Left ventricular hypertrophy as a risk factor: the Framingham experience

Abstract

Left ventricular hypertrophy (LVH) is one of the less common but ominous risk factors for coronary disease, stroke and cardiac failure. The chief determinants of LVH, aside from age, are elevated blood pressure, obesity, stature and glucose intolerance. Cardiac valve disease and chronic heart disease (CHD) also cause LVH. Downward trends in the prevalence of LVH over four decades indicate that LVH is preventable, and this has coincided with improved hypertension control. When evidence of LVH disappears, the risk of all-cause, cardiovascular and CHD mortality is substantially reduced. Cardiovascular events occur incrementally in relation to left ventricular mass with no discernible critical value identifying pathological hypertrophy. LVH as evidenced by electrocardiogram (ECG-LVH), manifested by repolarization abnormality as well as increased voltage, was a lethal finding; with 5 years, 33% of men and 21% of women were dead. ECG-LVH was associated with ventricular ectopy and a sudden death risk comparable to that of CHD or cardiac failure. ECG-LVH was associated with a 3-15-fold increase of cardiovascular events with greatest risk ratios for cardiac failure and stroke. However, CHD is the predominant clinical sequel. No other risk factor approaches LVH in potency. Anatomical (echocardiographic or X-ray) LVH and ECG-LVH each independently contribute to the risk of cardiovascular disease, and having both confers a greater risk than having either alone. LVH is a clinical finding which should be taken seriously and corrected as soon as detected. It should not be regarded as an innocuous adaptive process, augmenting cardiac function.