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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
12:03

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

Beta-adrenergic receptor blockade and the angiotensin-converting enzyme deletion polymorphism in patients with

Pascal de Groote1, Nicole Helbecque, Nicolas Lamblin

  • 1Service de Cardiologie C, Hôpital Cardiologique, Centre Hospitalier Universitaire de Lille, Boul Prof J Leclercq, 59037 Lille, France.

European Journal of Heart Failure
|March 12, 2004
PubMed

Insights

Beta-blocker therapy effectively improves heart failure (HF) outcomes, regardless of the angiotensin-converting enzyme (ACE) I/D polymorphism. This study found no evidence of a pharmacogenetic interaction influencing myocardial function or survival in HF patients treated with beta-blockers.

Area of Science:

  • Cardiology
  • Pharmacogenetics
  • Genetics

Background:

  • Beta-adrenergic receptor blockade is a standard treatment for chronic heart failure (HF).
  • Previous research suggested a potential pharmacogenetic interaction between beta-blocker therapy and the angiotensin-converting enzyme (ACE) I/D polymorphism in HF patients.

Purpose of the Study:

  • To investigate the impact of the ACE I/D polymorphism on myocardial function changes in HF patients undergoing beta-blocker therapy.
  • To determine if the ACE I/D genotype influences the response to beta-blocker treatment in chronic heart failure.

Main Methods:

  • 199 patients with chronic HF, not on beta-blockers, were studied.
  • Echocardiography, radionuclide angiography, and cardiopulmonary exercise tests were performed before and after beta-blocker initiation.
  • Genomic DNA was analyzed to determine the ACE I/D polymorphism (II, ID, DD genotypes).

Main Results:

  • All ACE I/D genotypes (II, ID, DD) showed significant and similar improvements in left ventricular ejection fraction (LVEF) after beta-blocker therapy.
  • Peak oxygen consumption and the proportion of responders to beta-blockers were comparable across all ACE I/D genotype groups.
  • No effect of the ACE I/D polymorphism on cardiac survival was observed during a median follow-up of 933 days.

Conclusions:

  • There is no evidence of a pharmacogenetic interaction between the ACE I/D polymorphism and the efficacy of beta-blockade in chronic HF patients.
  • Beta-blocker therapy is recommended for all HF patients, irrespective of their ACE I/D genotype (II, ID, or DD).
Abstract

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