【经验】冠状动脉旁路移植术（CABG）后房颤的处理

帕普沃斯医院Andrew Grace 博士

我在英国接诊量最大的心脏病机构帕普沃斯医院工作，医院每年会进行超过2000例心内直视手术。与其他一些机构相比，我们的患者具有手术结局更为严重、危险因素更多、以及同期接受更多瓣膜手术的趋势。总体而言，我们的患者中约有30%-40%将在CABG后发生房颤（AF）。

患者通常会转诊至外科接受电生理治疗。首诊时将考虑患者的情况、手术时间、何时开始出现支持AF诊断的迹象、以及相关的术前因素，尤其是既往有AF病史。左室功能和目前数值与术前观察的比较将具有意义，我们也会考虑现行的治疗方案。我们需要立即达成共识的是，需在多快时间内对心脏节律进行分类。如果我们立即对患者进行复诊或是在之后的常规流程中对其进行复查是否明智？这类决策，毫无疑问全部有赖于一致的病情概要。

我们会在床边与外科住院医生和护士一起对所有病历进行复习。我们需要一致认定这确实是AF而非对噪音干扰的过度解读，或有时可能是房扑等节律特征，但这或许需使用相同的治疗方案。我们将深入探索AF发生的准确时间，并将尤其注意是否有低血压、急性肾功能衰竭或肺水肿等血液动力学损害的迹象。我们在回顾药物方案时将关注抗血栓治疗，无论是口服药物、静脉给药还是皮下给药方案均包括在内。我们会探索是否可能存在特异性可纠正性促进因素，但几乎所有病例都排除了这一可能。

决定我们如何处理患者的重要因素是心室率。我们的治疗决策会考虑到通过遥测术和/或动态ECG测得的心动过缓。无论是观察到阵发性还是持续性心动过缓（未使用负性心率药物时），我们均会建议安装永久性起搏器。我们的患者在手术时心房及心室放置心外膜导线，我们会了解这些是否能正常运行。如果通过心外膜导线放置失败，则或许更需要在短时间内放置永久性系统。

如患者突发症状，则我们会进行经胸超声心动图检查，并考虑立即实施心脏电复律。这可能发生于低血压的情况下，或者是尿排出量开始减少的情况下。如AF病程超过24小时且缺乏抗凝治疗，通常我不建议在未行经食道检查的情况下进行化学或电击复律。多数情况下，我偏向于相对简单的电击而非化学心脏复律。除非是既往有术后早期阵发性AF迹象的患者，在这种情况下，几乎可以肯定患者在无抗心律失常治疗时使用电复律将迅速导致AF复发。在那种情形下，我会建议通过大的中央静脉（通常是颈内静脉）给予胺碘酮静脉给药。为了避免可能的血管/皮肤影响，我不建议通过外周静脉插管进行胺碘酮给药的做法。

在多数无明显症状或血流动力学损害的患者中，控制心率是合适的处理方式。在无心动过缓或其他禁忌症的情况下，患者可使用β受体阻滞剂及美托洛尔等半衰期较短的药物。几乎所有患者均对口服（与静脉制剂相反）心率控制药物产生应答。对于AF病程超过24小时且未接受抗凝治疗或经食道超声心动图的患者而言，我不建议其使用胺碘酮。我会顾虑到该药可导致不必要的即时心律纠正并带来脑血管风险。

对于所有患者，我都会评估其出血风险，如果评估结果显示风险是可以接受的，那么将开始进行抗血栓治疗，如果术前是窦性节律则加用胺碘酮。我个人倾向于在无劳动负荷的情况下使用胺碘酮 200 mg/天的给药方案，以使药物间相互作用降至最低并能顺利引入药物治疗。如果患者抗凝治疗充分，且因持续性快速心室应答（心脏电复律不在计划范围内）而受到损害，则可能要考虑更加快速地引入胺碘酮治疗。

一旦患者心律恢复稳定，无论是窦性心律还是适当的心率控制（可能置入了起搏器装置），则从点生理角度来看，该患者已具备出院条件。患者的CHA2DS2-VASc评分将决定其接下来的持续抗凝治疗需求。

在适当的时候，通常是在约第6周时，患者将再次接受检查。如手术随访时患者具有AF问题，则其将仅回访接受电生理治疗。如果治疗后AF持续存在，则通常会建议进行心脏电复律以及可能辅以胺碘酮治疗。如之后AF复发，则常用的治疗策略遵循普遍认可的方案——需要时可使用消融和/或起搏器装置。小部分接受了CABG的患者可能需要使用这些更为复杂的处理方案。

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Andrew Grace MD, PhD, FRCP, FACC

Consultant Cardiologist at Papworth Hospital and Research Group Head in the University of Cambridge, Cambridge

I work at the highest-volume cardiac facility in the United Kingdom, with over 2000 open-heart procedures annually. The patients tend to the more severe end of the surgical spectrum, with more risk factors, and more undergo concomitant valve procedures compared with some other units. Overall, around 30% to 40% of our patients will develop atrial fibrillation (AF) post CABG.

Patients are usually referred to the electrophysiology service from the operating surgeon. The initial conversation considers the patient’s condition, the timing of the operation, when AF started with the evidence to support the diagnosis, and relevant preoperative factors, particularly any prior AF history. The left ventricular function and how current values compared with observations preoperatively would be of interest, and we would also consider current therapy. The immediate decision to agree on would be how urgently the rhythm needed sorting. Would it be wise for us to review the patient straight away or see him or her on the general round later on? This sort of decision, of course, would all depend on the agreed summary condition.

Along with the surgical resident and nurses, we would review all available charts at the bedside. We would need to agree that this was indeed AF and not over-interpretation of, for example, a noisy trace or, as often happens, rhythms such as atrial flutter that might anyway require the same therapeutic approach. We would try to drill down precisely on the time of onset, and would be particularly interested as to any evidence of hemodynamic compromise evinced by hypotension, acute renal failure, or pulmonary edema. We would review drug charts focusing on antithrombotic therapy, whether oral, intravenous, or subcutaneous. We would be exploring the possibility that there was a specific correctable promoting cause; however, in nearly all cases, these are pretty readily excluded.

An important determinant of how we might proceed would be the ventricular rate. Our decision would take into account evidence of bradycardia obtained through telemetry and/or ambulatory ECG recordings. With either paroxysmal or persistent patterns with observed bradycardia (in the absence of implicated negatively chronotropic agents) then we may advise a permanent pacemaker. Our patients receive at surgery atrial and ventricular epicardial pacing wires and we would want to know that these were functioning correctly. If there was a failure to pace through epicardial wires, then a permanent system may be required sooner.

If a patient were suddenly compromised, we would order a transthoracic echocardiogram and consider immediate cardioversion. This would be the case with hypotension and if urine output was starting to drop. I am generally not happy to advise chemical or electrical cardioversion if AF duration is in excess of 24 hours without the reassurance of a transesophageal study in the absence of therapeutic anticoagulation. In most cases, I prefer relatively uncomplicated electrical rather than chemical cardioversion. The exception would be where there was evidence of prior early postop paroxysmal AF, in which case it would be almost certain that with electrical cardioversion in the absence of anti-arrhythmic therapy the patient would revert rapidly to AF. Under those circumstances, then, I would advise intravenous amiodarone given through a large central (usually internal jugular) vein. I would counter suggestions to administer amiodarone through peripheral venous cannulae to protect against possible vascular/dermatological consequences.

In most patients, without significant symptomatic or hemodynamic compromise, then rate control would be appropriate. In the absence of bradycardia/other contraindications, one would use beta blockers and something like metoprolol with its somewhat shorter half-life. Almost all patients respond to oral (as opposed to intravenous) rate-controlling agents. In any patient who had had AF for longer than 24 hours, and, in the absence of therapeutic anticoagulation or a transesophageal echocardiogram, I would not advise amiodarone. I would be concerned that it could lead to unwanted immediate rhythm correction with cerebrovascular risk.

In all cases, I would assess bleeding risk and, if judged acceptable, antithrombotic therapy would be instituted and amiodarone added assuming preoperative sinus rhythm. My own general preference would be to use amiodarone 200 mg/day without forced loading in order to minimize interactions and provide a smooth introduction. If the patient was adequately anticoagulated with compromise due to continuing rapid ventricular responses (and electrical cardioversion was not planned), then more accelerated amiodarone introduction might be considered.

Once the rhythm had been settled, either with the patient in sinus rhythm or, alternatively, appropriately rate-controlled (and possibly with a pacemaker in place), then he or she would, from our electrophysiological perspective, be ready for discharge from the hospital. The CHA2DS2-VASc score would determine the requirement for immediate on-going anticoagulation.

In due course, and usually at around 6 weeks, patients would be reviewed. They would only be referred back to the electrophysiology service if, at surgical follow-up, AF was seen to be an issue. If AF at that point was persistent, then electrical cardioversion with possible adjunctive amiodarone would usually be advised. With any subsequent reversion to AF, then the usual strategies would follow generally accepted approaches that might use ablation and/or pacemakers, as needs be. These more complex maneuvers would be required in a small subset of patients undergoing CABG.

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