What type of cardiac hypertrophy occurs in aortic regurgitation (aortic valve regurgitation)?

From the Guidelines

Aortic regurgitation primarily causes eccentric left ventricular hypertrophy. This condition is characterized by the backflow of blood from the aorta into the left ventricle during diastole, resulting in an increased volume load on the left ventricle 1. The left ventricle responds to this increased preload by dilating and developing eccentric hypertrophy, where the ventricular chamber enlarges and the walls thicken proportionally. This is in contrast to concentric hypertrophy, which is typically seen in pressure overload conditions such as aortic stenosis.

The development of eccentric hypertrophy in aortic regurgitation is a compensatory mechanism that allows the left ventricle to maintain forward cardiac output despite the increased volume load 1. The ventricle achieves this by increasing its stroke volume, which is made possible by the addition of new sarcomeres and the rearrangement of myocardial fibers. As a result, the left ventricle is able to eject a large total stroke volume and maintain normal forward stroke volume, at least initially 1.

However, if left untreated, the chronic volume overload can eventually lead to left ventricular dysfunction as the compensatory mechanisms fail, resulting in heart failure 1. Therefore, early surgical intervention is often recommended to prevent significant ventricular dysfunction and improve outcomes. Key factors that determine the outcome of surgical intervention include left ventricular systolic function and end-systolic size, which are critical in predicting survival and postoperative left ventricular function in patients undergoing aortic valve replacement for chronic aortic regurgitation 1.

Some of the key points to consider in the management of aortic regurgitation include:

• The importance of early surgical intervention to prevent left ventricular dysfunction and improve outcomes
• The role of left ventricular systolic function and end-systolic size in predicting survival and postoperative left ventricular function
• The potential benefits of vasodilator therapy in reducing the hemodynamic burden in patients with aortic regurgitation 1
• The need for close monitoring and follow-up to detect any signs of left ventricular dysfunction or other complications.

From the Research

Cardiac Hypertrophy in Aortic Regurgitation

• In aortic regurgitation, the type of cardiac hypertrophy that occurs is eccentric hypertrophy, which is an adaptive response to volume overload 2.
• This eccentric hypertrophy can be combined with concentric hypertrophy of the left ventricle, allowing the ventricle to normalize its afterload and maintain normal ejection performance 2.
• However, progressive dilatation of the left ventricle can lead to depressed left ventricular contractility and myocardial structural changes, including cellular hypertrophy and interstitial fibrosis, which is known as pathological hypertrophy 2.
• The left ventricular remodeling and systolic function triggers for intervention in aortic regurgitation may be lower than previously recommended, emphasizing the importance of LV volumes in risk stratification 3.

Key Characteristics of Cardiac Hypertrophy in Aortic Regurgitation

• Eccentric hypertrophy is characterized by an increase in left ventricular volume and a decrease in left ventricular wall thickness 2.
• Concentric hypertrophy is characterized by an increase in left ventricular wall thickness and a decrease in left ventricular volume 2.
• Pathological hypertrophy is characterized by advanced cellular hypertrophy and excessive interstitial fibrosis, leading to myocardial contractile dysfunction and ventricular remodeling 2.

Diagnosis and Management of Aortic Regurgitation

• The diagnosis of aortic regurgitation relies on electrocardiography, chest radiographs, and echocardiography, with cardiac magnetic resonance imaging potentially incorporated in chronic AR diagnosis 4, 3.
• The management of chronic aortic regurgitation aims to control hypertension and delay left ventricular dysfunction, with angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and potentially calcium-channel blockers recommended 4, 5.