Domenico Galzerano, Paolo Tammaro, Diana Lama, Carmen De Martino, Antonio Galzerano, Roberto Breglio and Paolo Capogrosso Pages 187 - 192 ( 6 )
Left ventricular hypertrophy (LVH) is a common form of target organ damage associated with hypertension that increases the risk for cardiovascular morbidity and mortality. Regression of left ventricular mass (LVM) substantially reduces this risk, and antihypertensive treatment is associated with reduction in LVM. Identifying the optimal therapeutic strategy that brings effective BP reductions and superior LVM regression is therefore important for the effective management of patients with LVH. Hypertension, both mean load and variability (for example, the early morning blood pressure [BP] surge), causes LVH. LVH also results from abnormalities in neurohormonal systems (such as the renin-angiotensinaldosterone system [RAAS]), and metabolic abnormalities. Agents that block the RAAS (angiotensin receptor blockers [ARBs], angiotensin-converting enzyme inhibitors) have particular efficacy. Telmisartan is a long-acting ARB that has shown regression of LVH and improved diastolic function in several clinical trials. Compared with carvedilol, telmisartan induces more regression of LVM for the same degree of BP control, and compared with hydrochlorothiazide the regression of LVM for a given degree of BP lowering is greater. As part of the ONTARGET study that compares telmisartan, ramipril, and the combination, a substudy will assess the effects of the three therapeutic strategies on the regression of LVH
Left ventricular hypertrophy, echocardiography, magnetic resonance imaging, telmisartan, angiotensin receptor blocker.
Transoesophageal and Three-Dimensional Echocardiography Laboratory, Division of Cardiology, San Gennaro Hospital, via Francesco Giordani 42, 80122 Naples, Italy.