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Cardiovascular Pharmacology Fellow, School of Pharmacy, University of Connecticut; Divisions of Cardiology and Drug Information, Hartford Hospital, Hartford, CT
Associate Professor of Pharmacy Practice, School of Pharmacy, University of Connecticut; Co-Director, Arrhythmia and Cardiac Pharmacology Research, Divisions of Cardiology and Drug Information, Hartford Hospital
Reprints: Dr. White, Divisions of Cardiology and Drug Information, Hartford Hospital, 80 Seymour St., Hartford, CT 06102, fax 860/545-2277, cmwhite{at}harthosp.org
OBJECTIVE: To review the available literature addressing preventive strategies of post-cardiothoracic surgery atrial fibrillation (post-CTS atrial fibrillation).
DATA SOURCES: Pertinent articles related to the etiology, risk factors, and preventive strategies were identified through a MEDLINE search (1966–March 2007) using the MeSH terms atrial fibrillation, cardiothoracic surgery, cardiac surgery, etiology, neurohormonal, sympathetic, volume, fluid, inflammation, risk factors, operative, pacing, ß-adrenergic blockers, amiodarone, sotalol, calcium-channel blockers, magnesium, HMG-CoA reductase inhibitors, statins, fatty acids, PUFA, steroids, and nonsteroidal antiinflammatory drugs.
STUDY SELECTION AND DATA EXTRACTION: Articles evaluated were limited to human studies, published in the English language, with a Jadad score greater than 3. References of identified articles were reviewed for additional pertinent articles.
DATA SYNTHESIS: Post-CTS atrial fibrillation most commonly occurs on the second or third postoperative day, with an incidence of 20–50%. Etiology theories include neurohormonal activation, volume overload, and inflammation. Studies examining nonpharmacologic therapies have shown that maintenance of the anterior epicardial fat pad is not a viable prophylactic strategy. Biatrial cardiac pacing, especially in combination with amiodarone, is a viable preventive option. Withdrawal of preoperative ß-blockers places patients at higher risk for atrial fibrillation; these drugs should be continued postoperatively. Evidence exists supporting the use of amiodarone, sotalol, and magnesium in addition to ß-blockers. Since most of these strategies work by attenuating neurohormonal activation, adverse events, including hypotension and bradycardia, are of concern. Adding agents with antiinflammatory properties, including hydroxymethylglutaryl coenzyme A reductase inhibitors or corticosteroids, may prove to be of benefit. Additional studies using novel therapies are needed in addition to established preventive strategies.
CONCLUSIONS: Available evidence supports the continuation of preoperative ß-blockers, as well as prophylactic amiodarone, sotalol, and magnesium. Other novel therapies, mostly targeting inflammation, are under investigation and may provide additional strategies.
Key Words: atrial fibrillation, cardiothoracic surgery
Published Online, March 20, 2007. www.theannals.com, DOI 10.1345/aph.1H594
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