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
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
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
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