Renin-angiotensin-aldosterone System (RAAS), Inflammation, and Post-Operative Atrial Fibrillation (AF)
Status:
Completed
Trial end date:
2010-08-01
Target enrollment:
Participant gender:
Summary
Atrial fibrillation (AF) is the most prevalent, sustained type of irregular heartbeat and
affects over 2 million Americans. Post-operative AF, which leads to significant morbidity and
a prolonged hospital stay, complicates 20% to 40% of cardiopulmonary bypass (CPB) surgical
procedures. While recent studies indicate that interruption of the
renin-angiotensin-aldosterone system by either angiotensin-converting enzyme (ACE) inhibition
or AT1 receptor antagonism decreases the incidence of AF following a heart attack or
cardioversion (electric shock to the heart), its effect on the incidence of post-operative AF
has not been throughly studied. Studies in both animals and humans suggest that
inflammation-induced atrial remodeling plays an important role in the cause of AF. Recent
studies also provide evidence that activation of the renin-angiotensin-aldosterone system
induces inflammation, myocyte injury, proarrhythmic electrical remodeling, and fibrosis
through aldosterone.
Phase:
Phase 2/Phase 3
Details
Lead Sponsor:
Vanderbilt University Vanderbilt University Medical Center