ABSTRACT
LVH has become an important parameter in the assessment of hypertensive patients. LVH is a strong independent predictor of cardiovascular morbidity and mortality. In cases of hypertension, it increases the risk of stroke, ischemic heart disease, and, eventually, congestive heart failure (1). The prevalence of LVH in a mild-to moderate-hypertensive population is 20-50% (2,3). There are now various methods to assess LVH in hypertensive patients (4). These include the classical electrocardiogram, echocardiography (both two-and three-dimensional), and cardiac magnetic resonance imaging.
Although LVH is usually regarded as a consequence of chronic elevation of arterial pressure, this may not always be the case. LVH is a pressure-independent predictor of cardiovascular morbidity and mortality. In fact, up to 60% of the variance of LVH may be due to genetic factors independent of BP (5). An increasing number of genes have been identified that contribute to LVH. Among these genes, most target the reninangiotensin-aldosterone system (RAAS), the natriuretic peptide family, or the adrenoceptor signaling cascade (6).
