Cardiac remodeling involves molecular, cellular, and in-terstitial changes that manifest clinically as changes in size, shape, and function of the heart after injury or stress stimulation. 1 Although the term cardiac remodeling was initially coined to describe the prominent changes that occur after myocardial infarction, 2, 3 it is clear that similar processes transpire after other types of injury such as with pressure overload (aortic valve stenosis, hypertension), inflammatory disease (myocarditis), idiopathic dilated cardiomyopathy, and volume overload (valvular regurgitation). Although the causes of these diseases are different, they share molecular, biochemical, and cellular events to collectively change the shape of the myocardium.

Cardiac hypertrophy is a common type of cardiac remodeling that occurs when the heart experiences elevated workload. The heart and individual myocytes enlarge as a means of reducing ventricular wall and septal stress when faced with increased workload or injury. Cardiac hypertrophy is classified as “physiological” when it occurs in healthy individuals after exercise or pregnancy and is not associated with cardiac damage. In contrast, hypertrophy that results from pressure or volume overload or after myocardial infarction is usually referred to as “pathological.” This name may be misleading, however, because pathological hypertrophy may also involve a compensatory and adaptive phase that tends to reduce wall stress and maintain output, although ultimately these positive aspects are lost and ventricular function declines, often leading to heart failure.