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, beta-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 beta-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 beta-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 beta-blockers, as well as prophylactic amiodarone, sotalol, and magnesium. Other novel therapies, mostly targeting inflammation, are under investigation and may provide additional strategies.
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, beta-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 beta-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 beta-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 beta-blockers, as well as prophylactic amiodarone, sotalol, and magnesium. Other novel therapies, mostly targeting inflammation, are under investigation and may provide additional strategies.
Authors: Erin Harleton; Alessandra Besana; George M Comas; Peter Danilo; Tove S Rosen; Michael Argenziano; Michael R Rosen; Richard B Robinson; Steven J Feinmark Journal: J Biol Chem Date: 2012-12-10 Impact factor: 5.157
Authors: Y Zhang; J A Fraser; C Schwiening; Y Zhang; M J Killeen; A A Grace; C L-H Huang Journal: Acta Physiol (Oxf) Date: 2009-11-03 Impact factor: 6.311