Pathophysiology and treatment of hypertensive left ventricular hypertrophy

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 fibro- genic cytokines and neurohumoral factors, notably angiotensin II, which favor interstitial collagen depo- sition and perivascular fibrosis. These tissue changes, in conjunction with geometric abnormalities, primarily concentric hypertrophy, are responsible for the insidi- ous dysfunction associated with LVH, beginning with decreased coronary reserve and altered diastolic ven- tricular filling and relaxation. The cardinal investiga- tion 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 my- ocardial ischemia). All antihypertensive drugs regress LVH, notably the angiotensin-converting enzyme in- hibitors, which may also target the detrimental tissue changes. Regression enhances systolic midwall per- formance, normalizes autonomic function, and restores coronary reserve. The resulting improvement in prog- nosis has enshrined the detection, prevention, and reversal of LVH in the current guidelines of hyperten- sion management