Mechanisms of biatrial pacing for prevention of postoperative atrial fibrillation--insights from a clinical trial.

Katherine Fan, Kathy Lee, Chu-Pak Lau
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引用次数: 16

Abstract

Atrial fibrillation (AF) occurs in a high proportion of patients after cardiac surgery and is associated with increased morbidity and longer hospital stay. Beta-blockers and amiodarone have been shown to reduce the incidence, but AF still occurs in up to 25% despite pre-treatment. The mechanisms of AF after cardiac surgery are presumably multifactorial. The transient nature of postoperative AF suggests a reversible trigger in patients with susceptible underlying electrophysiological substrates such as abnormal automaticity and conduction delay due to atrial incisions, ischemia and preexisting disease). These could result in atrial premature beats (APBs) and prolonged atrial activation causing lengthening of the P wave. Prophylactic atrial pacing (single- or multi-site) is reported to be effective in patients at high risk for postoperative AF. The mechanisms are probably a combination of preventing bradycardia-induced arrhythmias, overdrive suppression of APBs, eliminating compensatory pauses after APBs and reduction of dispersion of refractoriness. By reducing non-uniform and asynchronous activation resulting from anatomic or functional block, multi-site pacing could improve local excitability and reduce the window of opportunity for AF initiation. We found that the incidence of AF after coronary bypass surgery (CABG) was significantly reduced in patients who received prophylactic biatrial overdrive pacing (BiA) compared with single site left atrial (LA) or right atrial (RA) pacing or no pacing. (BiA 12.5% versus LA 36.4%; RA 33.3% or control 41.9%; P < 0.05). BiA pacing was associated with the greatest reduction of P wave dispersion compared with single site pacing or control (BiA 42 +/- 8%; LA 13 +/- 6%; RA 10 +/- 9%; P < 0.05). Prophylactic postoperative BiA pacing is thus a reasonable and attractive strategy for reducing the risk for postoperative AF.

双房起搏预防术后房颤的机制——来自临床试验的见解。
心房颤动(AF)在心脏手术后患者中发生的比例很高,并与发病率增加和住院时间延长有关。β受体阻滞剂和胺碘酮已被证明可以降低发病率,但尽管进行了治疗,心房颤动的发生率仍高达25%。心脏手术后房颤的发生机制可能是多因素的。术后房颤的短暂性表明,在具有易感的潜在电生理底物(如心房切口、缺血和先前存在的疾病导致的异常自动性和传导延迟)的患者中,房颤是可逆的触发因素。这些可能导致心房早搏(APBs)和延长心房激活导致P波延长。据报道,预防性心房起搏(单位点或多位点)对术后房颤高危患者有效。其机制可能是预防心动过缓引起的心律失常、过度抑制房颤、消除房颤后代偿性暂停和减少房颤难治性分散的综合作用。通过减少由解剖或功能阻滞引起的非均匀和异步激活,多点起搏可以改善局部兴奋性,减少心房颤动起始的机会窗口。我们发现,与单部位左房(LA)或右房(RA)起搏或不起搏相比,接受预防性双房超速起搏(BiA)的患者冠状动脉搭桥手术(CABG)后房颤的发生率显著降低。BiA 12.5% vs LA 36.4%;RA 33.3%或对照41.9%;P < 0.05)。与单位点起搏或对照组相比,BiA起搏与P波弥散度降低最大相关(BiA 42 +/- 8%;La 13 +/- 6%;Ra 10 +/- 9%;P < 0.05)。因此预防性术后BiA起搏是降低术后房颤风险的一种合理且有吸引力的策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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