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The renin-angiotensin-aldosterone system (RAAS) and cardiac arrhythmias
Shahriar Iravanian1, Samuel C Dudley
1Division of Cardiology, Department of Medicine, Emory University, Atlanta, Georgia, USA.
Insights
The renin-angiotensin-aldosterone system (RAAS) contributes to cardiac arrhythmias by affecting ion channels and increasing oxidative stress. RAAS modulators show promise in preventing and treating these arrhythmias.
Area of Science:
- Cardiovascular Science
- Electrophysiology
- Pharmacology
Background:
- The renin-angiotensin-aldosterone system (RAAS) is implicated in cardiovascular diseases like hypertension and hypertrophy.
- Its role in cardiac arrhythmias is an emerging area of research.
Purpose of the Study:
- To review the proarrhythmic effects of RAAS on cardiac electrophysiology.
- To explore the contribution of oxidative stress to RAAS-mediated arrhythmias.
- To summarize ongoing clinical trials on RAAS modulators for arrhythmia management.
Main Methods:
- Review of experimental results on RAAS effects on ion channels.
- Analysis of the role of oxidative stress in RAAS-induced arrhythmias.
- Compilation of data from ongoing clinical trials.
Main Results:
- RAAS influences membrane and sarcoplasmic reticulum ion channels, potentially causing proarrhythmic effects.
- Increased oxidative stress is a likely mechanism contributing to RAAS-related arrhythmias.
- RAAS modulators have demonstrated a reduced incidence of certain arrhythmias.
Conclusions:
- The RAAS plays a significant role in the development of cardiac arrhythmias.
- Targeting RAAS with modulators may be a viable strategy for arrhythmia prevention and treatment.
- Further clinical trials are needed to confirm the therapeutic utility of RAAS modulators in arrhythmias.
Abstract:
The role of the renin-angiotensin-aldosterone system (RAAS) in many cardiovascular disorders, including hypertension, cardiac hypertrophy, and atherosclerosis, is well established, whereas its relationship with cardiac arrhythmias is a new area of investigation. Atrial fibrillation and malignant ventricular tachyarrhythmias, especially in the setting of cardiac hypertrophy or failure, seem to be examples of RAAS-related arrhythmias because treatment with RAAS modulators, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and mineralocorticoid receptor blockers, reduces the incidence of these arrhythmias. RAAS has a multitude of electrophysiological effects and can potentially cause arrhythmia through a variety of mechanisms. We review new experimental results that suggest that RAAS has proarrhythmic effects on membrane and sarcoplasmic reticulum ion channels and that increased oxidative stress is likely contributing to the increased arrhythmic incidence. A summary of ongoing clinical trials that will address the clinical usefulness of RAAS modulators for prevention or treatment of arrhythmias is presented.
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