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Angiotensin II type 1 receptor blockade prevents alcoholic cardiomyopathy

Che-Ping Cheng1, Heng-Jie Cheng, Carol Cunningham

  • 1Cardiology Section, Department of Internal Medicine, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1045, USA. ccheng@wfubmc.edu

Circulation
|July 13, 2006
PubMed
Abstract

Insights

Alcohol consumption activates the renin-angiotensin system (RAS), leading to alcoholic cardiomyopathy. Blocking the angiotensin II (Ang II) type 1 receptor (AT1) with irbesartan prevents this cardiac dysfunction.

Area of Science:

  • Cardiology
  • Pharmacology
  • Toxicology

Background:

  • Alcoholic cardiomyopathy is a potential consequence of chronic alcohol consumption.
  • The renin-angiotensin system (RAS) may play a role in the development of alcoholic cardiomyopathy.

Purpose of the Study:

  • To investigate the effect of angiotensin II (Ang II) type 1 receptor (AT1) blockade on alcoholic cardiomyopathy development.
  • To evaluate the impact of irbesartan on cardiac function and RAS activation in alcohol-fed dogs.

Main Methods:

  • Instrumented dogs were divided into three groups: alcohol, alcohol plus irbesartan, and control.
  • Left ventricular (LV) and cardiomyocyte function, along with RAS markers, were monitored over six months.
  • Measurements included LV contractility, myocyte shortening and relengthening, and calcium transients.

Main Results:

  • Alcohol ingestion led to sustained RAS activation, evidenced by increased Ang II, renin activity, and AT1 receptor expression.
  • Cardiac dysfunction manifested as decreased LV contractility, impaired myocyte function, and reduced calcium handling.
  • Irbesartan treatment prevented alcohol-induced cardiac dysfunction and suppressed RAS activation.

Conclusions:

  • Chronic alcohol consumption activates the RAS, causing progressive cardiac dysfunction.
  • AT1 receptor blockade effectively prevents the development of alcoholic cardiomyopathy.

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