Ventricular hypertrophy is a compensatory change related to alterations in pressure and/or volume imposed on the wall of the ventricle.
Pathogenesis of left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH)
1. Sustained pressure in the ventricles increases wall stress.
2. Changes in wall stress alter gene expression in the muscle.
3. Changes in gene expression lead to duplication of sarcomeres. Definition: Sarcomeres are the contractile elements of muscle.
4. Changes occur in wall stress when there is an increase in afterload.
a. Definition: Afterload is the resistance the ventricle contracts against to eject blood in systole.
b. Increased afterload produces concentric hypertrophy of the ventricular wall. Sarcomeres duplicate parallel to the long axis of the cells, causing the individual muscle fibers to be thicker.
c. Causes of concentric LVH due to increased afterload include primary hypertension
(HTN; most common), aortic valve (AV) stenosis, and hypertrophic cardiomyopathy(HCM).
d. Causes of concentric RVH due to increased afterload include pulmonary HTN and pulmonary valve (PV) stenosis.
5. Changes occur in wall stress when there is an increase in preload.
a. Definition: Preload refers to the volume of blood in the ventricle that must be expelled during systole.
b. Preload correlates with left and right ventricle end-diastolic volumes (LVEDV, RVEDV).
c. Increased preload increases stroke volume (SV; volume of blood ejected) via the Frank-Starling pressure relationship.
d. Increased preload causes dilation and hypertrophy (eccentric hypertrophy) of the ventricular wall . Sarcomeres duplicate in series (on top of each other), causing the individual muscle fibers to increase in length and width.
e. Causes of eccentric hypertrophy of the left ventricle (LV) due to increased preload include:
(1) mitral valve (MV) or AV regurgitation.
(2) left-to-right shunting of blood (e.g., ventricular septal defect [VSD]). In left-to-right shunting, more blood returns to the left side of the heart because the right side of the heart is receiving more blood than usual.
f. Causes of eccentric hypertrophy of the right ventricle (RV) due to increased preload include tricuspid valve (TV) and PV regurgitation.
C. Consequences of ventricular hypertrophy
1. Left- and right-sided heart failure (LHF, RHF discussed later)
a. Excess work is imposed on the ventricles (LVH and/or RVH).
b. Excess work is caused by either an increase in afterload or an increase in preload.
2. Angina pectoris (AP; chest pain) with exercise (only a complication of LVH; discussed later)
a. In the normal LV, the sub endocardium receives the least amount of blood from the coronary arteries (CAs).
b. Therefore, if the muscle is concentrically thickened, angina may occur with exercise because the muscle wall is so thick that the subendocardium tissue receives dangerously low levels of O2, causing chest pain. Recall that with exercise, the heart rate (HR) increases, which decreases the time for diastole and the filling of the CAs. Therefore, there is even less blood flow to the subendocardium.
3. Pathologic S4 heart sound is commonly present in either LVH and/or RVH.
a. Abnormal heart sound that correlates with atrial contraction in late diastole. S4 heart sound produces an atrial gallop .
b. Caused by blood entering a noncompliant ventricle (problem in filling the ventricle)
(1) Noncompliant ventricle is present in concentric hypertrophy involving the LV and/or RV.
(2) Noncompliant ventricle is also present in left- and/or right-sided eccentric hypertrophy because the ventricles are volume overloaded and resist receiving more blood in late diastole.
c. Examples of a noncompliant ventricle producing an S4 heart sound include:
(1) concentric LVH in primary HTN or AV stenosis (↑afterload).
(2) concentric RVH in pulmonary hypertension (PH) or PV stenosis (↑afterload).
(3) eccentric hypertrophy from volume overload in MV or TV regurgitation (↑preload).
(4) eccentric hypertrophy from volume overload in AV or PV regurgitation (↑preload).
4. Pathologic S3 heart sound is commonly present in either left- or right-sided eccentric
hypertrophy.
a. S3 heart sound is caused by blood entering a volume overloaded chamber in early
diastole
b. Examples of volume overloaded ventricles producing an S3 heart sound include:
(1) volume overload in MV or TV regurgitation.
(2) volume overload in AV or PV regurgitation.