Ventricular and Atrial Hypertrophy and Dilation
Ventricular and Atrial Hypertrophy
Ventricular hypertrophy is an increase in the size and mass of the involved ventricle. This can be a normal response to cardiovascular conditioning as occurs in athletes and enables the heart to pump more effectively. This type of hypertrophy is physiological, not abnormal, and is reversible. In contrast, other forms of hypertrophy are caused by the ventricle adapting to increased stress, such as chronically increased volume load (preload) or increased pressure load (afterload). This hypertrophy is an adaptation to the stress; however, prolonged stress-induced hypertrophy can lead the ventricular failure. Hypertrophy can also result from disease of the heart (valve disease, cardiomyopathies), genetic abnormalities (e.g., hypertrophic cardiomyopathy), and as a consequence of coronary artery disease.
In the case of chronic pressure overload as occurs with chronic hypertension or aortic valve stenosis, the ventricular 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. Sometimes the chamber radius is increased and the wall thickness is increased moderately - this is termed eccentric hypertrophy - and can occur when there is both volume and pressure overload. An example of this would be when systolic dysfunction and a volume overload state occur in a concentrically hypertrophied heart, thus stimulating chronic chamber dilation. Chamber dilation occurs as new sarcomeres are added in-series to existing sarcomeres.
Atria, like the ventricles, can undergo hypertrophy in response to increased afterload. For example, mitral valve stenosis increases resistance to blood flow across the valve, which requires higher pressures in the left atrium to drive ventricular filling. This pressure afterload stimulates wall thickening in the left atrium.
Ventricular and Atrial Dilation
Chronic ventricular dilation occurs in response to:
- chronic volume overload stimulated by elevated ventricular end-diastolic pressures (e.g., as occurs in aortic and mitral regurgitation; systolic dysfunction)
- hypervolemic states triggered by ventricular failure or renal failure.
- intrinsic disease such as idiopathic dilated cardiomyopathy or known causes of dilated cardiomyopathy (e.g., alcohol-induced; viral).
Ventricular dilation occurs as new sarcomeres are added in-series to existing sarcomeres. Mechanically, dilation increases the ventricular compliance. The dilated ventricle has high wall stress, elevated oxygen demand, and lower mechanical efficiency. Clinically, it is generally associated with symptoms of heart failure and reduced ejection fraction.
The atria can also undergo dilation in response to chronic volume overload. For example, in mitral valve regurgitation, the volume and pressure of the left atrium are greatly increased. The left atrium responds by undergoing chronic dilation, which enables it to accommodate the increased volume without as large an increase in pressure because of its increased compliance.
Hypertrophy and dilation are results of cardiac remodeling. Under some conditions (e.g., exercise training) remodeling is beneficial; however, under other conditions (e.g., heart failure) this remodeling is deleterious because it increases the oxygen demand of the heart and decreases mechanical efficiency. Certain drugs, such as beta-blockers, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have been shown to prevent or partially reverse remodeling under pathologic conditions.