Hypertension and the heart

It has been clearly demonstrated that left ventricular (LV) hypertrophy is a strong blood pressure independent risk factor for cardiovascular morbidity and mortality in the general population, in primary and secondary hypertension and in cardiac patients. LV hypertrophy in arterial hypertension develops in response to an increased afterload, but underlying pathophysiological mechanisms include a variety of non-haemodynamic factors. Due to the prognostic importance of LV hypertrophy, normalisation of LV mass emerged as a desirable goal of antihypertensive treatment. Indeed, several prospective studies now indicate that regression of LV hypertrophy reduced cardiovascular complications. As a consequence, the question was raised whether certain antihypertensive drugs differ in their ability to reduce LV mass. Several comparative studies and meta-analyses have been carried out to resolve this issue. The available data seem to indicate that angiotensin-converting enzyme (ACE)-inhibitors and calcium channel blockers were more potent than beta -blockers in their ability to reduce LV hypertrophy, with diuretics in the intermediate range. The role of new antihypertensive agents such as angiotensin II AT(1)-receptor blockers appears similar to the one of ACE-inhibitors, since in some studies angiotensin II AT(1)-receptor blockers were superior to beta -blockers and diuretics. Various aspects of LV hypertrophy including its prevalence, determinants, prognosis and regression are discussed in this article.