Being a "classical" sequel of hemodynamic burdens (pressure and/or volume), the untoward results of left ventricular hypertrophy (LVH) were traditionally related to its underlying causes. The Framingham study was the first to demonstrate the increased independent risk associated with LVH detected by ECG and/or by echocardiography. The presence of LVH in "nonhypertensive" individuals (e.g., obese), the association of LVH with age and gender, and the possibility of genetic control of left ventricular size via "nonhemodynamic" mechanisms had underscored the importance of LVH per se as a prognostic indicator. The presence of LVH in patients with hypertensive or coronary artery disease results in a severalfold increase in risk compared to similar patients without LVH. Early studies have indicated that the presence of LVH is associated with a significantly worse prognosis in patients recovering from myocardial infarction. We have studied the effect of LVH on long-term (mean 5.5 years) mortality in patients surviving myocardial infarction registered in the SPRINT database. The LVH patients were older and had more complications during hospitalization. The 1- and 5-year mortality rates were doubled in patients with ECG-LVH. Review of the mechanisms operating in LVH reveals important changes in the anatomy and physiology of hypertrophied heart, leading to increased fibrosis, inadequate vascular growth, impaired myocardial function (systolic and diastolic), reduced coronary reserve, and abnormal electrophysiological properties. Regression of LVH by proper treatment (achieved mainly by calcium antagonists and ACE inhibitors) may correct many of the above-mentioned adverse phenomena. Whether the regression of LVH per se will lead to improved prognosis remains to be answered in the future.