Potential mechanisms explaining the risk of left ventricular hypertrophy

Abstract

Major risk factors have been identified that enhance the chances of cardiovascular morbidity and mortality. These include such modifiable factors as hypertension, hyperlipidemia, obesity, diabetes mellitus, smoking and hyperuricemia. Other factors that also increase risk are not modifiable and include advancing age, male gender and black race. The development of left ventricular (LV) hypertrophy imposes another significant risk for increased morbidity and mortality. Development of LV hypertrophy may be produced by hemodynamic as well as nonhemodynamic mechanisms. Included in the latter group are some of the same factors that in and of themselves participate in the production of increased LV mass (i.e., aging, gender and race, obesity, coronary disease, diabetes and the underlying mechanisms that subserve the hypertensive disease). This article discusses the concept, drawn from clinical and experimental studies, that demonstrate that the additional increased risk of LV hypertrophy may be ascribed to loss of reserve cardiac function, accelerated atherosclerosis, development of abnormal cardiac rhythm secondary to ischemia, fibrosis or drug-induced hypokalemia, inherent predisposition to ventricular dysrhythmias and sudden death, risks directly or coincidentally related to associated diseases or perhaps even the paradoxical risk of beneficial antihypertensive therapy.