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Cardiac arrhythmias: the possible role of the renin-angiotensin system

W C De Mello1

  • 1Department of Pharmacology, UPR, San Juan, Puerto Rico 00936-5067, USA. wmello@rcm.upr.edu

Journal of Molecular Medicine (Berlin, Germany)
|May 19, 2001
PubMed

Insights

The renin-angiotensin system in heart failure can cause arrhythmias by affecting cell communication. Blocking this system may help prevent dangerous heart rhythms.

Area of Science:

  • Cardiovascular Physiology
  • Cardiac Electrophysiology

Background:

  • Heart failure is associated with activation of the renin-angiotensin system.
  • This activation may contribute to malignant arrhythmias.
  • Reduced cell coupling and conduction velocity are implicated in arrhythmogenesis during heart failure.

Purpose of the Study:

  • To discuss the role of the renin-angiotensin system in modulating cardiac cell coupling and impulse propagation.
  • To explore the generation of reentrant rhythms in the failing heart.
  • To highlight the effects of renin-angiotensin system blockade on electrical properties.

Main Methods:

  • Review of existing literature on the renin-angiotensin system and cardiac electrophysiology.
  • Discussion of the mechanisms by which angiotensin II affects the failing heart.
  • Analysis of the impact of pharmacological interventions.

Main Results:

  • Activation of the renin-angiotensin system can decrease cell coupling and conduction velocity.
  • These changes facilitate the development of reentrant arrhythmias in heart failure.
  • Angiotensin II plays a key role in altering the electrical properties of the failing heart.

Conclusions:

  • The renin-angiotensin system is a significant factor in the development of arrhythmias in heart failure.
  • Inhibition of the renin-angiotensin system, via ACE inhibitors or AT1 receptor blockers, may offer protective effects against malignant arrhythmias.

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