Hypertension and the heart

It has been clearly demonstrated that left ventricular (LV) hypertrophy is a strong blood pressure independent risk factor for cardiovascular morbidit y and mortality in the general population, in primary and secondary hyperte nsion and in cardiac patients. LV hypertrophy in arterial hypertension deve lops in response to an increased afterload, but underlying pathophysiologic al mechanisms include a variety of non-haemodynamic factors. Due to the pro gnostic 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 cardiovascul ar 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 enz yme (ACE)-inhibitors and calcium channel blockers were more potent than bet a -blockers in their ability to reduce LV hypertrophy, with diuretics in th e intermediate range. The role of new antihypertensive agents such as angio tensin II AT(1)-receptor blockers appears similar to the one of ACE-inhibit ors, since in some studies angiotensin II AT(1)-receptor blockers were supe rior to beta -blockers and diuretics. Various aspects of LV hypertrophy inc luding its prevalence, determinants, prognosis and regression are discussed in this article.