Effects of Antihypertensive Agents on the Left Ventricle

Abstract

Hypertensive heart disease (HHD) is characterized by left ventricular hypertrophy (LVH), alterations of cardiac function, and coronary flow abnormalities. LVH is an independent cardiovascular risk factor related to cardiovascular complications in patients with hypertension. Therefore, a decrease in left ventricular mass is a therapeutic goal in these patients. The effect of the different antihypertensive agents on LVH regression has been studied in nearly 500 clinical trials. Most studies conclude that there is regression of LVH after significant decrease in blood pressure with most commonly prescribed antihypertensive agents. However, the ability to regress LVH is different between antihypertensive drug classes. ACE inhibitors and calcium channel antagonists are more potent in reducing left ventricular mass than beta-blockers, with diuretics falling in the intermediate group. Recent data suggest that angiotensin AT(1) receptor antagonists reduce left ventricular mass to a similar extent as ACE inibitors or calcium channel antagonists. Although a large number of studies have established that reversal of LVH decreases the occurrence of adverse cardiovascular events in patients with hypertension, the hypothesis that LVH regression is beneficial has not yet been conclusively proven. On the other hand, the time has come to revisit the current management of HHD simply focused on controlling blood pressure and reducing left ventricular mass. In fact, it is necessary to develop new approaches aimed to repair myocardial structure and protect myocardial perfusion and function and, in doing so, to reduce in a more effective manner, adverse risk associated with HHD. The identification of genes involved in both the process of HHD and the response to therapy may be critical for the development of these new approaches. This article will review briefly the available data on the effects of antihypertensive agents on HHD. In addition, the emerging new concepts on the pharmacology of hypertensive myocardial remodeling and the pharmacogenetic basis of the treatment of HHD will be also considered.

Recombinant frizzled1 protein attenuated cardiac hypertrophy after myocardial infarction via the canonical Wnt signaling pathway

“…Cardiac hypertrophy is not only a predictor but also a mediator of cardiovascular events predisposing patients to arrhythmias and heart failure [ 19 ]. Therefore, prevention of cardiac hypertrophy is considered as a promising strategy in the treatment of MI [ 20 ]. To our knowledge, this is the first report that immunization of FZD1 with RFP attenuated cardiac hypertrophy occurred in the early stage of MI.…”