PubMed Health⌕ Search

PubMed · 9495620

Decrease of left ventricular mass is a clinically valuable intermediate end-point of antihypertensive treatment.

Abstract

The presence of left ventricular hypertrophy (LVH) in hypertensive patients, recognized clinically by electrocardiography or echocardiography, is an adverse prognostic sign and a powerful predictor of cardiovascular morbidity and mortality, independent of blood pressure and other cardiovascular risk factors. Several pathophysiological changes accompany the myocytic growth and fibrosis that characterize hypertensive LVH and have been invoked to explain the association of LVH with increased cardiovascular risk. These include: impairment of diastolic function, and probably also of systolic performance, at least during exercise; reduced coronary blood flow reserve; predisposition to ventricular arrhythmias; alteration in cardiac autonomic nervous system activity. All these data have led to the opinion that regression of LVH should be a major goal in the treatment of hypertensive patients and might predict an improvement in prognosis.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E Agabiti-Rosei. 1997. Decrease of left ventricular mass is a clinically valuable intermediate end-point of antihypertensive treatment.. https://pubmed.ncbi.nlm.nih.gov/9495620/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Antioxidant action of the antihypertensive drug, carvedilol, against lipid peroxidation.

The action of carvedilol, a vasodilating, beta-adrenoceptor blocking agent, against lipid peroxidation has been the subject of many studies, but the results reported thus far are contradictory. In an attempt to define the antioxidant mechanism of carvedilol against lipid peroxidation, the dynamics of the action of carvedilol were studied in several oxidation systems. We investigated the reactivity of carvedilol toward radicals and its inhibitory effect on lipid peroxidation induced by several kinds of initiating species such as azo compounds and metal ions in solution, micelles, membranes, and low-density lipoprotein. Carvedilol exerted poor reactivity toward phenoxyl, alkoxyl, and peroxyl radicals in acetonitrile solution nor did it show an appreciable antioxidant effect against either the peroxyl radical-induced oxidation of methyl linoleate in acetonitrile or against phosphatidylcholine liposomal membranes in aqueous suspension. Carvedilol completely inhibited the ferric ion-induced oxidation of methyl linoleate micelles by sequestering ferric ions, but not by reducing hydroperoxide. It was shown that carvedilol enhanced the oxidation of micelles induced by either methemoglobin or peroxyl radical. Carvedilol, which was added exogenously, did not suppress the oxidation of isolated low-density lipoprotein induced by peroxyl radical or cupric ion. These results show that carvedilol does not act as a radical-scavenging antioxidant, but that it does act most efficiently as an antioxidant against ferric ion-induced oxidation by sequestering ferric ion.

Antihypertensive Agents↗