At some point in the natural history of hypertension, the compensatory increase in left ventricular (LV) mass ceases to be beneficial. LV hypertrophy (LVH) becomes a preclinical disease and an independent risk factor for congestive heart failure, ischemic heart disease, arrhythmia, sudden death, and stroke. The multiple mechanisms involved, in addition to elevated blood pressure, include body size (obesity), demographics (age, gender, and race), and contributions by fibrogenic cytokines and neurohumoral factors, notably angiotensin II, which favor interstitial collagen deposition and perivascular fibrosis. These tissue changes, in conjunction with geometric abnormalities, primarily concentric hypertrophy, are responsible for the insidious dysfunction associated with LVH, beginning with decreased coronary reserve and altered diastolic ventricular filling and relaxation. The cardinal investigation is echocardiography: [Doppler transmitral flow velocities expressed as the early (E) to atrial (A) wave ratio reveal LVH as a state of potential or actual myocardial ischemia]. All antihypertensive drugs regress LVH, notably the angiotensin-converting enzyme inhibitors, which may also target the detrimental tissue changes. Regression enhances systolic midwall performance, normalizes autonomic function, and restores coronary reserve. The resulting improvement in prognosis has enshrined the detection, prevention, and reversal of LVH in the current guidelines of hypertension management...