Pharmacological strategies for prevention of postoperative atrial fibrillation

Abstract

Atrial fibrillation (AF) complicating cardiac surgery continues to be a major problem that increases the postoperative risk of stroke, myocardial infarction, heart failure and costs and can affect long-term survival. The incidence of AF after surgery has not significantly changed over the last two decades, despite improvement in medical and surgical techniques. The mechanism and pathophysiology underlying postoperative AF (PoAF) is incompletely understood and results from a combination of acute and chronic factors, superimposed on an underlying abnormal atrial substrate with increased interstitial fibrosis. Several anti-arrhythmic and non-anti-arrhythmic medications have been used for the prevention of PoAF, but the effectiveness of these strategies has been limited due to a poor understanding of the basis for the increased susceptibility of the atria to AF in the postoperative setting. In this review, we summarize the pathophysiology underlying the development of PoAF and evidence behind pharmacological approaches used for its prevention in the postoperative setting.

Keywords: amiodarone; anti-arrhythmic agents; antioxidants; cardiac surgery; postoperative atrial fibrillation; prevention; statins; β-blockers.

Figure 1. Acute and Chronic Factors Increasing Susceptibility to Postoperative Atrial Fibrillation

CPB: cardiopulmonary bypass, CRP: c-reactive protein, IL: interleukin, PAI: plasminogen activator inhibitor, ROS: reactive oxygen species, RNS: reactive nitrogen species.

Figure 2. Pathophysiological Factors Increasing Predisposition to Postoperative Atrial Fibrillation (PoAF) and Therapeutic Interventions That Has Been Tested in Clinical Trials to Prevent PoAF

PUFA: polyunsaturated fatty acids, RAAS: renin angiotensin aldosterone system, ACEI: angiotensin converting enzymes inhibitor, ARB: angiotensin receptor blocker, NAC: N-acetyl cysteine, CCB: calcium channel blockers.