Mechanism of angiotensin II type 1 receptor blocker action in the regression of left ventricular hypertrophy. Article Report uri icon

Overview

MeSH Major

  • Cardiovascular Diseases
  • Cause of Death
  • Electrocardiography
  • Signal Processing, Computer-Assisted

abstract

  • Left ventricular hypertrophy refers to a pathologic increase in left ventricular mass and is associated with an increased risk of subsequent cardiovascular morbidity and mortality from any cause. In the development of left ventricular hypertrophy there is growth of cardiomyocytes and accumulation of extracellular matrix and fibrosis. The actions are partly induced by angiotensin II, the principal effector of the renin-angiotensin-aldosterone system, binding to the AT1 receptor. Biochemical markers, some implicated in inflammatory changes, correlate with changes in left ventricular mass. The reduction in left ventricular mass brought about with angiotensin-converting enzyme inhibitor or angiotensin receptor blocker (ARB) therapy correlates with a reduction in these inflammatory changes, monitored by brain natriuretic peptide. Recent studies incorporating trials of ARBs have found ARBs to be more effective in reducing left ventricular mass than beta blockers and possibly more effective than calcium antagonists. Initial studies suggest that ARBs and angiotensin-converting enzyme inhibitors may have similar effects in terms of reducing left ventricular hypertrophy, and the combination of angiotensin-converting enzyme inhibitors and ARBs is thought to be synergistic due to a more complete inhibition of the renin-angiotensin-aldosterone system. In conclusion, these agents are efficacious in antihypertensive therapy and can play an important role in the prevention or regression of left ventricular hypertrophy due to hypertension.

publication date

  • July 2006

Research

keywords

  • Report

Identity

Digital Object Identifier (DOI)

  • 10.1111/j.1524-6175.2006.05366.x

PubMed ID

  • 16849902

Additional Document Info

start page

  • 487

end page

  • 92

volume

  • 8

number

  • 7