Cardiac hypertrophy is a common response of the heart to all forms of stress, whether internal, such as a genetic defect in hypertrophic cardiomyopathy (HCM), or external, such as increased afterload in hypertension. It is diagnosed commonly on an electrocardiogram or an echocardiogram showing increased cardiac mass. A diverse array of stimuli could induce cardiac hypertrophy, including physiological stimuli such as exercise, which induces physiological hypertrophy that is beneficial for cardiac function. In contrast, pathological hypertrophy is responsible for diastolic heart failure and is associated with increased morbidity and mortality. Pathogenesis of cardiac hypertrophy entails sensing the stress through transmembrane, nuclear, or cytoplasmic receptors followed by activation of a cascade of signal transducers that ultimately enter the nucleus and activate gene transcription and expression, protein synthesis, cellular organization, and hypertrophy.

Genetic factors are important determinants of cardiac hypertrophy. HCM is the prototype of genetic cardiac hypertrophy and is caused by mutations in contractile sarcomeric proteins. It is the most common cause of sudden cardiac death in the young, particularly young competitive athletes, and a major cause of morbidity in elderly. Genetic factors also influence the magnitude of hypertrophic response in acquired cardiac hypertrophy. Clinical studies in humans and experimental studies in animals show that hypertrophy is reversible on removal of the primary stimulus (such as treatment of hypertension or replacement of a stenotic valve) or through blockade of signal mediators that are essential for cardiac hypertrophic response. Regression of cardiac hypertrophy is associated with significant improvement in cardiovascular mortality and morbidity.