trans fatty acids are more deleterious with respect to CHD than saturated fatty acids" [3].
The Harvard Medical School has shown that most oils reduce blood cholesterol. However, more importantly they showed that hydrogenated, or trans fats, which are present in margarine and are extensively used for packaged food manufacturing, may be harmful. One of their studies published in 2005 has determined that a positive relationship exists between the consumption of trans fat and the development of endothelial dysfunction, a precursor to atherosclerosis.[9]
Trans fats are harmful because they are absorbed by the body's cell membranes as if they were cis fats, causing the cells to become partially hydrogenated, which disrupts cell metabolism.[4]
Other studies have found that hydrogenated fats made from vegetable oils block the use of essential fatty acids, which could contribute to sexual dysfunction, increased blood cholesterol and negatively affect the immune system.[10][11][12][13][14]

Salt
Main article: Edible salt
The UK Scientific Advisory Committee on Nutrition (SACN) review Salt and Health is probably the most authoritative single document on its stated topic. It concludes:
Hypertension (high blood pressure). "Since 1994, the evidence of an association between dietary salt intakes and blood pressure has increased. The data have been consistent in various study populations and across the age range in adults." (SACN, p3).
Left Ventricular Hypertrophy (LVH). "Evidence suggests that high salt intake causes left ventricular hypertrophy, a strong risk factor for cardiovascular disease, independently of blood pressure effects." (SACN, p3)

Homogenised milk
Main Articles: Unpasteurised milk: Homogenisation & heart disease; also Milk: Creaming & homogenisation
In recent years, there has been increased attention placed on potential health concerns relating to the homogenisation of milk and other dairy products. Studies conducted by Dr Kurt A Oster and his colleague D.J. Ross from the early 1960s to the mid 1980s suggested that homogenised milk could be a major factor in arterial plaque formation, causing heart disease.
Oster and Ross hypothesised that the homogenisation of milk increased the dietary availability of xanthine oxidase, which could lead to the formation of arterial, or atheromatous, plaque. However a team lead by A.J. Clifford in the early 1980s asserted that Oster and Ross had not sufficiently established their arguments.[15]
While the xanthine oxidase/plasmalogen hypothesis has been disproved, the debate is hardly over. Lipids expert Mary Enig has remarked that while Oster's work has been discounted, it does not prove that the homogenisation process is benign, as it vastly increases the surface area of fat globules, and causes new globule mebranes to be formed which have a different composition to raw milk fat globules.[5] Examination of the xanthine oxidase issue has continued, with recent research by R.J. Hajjar and J.A. Leopold, "Xanthine oxidase inhibition and heart failure: novel therapeutic strategy for ventricular dysfunction", published in Circulation Research (2006) (journal of the American Heart Association).

Preventive diets

Vegetarian diet
Vegetarians have been shown to have a 24% reduced risk of dying of heart disease.[16]
One of the earliest and well-known popularizers of a diet approach to heart disease was the Pritikin diet. The Pritikin Plan was created by a non-physician, Nathan Pritikin, and consisted of diet and exercise changes in a residential program.
The Ornish Diet is widely believed to have proven that a low fat, low cholesterol diet prevents heart disease.[citation needed] The AHA-1 Diet is recommended by the American Heart Association. Some food manufacturers produce cholesterol-reducing products which they suggest may help to reduce the risk of heart disease. [citation needed]
In addition to Ornish, Dr. Gabe Mirkin and Dr. John McDougall have been proponents of a diet approach to avoiding heart disease. McDougall sells "just add water" vegetarian meals in a cup on his rightfoods site.
The most powerful cholesterol-lowering agents are soluble fiber, unsaturated fats, and phytochemicals, all of which are found almost exclusively in plant foods. In the seventeen studies conducted between 1978 and 2002, the average vegan’s cholesterol level was 160 mg/dl, while the average non-vegetarian’s cholesterol was 202 mg/dl.[17]
Despite the benefits of a vegetarian diet, it is likely that with a few changes to the typical vegetarian diet, the risks of heart disease could be reduced even further. Vegetarian diets are sometimes low in Vitamin B12, which can lead to increased homocysteine levels--a risk factor for heart diease. Since vegetarians do not eat fish, some vegetarians don't have high intakes of Omega-3 fatty acids. There is strong evidence that higher intakes of Omega-3 fatty acids reduce the risk of heart disease. Both of these shortcomings can easily be overcome by taking a vitamin B12 supplement, along with spirulina or fermented soy products and increasing intake of omega-3 fatty acids via ground flax seeds or flax seed oil, soy products, and walnuts. There is some evidence that flax may be even more beneficial than fish oil in its effectiveness in reducing C-reactive protein, an indicator of heart disease.[citation needed] It should also be noted that while canola oil contains Omega-3 fatty acids, it has a high sulphur content and goes rancid easily. If canola oil is deodorised, these Omega-3 fatty acids are transformed into trans fatty acids, which are harmful.[6]

Cretan Mediterranean-style diet
The Seven Country Study[18] found that Cretan men had exceptionally low death rates from heart disease, despite moderate to high intake of fat. The Cretan diet is similar to other traditional Mediterranean diets: consisting mostly of olive oil, bread, abundant fruit and vegetables, a moderate amount of wine, and fat-rich animal products such as lamb, sausage and goat cheese.[19][20][21] However, the Cretan diet consisted of less fish and wine consumption than some other Mediterranean-style diets, such as the diet in Corfu, another region of Greece, which had higher death rates.[citation needed]
The Lyon Heart Study[22] set out to mimic the Cretan diet, but adopted a pragmatic approach. Realizing that some of the people in the study would be reluctant to move from butter to olive oil, they used a margarine based on rapeseed (canola) oil. The dietary change also included 20% increases in vitamin C rich fruit and bread and decreases in processed and red meat. On this diet, mortality from all causes was reduced by 70%. This study was so successful that the ethics committee decided to stop the study prematurely so that the results of the study could be made available to the public immediately.[23]

Alcohol
Main article: Alcohol and heart attacks
The World Health Organization (WHO) states there is convincing evidence that "low to moderate alcohol intake" reduces the risk of coronary heart disease but also that "high alcohol intake" increases the risk of stroke.[24].

Summary
Current indications suggest that the best way forward at present may be to be wary of manufactured foods (especially those containing hydrogenated oils), to increase intakes of fresh fruits and vegetables, and to consider eating unrefined foods including dairy products, meats, nuts and grains.
Avoiding smoking and homogenised milk, reducing salt and sugar consumption, and adopting regular physical activity are also likely to be beneficial
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Coronary heart disease

2006-12-19T01:00:00.000-08:00

Coronary heart disease (CHD), also called coronary artery disease (CAD) and atherosclerotic heart disease, is the end result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium (the muscle of the heart). While the symptoms and signs of coronary heart disease are noted in the advanced state of disease, most individuals with coronary heart disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "sudden" heart attack, finally arise. After decades of progression, some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. The disease is the most common cause of sudden death, and is also the most common reason for death of men and women over 65 years of age.
Contents
1 Overview
2 Pathophysiology
3 Angina
4 Risk factors
5 Prevention
5.1 Preventive diets
6 Recent research
7 References
8 See also
9 External links

Overview
Atherosclerotic heart disease can be thought of as a wide spectrum of disease of the heart. At one end of the spectrum is the asymptomatic individual with atheromatous streaks within the walls of the coronary arteries (the arteries of the heart). These streaks represent the early stage of atherosclerotic heart disease and do not obstruct the flow of blood. A coronary angiogram performed during this stage of disease may not show any evidence of coronary artery disease, because the lumen of the coronary artery has not decreased in calibre.
Over a period of many years, these streaks increase in thickness. While the atheromatous plaques initially expand into the walls of the arteries, eventually they will expand into the lumen of the vessel, affecting the flow of blood through the arteries. While it was originally believed that the growth of atheromatous plaques was a slow, gradual process, some recent evidence suggests that the gradual buildup of plaque may be complemented by small plaque ruptures which cause the sudden increase in the plaque burden due to accumulation of thrombus material.
Atheromatous plaques that cause obstruction of less than 70 percent of the diameter of the vessel rarely cause symptoms of obstructive coronary artery disease. As the plaques grow in thickness and obstruct more than 70 percent of the diameter of the vessel, the individual develops symptoms of obstructive coronary artery disease. At this stage of the disease process, the patient can be said to have ischemic heart disease. The symptoms of ischemic heart disease are often first noted during times of increased workload of the heart. For instance, the first symptoms include exertional angina or decreased exercise tolerance.
As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium. Individuals with this degree of coronary heart disease typically have suffered from one or more myocardial infarctions (heart attacks), and may have signs and symptoms of chronic coronary ischemia, including symptoms of angina at rest and flash pulmonary edema.
A distinction should be made between myocardial ischemia and myocardial infarction. Ischemia means that the amount of oxygen supplied to the tissue is inadequate to supply the needs of the tissue. When the myocardium becomes ischemic, it does not function optimally. When large areas of the myocardium becomes ischemic, there can be impairment in the relaxation and contraction of the myocardium. If the blood flow to the tissue is improved, myocardial ischemia can be reversed. Infarction means that the tissue has undergone irreversible death due to lack of sufficient oxygen-rich blood.
An individual may develop a rupture of an atheromatous plaque at any stage of the spectrum of coronary heart disease. The acute rupture of a plaque may lead to an acute myocardial infarction (heart attack).

Pathophysiology
Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. When myocardial cells die from lack of oxygen, this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle damage, heart muscle death and later scarring without heart muscle regrowth.
Myocardial infarction usually results from the sudden occlusion of a coronary artery when a plaque ruptures, activating the clotting system and atheroma-clot interaction fills the lumen of the artery to the point of sudden closure. The typical narrowing of the lumen of the heart artery before sudden closure is typically 20%, according to clinical research completed in the late 1990s and using IVUS examinations within 6 months prior to a heart attack. High grade stenoses as such exceeding 75% blockage, such as detected by stress testing, were found to be responsible for only 14% of acute heart attacks the rest being due to plaque rupture/ spasm. The events leading up to plaque rupture are only partially understood. Myocardial infarction is also caused, far less commonly, by spasm of the artery wall occluding the lumen, a condition also associated with atheromatous plaque and CHD.
CHD is associated with smoking, obesity, hypertension and a chronic sub-clinical lack of vitamin C. A family history of CHD is one of the strongest predictors of CHD. Screening for CHD includes evaluating homocysteine levels, high-density and low-density lipoprotein (cholesterol) levels and triglyceride levels.

Angina
The pain associated with very advanced CHD is known as angina, and usually presents as a sensation of pressure in the chest, arm pain, jaw pain, and other forms of discomfort. The word discomfort is preferred over the word pain for describing the sensation of angina, because it varies considerably among individuals in character and intensity and most people do not perceive angina as painful, unless it is severe. There is evidence that angina and CHD present differently in women and men.
Angina that occurs regularly with activity, upon awakening, or at other predictable times is termed stable angina and is associated with high grade narrowings of the heart arteries. The symptoms of angina are often treated with nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms, and may be administered transdermally, sublingually or orally. Many other more effective treatments, especially of the underlying atheromatous disease, have been developed.
Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction, and requires urgent medical attention. It is treated with morphine, oxygen, intravenous nitroglycerin, and aspirin. Interventional procedures such as angioplasty may be done.

Risk factors
The following are confirmed independent risk factors for the development of CAD, in order of decreasing importance:
Hypercholesterolemia (specifically, serum LDL concentrations)
Smoking
Hypertension (high systolic pressure seems to be most significant in this regard)
Hyperglycemia (due to diabetes mellitus or otherwise)
Hereditary differences in such diverse aspects as lipoprotein structure and that of their associated receptors, homocysteine processing/metabolism, etc.
Significant, but indirect risk factors include:
Lack of exercise
Stress
Diet rich in saturated fats
Diet low in antioxidants
Obesity
Men or Women over 65

Prevention
Coronary heart disease is the most common form of heart disease in the Western world. Prevention centers on the modifiable risk factors, which include decreasing cholesterol levels, addressing obesity and hypertension, avoiding a sedentary lifestyle, making healthy dietary choices, and stopping smoking. There is some evidence that lowering uric acid and homocysteine levels may contribute. In diabetes mellitus, there is little evidence that blood sugar control actually improves cardiac risk. Some recommend a diet rich in omega-3 fatty acids and vitamin C. The World Health Organization (WHO) recommends "low to moderate alcohol intake" to reduce risk of coronary heart disease [1].
An increasingly growing number of other physiological markers and homeostatic mechanisms are currently under scientific investigation. Among these markers are low density lipoprotein and asymmetric dimethylarginine. Patients with CHD and those trying to prevent CHD are advised to avoid fats that are readily oxidized (e.g., saturated fats and trans-fats), limit carbohydrates and processed sugars to reduce production of Low density lipoproteins while increasing High density lipoproteins, keeping blood pressure normal, exercise and stop smoking. These measures limit the progression of the disease. Recent studies have shown that dramatic reduction in LDL levels can cause mild regression of coronary heart disease.
Risk factor management is carried out during cardiac rehabilitation, a 4-phase process beginning in hospital after MI, angioplasty or heart surgery and continuing for a minimum of three months. Exercise is a main component of cardiac rehabilitation along with diet, smoking cessation and blood pressure and cholesterol management.

Preventive diets
Main article: Diet and Heart Disease
Vegetarian diet: Vegetarians have been shown to have a 24% reduced risk of dying of heart disease (source: Key TJ, Fraser GE, et al. 1999, Sep. Mortality in vegetarians and nonvegetarians: detailed findings from a collaborative analysis of 5 prospective studies. Am J Clin Nutr, 70:516S-524S).
Cretan Mediterranean-style diet: The Seven Country Study found that Cretan men had exceptionally low death rates from heart disease, despite moderate to high intake of fat. The Cretan diet is similar to other traditional Mediterranean diets: consisting mostly of olive oil, bread, abundant fruit and vegetables, a moderate amount of wine and fat-rich animal products such as lamb, sausage and goat cheese.[1][2][3]. However, the Cretan diet consisted of less fish and wine consumption than some other Mediterranean-style diets, such as the diet in Corfu, another region of Greece, which had higher death rates.[citation needed]
A study published in 2005 has determined that a positive relationship exists between the consumption of trans fat (commonly found in hydrogenated products such as margarine) and the development of endothelial dysfunction, a precursor to atherosclerosis.[4]
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Congenital heart disease

2006-12-19T00:54:00.000-08:00

Congenital heart disease (CHD) is heart disease in the newborn, and includes structural defects, congenital arrythmias, and cardiomyopathies. CHD is a defect of the heart that exists primarily at birth, and can describe a wide variety of different abnormalities affecting the heart. CHD occurs when the heart or blood vessels near the heart does not develop properly before birth. Therefore, the heart does not pump because it is not completely developed. Also the blood flow is obstructed in the heart of the vessels nearby, causing an abnormal flow of blood through the heart. Blood flow obstructions put a strain on the heart muscle causing the heart to work harder and beat faster. Abnormal blood flow usually occurs when there is a hole in the walls of the heart and may be an abnormal connection between two arteries outside the heart.
Contents

Causes
CHD has many diverse causes. Some factors are environmental, such as chemicals, drugs, or infection. However, the bulk of CHD is thought to be genetic in nature. Infections such as German measles (i.e. rubella) can produce CHD. Women with diabetes and phenylketonuria are at high risk for their children to be born with this disease. Other causes include the mother's excessive intake of alcohol and illegal drugs while pregnant. There are many genetic conditions which can be a factor in causing CHD, such as DiGeorge syndrome (22q11 deletion syndrome), Holt-Oram syndrome, and Alagille syndrome. Although these factors are known causes of CHD, most are currently unknown. Therefore, the causes of most cases of CHD are unknown.

Diagnosis
Mild congenital heart diseases may not be observed or occur until adulthood. The physician or provider will find this through a series of questions in an examination. Echocardiography and cardiac magnetic resonance(MRI) are used to confirm CHD when signs or symptoms occur in the physical examination. An echocardiograph displays images of the heart and the sound waves it makes. It also finds abnormal rhythms or defects of the heart present with CHD. Fetal echocardiography is used to diagnose CHD in utero after 20 weeks of pregnancy. An ultrasound may be used to determine the defects in pregnant women. Cardiac MRI scans and uses magnetic fields and radio waves to determine these defects but is not always necessary in dianosing CHD. A chest x-ray may also be issued to look at the anatomical position of the heart and lungs. A Cat Scan(CT) can also be used to visualize CHD. All of these tests are ways to diagnose CHD by a physician.
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Ischaemic heart disease

2006-12-19T00:47:00.000-08:00

Ischaemic (or ischemic) heart disease is a disease characterized by reduced blood supply to the heart. It is the most common cause of death in most western countries.
Ischaemia means a "reduced blood supply". The coronary arteries supply blood to the heart muscle and no alternative blood supply exists, so a blockage in the coronary arteries reduces the supply of blood to heart muscle.
Most ischaemic heart disease is caused by atherosclerosis, usually present even when the artery lumens appear normal by angiography, see IVUS.

What is it?
Initially there is sudden severe narrowing or closure of either the large coronary arteries and/or of coronary artery end branches by debris showering downstream in the flowing blood. It is usually felt as angina, especially if a large area is affected.
The narrowing or closure is predominantly caused by the covering of atheromatous plaques within the wall of the artery rupturing, in turn leading to a heart attack (Heart attacks caused by just artery narrowing are rare).
A heart attack causes damage to heart muscle by cutting off its blood supply.
This can cause:
Temporary damage and pain (ischemia)
Loss of muscle activity (acute heart failure)
Permanent heart muscle damage, heart muscle does not grow back (acute myocardial infarction /infarct)
Long term loss of heart muscle activity (chronic heart failure)
Cardiac arrhythmias: irregular heartbeat which can be fatal. Most death is due to arrhythmias, usually tachyarrhythmias.
Other structural damage to the heart including damaged heart valves, actual perforation of the heart and a thin walled fibrous floppy heart.

Prevention
Prevent or delay atherosclerosis.
Do not smoke
Maintain low blood pressure - prevent/treat hypertension (high blood pressure)
Exercise frequently - exercising the heart muscle strengthens it, like any other muscle
Avoid obesity - increasing body fat stores, especially intra-abdominal fat, increases serum cholesterol, triglycerides, insulin requirements and promotes Diabetes Mellitus plus chronically increases heart muscle workload.
Avoid trans-fats - these are found in any chemically modified fat product, such as margarine, in hydrogenated fats, and especially in superheated fats (such as those used for commercial deep frying). These fats are unreactive (not fitting in the enzymes designed for cis-fats) and should not be consumed in any amount; however, in many western countries, limitation may be the only practical option. Some mono-unsaturated fats are beneficial in reducing the risk of heart disease when consumed in moderation. When consumed in excess, however, other health concerns arise. An increase in polyunsaturated fats is also warranted in most American diets. Dietary cholesterol intake is known to have only limited effect on serum cholesterol.
Monitor and reduce cholesterol - take LDLipoprotein cholesterol reducing and HDLipoprotein raising drugs and verfiy both LDLipoprotein particle counts and quantitative large HDLipoprotein response to treatment
Avoid shift work
Eat vitamin C - this micronutrient maintains healthy blood vessels (see scurvy), and prevents tears and fissures in the lumen wall that act as condensation nuclei on which the cholesterol molecules aglommerate

Treatment of a heart attack
The option required depends on the situation.
Specialised coronary care (the sooner the better); most deaths are due to sudden onset arrhythmias - time is crucial to survival.
Cardiopulmonary resuscitation (breathing support, pulse and BP monitoring & possible chest compressions).
A defibrillator can stop cardiac arrhythmias.
An artificial pacemaker can speed up cardiac bradyarrhythmias.
Drugs such as adrenaline can increase heart rate and strength of contractions, although also promote tachyarrhythmias.
Thrombolytic agents can clear away compounding blood clots.
Anticoagulation can impede additional blood clots.
Inotropic drugs will raise blood pressure.
Unblock arteries with angioplasty ("balloon angioplasty with or without stents") or surgery.

After a heart attack
Possible angioplasty or cardiac surgery.
Possibly the regular administration of anti-coagulants to prevent further blood clot complications.
Possibly the administration of drugs to reduce heart arrhythmias although they many also induce arrhythmias.
Lifestyle modifications are important in prevention of a second MI; increased exercise, reduction of stress, and improved dietary considerations are perhaps most important
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The Best Heart Disease Treatment

2006-11-21T18:27:00.000-08:00

The Best Heart Disease Treatment by Ernest Barby

Heart disease is a serious illness but luckily it can be treated. Whilst there are no cures to speak of, some treatments do manage to successfully control the condition and help you to live a happy life. So what options are open to you then?
The Various Heart Disease Treatment Options Available
There are quite a lot of treatment options including medical treatment, self help treatment and alternative treatments to choose from. Basically it all depends upon your own personal preferences and it is always a good idea to visit your doctor before starting any treatments as they will be able to give you a good idea on whether or not they are right for you. Every person's condition is different and whilst some sufferers of the disease may only suffer from angina, there are others who have suffered heart attacks or strokes.
So, once you have worked out the seriousness of your condition, it is then time to find the best heart disease treatment for you.
* Medical Treatments
Generally medical treatments are the best way to go. They have been tried and tested and most of them work. You will also be monitored by the doctor as you are taking the medication so that is another advantage as it makes the treatment safer.
Medications are available to treat high blood pressure, angina, heart failure and high blood cholesterol as well as many other heart problems. These treatments do need to be taken regularly and often beta blockers are one of the best medications to go for. Again it will depend upon what your doctor advises.
Another great medical treatment which works well to keep the heart beating regularly and safely is a pacemaker. Pacemakers are fitted into the body and attached the arteries of the heart. The device sends small electrical impulses and encourages the heart to beat.
There are also surgery options but before considering any type of surgery, always talk it through with your doctor.
* Alternative Treatment Options
Some people prefer to undergo alternative treatments, though it is worth remembering that medical treatments should also be taken.
Generally if you want to try out alternative treatments options then getting plenty of CoQ10 Protection is a good idea. GoQ10 Protection is a nutrient which naturally occurs in the body. It is known to reduce the blood pressure and you can also find it in meat and fish as well as in supplements.
There are many alternative treatments which are designed to help with the various symptoms of heart disease so if you are after something in particular visit your local health shop and ask the experts there whether they have anything suitable.
Overall the best heart disease treatments are usually medical ones. They work, they are monitored and they provide comfort for millions of people each year. Always talk to your doctor to ensure that you are getting the right treat options for you and that way you should start to realize the benefits of the treatment as soon as possible.
About the Author
Ernest is the owner of www.HeartDiseaseToday.us you can view the website at: http://heartdiseasetoday.us/ , the site offers up-to-date information and tips about acne and many of the latest treatments.
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Smoking - The Silent Killer

2006-11-21T18:25:00.000-08:00

Smoking - The Silent Killer by Embla Verandi

Do you know that Ten Thousands of people around the World are dying everyday because of Tobacco?
One out of each six men is dying in United States because of smoking. It is pretty clear now that smoking is one of the main causes of death. If you smoke then you are also enhancing the chances of diseases that will end up in death. The main diseases due to smoking are the coronary heart disease, lung cancer, mouth cancer and severe problems concerning throat, bladder, kidney and pancreas. Most of the diseases are so severe that there are no treatments available for them. The severe gangrene problem has been found in the Diabetic patients, who smoke a lot.
Now, this is the high time and you must quit smoking immediately. Do not think that it is impossible for you to quit it, as there are many chain smokers, who have quit smoking. The only thing one needs is the determination and once you achieve your destination then you will feel happy and contented.
You Must Follow these rules to see the results:
First of all, you have to a firm willpower of give up this terrible habit. When you have determined firmly, and then make a decision of a day and date. Now, from this specific date, you will not lay a hand on the cigarette determine it firmly.
For a smoker, smoking is one of the fundamentals. Now you have decided to give up it and to attain the quit, try some other work at the time of smoking.
As the time of quit is forthcoming, try to reduce the intake of cigarettes and the circumstances when you smoke. Take a glass jar, fill up with water and drop all the butts of cigarette into it.
Try to concentrate on the advantages after Quit Cigarette, in your free time. You will find that quit smoking have much more advantages than smoking. If one quit smoking then there will be considerable minimization in the risk involved due to heart disease, cancer and other deadly diseases. Earlier you use to get tired up easily, but now you have more power. You will also gain resistance from cough, cold and flu.
Quit Cigarette will also save the money, which you were burning to destroy your health. Put all the money you spend on your cigarette in the glass jar and in one month see your savings.
In the primary phases, smoking will show its effects. It would be more or less impossible for you to handle this temptation. On the other hand, try to deflect your mind. You will as well have to expression a lot of troubles like headache, frustration and coughing. All these are positive signs. To steer clear of them drink water, make your hands and mouth active.
Do not bother about them, as they will decrease with the time. Throughout the early phases of quitting smoking, you may experience nervousness. To get rid of nervousness does not take caffeine drinks, inhale deep breaths and go for walk. The greatest way to handle the distaste is start-doing exercises.
Moreover, quantity of carbon monoxide in your blood will minimize and a considerable increment of oxygen. There will be glow at your face and your skin will turn pink. Your heartbeat will be normal and lungs become clearer.
Your risk to heart attack gradually decreases, if you are not smoking for a year or two.
To make it more interesting, look out for a friend interested in getting rid of it. Both of you can do wonders. Always try to avoid places that encourage smoking. After quit, many people usually put on a lot of weight. To avoid this, go for an exercise program, eat healthy food and improve your way of living.
Some drugs can replace the harmful nicotine. But, it should not be taken without the advice of Doctor. For instance, Nicotine gum, Bupropion, Nicotine inhaler and Nicotine nasal spray. These drugs will surely helpful in Quit Cigarette.
Now, you have acquired your destination. It is the time to reward you for your achievement. Get that glass jar and you will be wondered to find the amount you have saved.
Many times, even after quitting people smoke. Do not think that your efforts have gone wasted. You should only consider the advantages of not smoking and start following the path of not smoking. The best thing one can do for quitting smoking is the faith in oneself. Have faith in yourself and you will attain the unachievable.
Author: Embla Verandi - You can find more great info about quit Smoking on: http://www.smokingstopsite.com/ You may publish the article on your website if you do not change the article, and include all html as direct links to our site.

The Best Heart Disease Treatment by Ernest Barby

Heart disease is a serious illness but luckily it can be treated. Whilst there are no cures to speak of, some treatments do manage to successfully control the condition and help you to live a happy life. So what options are open to you then?
The Various Heart Disease Treatment Options Available
There are quite a lot of treatment options including medical treatment, self help treatment and alternative treatments to choose from. Basically it all depends upon your own personal preferences and it is always a good idea to visit your doctor before starting any treatments as they will be able to give you a good idea on whether or not they are right for you. Every person's condition is different and whilst some sufferers of the disease may only suffer from angina, there are others who have suffered heart attacks or strokes.
So, once you have worked out the seriousness of your condition, it is then time to find the best heart disease treatment for you.
* Medical Treatments
Generally medical treatments are the best way to go. They have been tried and tested and most of them work. You will also be monitored by the doctor as you are taking the medication so that is another advantage as it makes the treatment safer.
Medications are available to treat high blood pressure, angina, heart failure and high blood cholesterol as well as many other heart problems. These treatments do need to be taken regularly and often beta blockers are one of the best medications to go for. Again it will depend upon what your doctor advises.
Another great medical treatment which works well to keep the heart beating regularly and safely is a pacemaker. Pacemakers are fitted into the body and attached the arteries of the heart. The device sends small electrical impulses and encourages the heart to beat.
There are also surgery options but before considering any type of surgery, always talk it through with your doctor.
* Alternative Treatment Options
Some people prefer to undergo alternative treatments, though it is worth remembering that medical treatments should also be taken.
Generally if you want to try out alternative treatments options then getting plenty of CoQ10 Protection is a good idea. GoQ10 Protection is a nutrient which naturally occurs in the body. It is known to reduce the blood pressure and you can also find it in meat and fish as well as in supplements.
There are many alternative treatments which are designed to help with the various symptoms of heart disease so if you are after something in particular visit your local health shop and ask the experts there whether they have anything suitable.
Overall the best heart disease treatments are usually medical ones. They work, they are monitored and they provide comfort for millions of people each year. Always talk to your doctor to ensure that you are getting the right treat options for you and that way you should start to realize the benefits of the treatment as soon as possible.
About the Author
Ernest is the owner of www.HeartDiseaseToday.us you can view the website at: http://heartdiseasetoday.us/ , the site offers up-to-date information and tips about acne and many of the latest treatments.

Heart Disease and Prevent Osteoporosis

2006-11-19T06:53:00.000-08:00

8 Ways to Prevent Osteoporosis and Heart Disease During Menopause by Riana Lance

Osteoporosis causes bones to lose mass and density. As the bones become porous and brittle, the chance of fracture is greatly increased. Often there are no symptoms and a person only discovers that they have osteoporosis when they suffer a fracture.
Heart disease includes a number of conditions affecting the structures or function of the heart. They includes coronary artery disease (including heart attack), abnormal heart rhythms or arrythmias, heart failure, heart valve disease, congenital heart disease, heart muscle disease (cardiomyopathy), pericardial disease, aorta disease and Marfan syndrome, vascular disease (blood vessel disease).
Cardiovascular disease is the leading cause of death in the U.S. thus, it is essential to learn how prevent heart disease. During menopause, many women are easily getting osteoporosis. Indeed, it would also be easy for them to get heart disease.
How is that?
Women, during menopause, might be lack of estrogen. This causes bones to lose calcium and become weaker, putting them at risk for severe bone loss or osteoporosis. A lack of estrogen also increases risk of heart disease.
However, there are steps you can do to prevent osteoporosis and heart disease, such as:
1. Get enough calcium to keep your bones strong. Before menopause, you need about 1,000 mg of calcium per day. After menopause, you need 1,500 mg per day. You also can talk with your physician about taking medicine to help preserve bone and slow down bone loss. Get at least 30 minutes of physical activity on most days of the week. Try weight-bearing exercises, like walking, running, or dancing.
2. Eat healthy by including plenty of whole grain products, vegetables, and fruits in your diet. Choose a diet low in total fat, saturated fat, and cholesterol.
3. Maintain a healthy weight. Ask your health care provider what a healthy weight is for you.
4. Control your blood pressure. Ask your health care provider what a healthy number is for you and how often you need it checked.
5. If you have diabetes, control and monitor your blood sugar levels.
6. Lower your cholesterol to the right level. Ask your health care provider what a healthy level is for you.
7. If you smoke, try to quit. Ask your health care provider for help or visit this special section of the NWHIC web site: www.4woman.gov/QuitSmoking
8. If you drink alcohol, limit it to no more than one drink per day.
So, if you think that your menopause has begun, it is important for you to pay attention to the eight essential ways to prevent osteoporosis and heart disease.
About the Author
Riana Lance has a deep concern on health. That brings her to create essential tips on how to become healthier. Get her inspirational e-mail guides at http://healthifca.com/30/a-gift-for-you.html Also, grasp her other motivational health tips at http://www.healthfica.com/news, a
worth-to-visit daily updated news.
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American Heart Assoc.Get Resources, Recipes and Tipsfrom the American Heart Associationwww.americanheart.orgAll about Heart DiseaseInformation you can trust onheart disease and more!www.heartcenteronline.comHeart DiseaseFind Heart Disease Info.Fast & Easywww.DiseaseHeart.infoHeart Disease InfoA complete guide to Heart Diseaseand Heart Health.www.HeartAuthority.com
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