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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.
Acknowledgements
This research effort was supported in part by National Heart, Lung, and Blood Institute grants (RO1 HL101240) and (R01 HL089542). The authors gratefully acknowledge J Pfaff and S Nord of Aurora Cardiovascular Services for editorial assistance.
Financial & competing interests disclosure
A Jahangir’s research effort was supported in part by National Heart, Lung, and Blood Institute grants (RO1 HL101240 and R01 HL089542) and intramural Cardiovascular Medicine and Surgery Research support from the Aurora Research Institute and Aurora Foundation. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
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 may decrease long-term survival.
Several anti-arrhythmic and non-anti-arrhythmic medications have been used for the prevention of postoperative AF, 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 fibrillation in the postoperative setting.
The interaction of acute surgery-related factors such as sympathetic activation, inflammation, renin–angiotensin–aldosterone system activation, trauma and oxidative stress with an underlying abnormal atrial structural substrate precipitates electrical instability and onset of AF in the immediate postoperative period, and these factors are the target for pharmacological prevention of postoperative AF.
The selection of prophylactic intervention needs to be individualized to a patient’s condition and the risks and adverse events associated with each intervention.
In patients at high risk for cardiovascular events or myocardial ischemia undergoing cardiac surgery, β-blockers should be continued or initiated to reduce postoperative AF with avoidance of hypotension or bradycardia. In patients with low surgical risk, β-blocker initiation or use of high dose without titration is not recommended.
In high-risk individuals undergoing cardiac surgery or in patients unable to tolerate β-blockers, amiodarone is recommended for reduction of postoperative AF or control of rapid ventricular rate response in patients with heart failure with reduced ejection fraction.
In patients with stable ventricular systolic dysfunction, it is reasonable to continue angiotensin-converting enzyme inhibitors with close hemodynamic monitoring. Initiation of angiotensin-converting enzyme inhibitors or angiotensin receptor antagonists for the prevention of postoperative AF is, however, not recommended.
Statins should be continued in patients undergoing vascular surgery, favoring statins with a long half-life, and its preoperative initiation considered 2 weeks before surgery in those at high risk for cardiovascular events. In patients without cardiovascular disease, preoperative initiation of statin is not indicated for primary prevention of AF.
The overall data at this time do not support the routine use of magnesium supplementation, anti-inflammatory agents or antioxidants such as corticosteroids, colchicine, N-acetyl cysteine, omega-3 polyunsaturated fatty acids or ascorbic acid for the prevention of postoperative AF in patients going for cardiac surgery.
Since current interventions for reduction of postoperative AF are only partially effective, additional research to improve understanding of molecular mechanisms underlying the development of AF is warranted to identify novel therapeutic targets that can help prevent or reverse the substrate that increases predisposition to postoperative AF.