Incidence of Atrial Fibrillation after Off-pump and On-pump Coronary Artery Surgery: Current Best Available Evidence

摘要

Coronary artery bypass graft (CABG) surgery is an effective form of treatment for patients with ischemic heart disease. This method is well tolerated by majority of patients; however it can cause some complications. The early postoperative atrial fibrillation (AF) is among the most common ones. Incidence of postoperative AF varies from 5 to over 40% according to definition of the arrhythmia, patients' characteristics, type of operation and method of heart rhythm monitoring. Some investigators consider postoperative AF to be a benign and self-limited arrhythmia. It rarely has a fatal outcome, however may lead to instability of the patient, prolongs hospital stay and increases costs. In some cases AF can be the reason of perioperative myocardial infarction, stroke, and persistent congestive heart failure. The use of cardiopulmonary bypass (CPB), the influence of cardioplegia and myocardial ischemia are possible factors responsible for postoperative occurrence of AF. For last few years off-pump coronary artery bypass (OPCAB) surgery on the beating heart, without cardiopulmonary bypass has become very popular. Rapid development of technology for OPCAB, especially stabilizing devices, has made it possible to approach almost all surfaces of the beating heart. OPCAB has excellent short-term results, however is not completely free from complications. The problem of atrial fibrillation in patients after beating heart surgery appears to be controversial. This review article analyses the available evidence to try and solve this controversy. Introduction Atrial fibrillation (AF) is one of the most common arrhythmias to occur after conventional coronary artery bypass grafting (CABG) with cardiopulmonary bypass (on-pump CABG).1,2 Postoperative AF has been associated with increased morbidity and prolonged hospitalization after on-pump CABG surgery. Several clinical factors have been associated with AF after on-pump CABG.3,4,5,6 Available evidence suggests that surgical “over-manipulation” of the right atrium7, surgical thoracic trauma8, use of cardioplegic solutions1, cross-clamping of the aorta1, withdrawal of β-blockers administered preoperatively9, structural changes in the heart such as those related to age, as well as the effects of postoperative hypoxia, hypovolemia, and electrolyte imbalance7 could trigger AF in patients undergoing on-pump CABG. Clinical factors that predispose persons to AF may act through a common denominator: “the dispersion of refractoriness,” a term used to describe the heterogeneity of local atrial refractory periods.10,11 Electrophysiologic mechanism of postoperative atrial fibrillation The electrophysiologic mechanism of postoperative AF is believed to be reentry that results from dispersion of atrial refractoriness.10,12,13 When adjacent atrial areas have dissimilar or nonuniform refractoriness, a depolarizing wavefront becomes fragmented as it encounters both refractory and excitable myocardium.10,12,13 This allows the wavefront to return and stimulate previously refractory but now repolarized myocardium leading to incessant propagation of the wavefront or reentry.10,12,13 Currently, there is not an adequate explanation for why some patients develop postoperative AF whereas others having the same surgical interventions remain in sinus rhythm. Individuals vulnerable to AF are speculated to have the electrophysiologic substrate (nonuniform dispersion of atrial refractoriness) before operation that is then aggravated by surgical perturbations.10 It is widely believed that enhanced sympathetic nervous system activity increases susceptibility to postoperative AF.14,15,16,17,18,19 Sympathetic activation, however, is highest the first 24 hours after operation, whereas the onset of AF usually occurs between the second and third postoperative days.1,3,7,20 Furthermore, the atrial electrophysiologic effects of autonomic nervous system stimulation are complex. In contrast to the ventricle where sympathetic activation d