Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During Resuscitation.
Effect of Amiodarone and Hypothermia on Arrhythmia Substrates During Resuscitation.
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胺碘酮和低温对复苏期间心律失常基质的影响。
DOI：
10.1161/jaha.120.016676
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发表时间：
2021-05-18
影响因子：
5.4
通讯作者：
Wilson LD
中科院分区：
文献类型：
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作者：
Piktel JS;Suen Y;Kouk S;Maleski D;Pawlowski G;Laurita KR;Wilson LD
在复苏期间使用胺碘酮，但其在目标温度管理期间的抗心律失常作用尚不清楚。本研究的目的是确定治疗性低温和胺碘酮对心脏骤停复苏期间心律失常底物的影响。我们采用了两种互补模型：(1)体外无血流全脑缺血犬左心室经壁楔块制备。在不同温度（36°C或32°C）下给予5µmol/L胺碘酮（36 - Amio或32 - Amio，每个n=8），然后进行缺血和再灌注。结果与既往对照比较。光学成像测量动作电位持续时间、复极化色散（DOR）和传导速度（CV）。(2)猪体内复苏模型。猪（对照组或目标温度管理，32-34°C）发生缺血性心脏骤停，在心室颤动8分钟后给予胺碘酮（或不给予胺碘酮）。体外：治疗性低温而不是胺碘酮延长动作电位持续时间。缺血期间，32‐Amio组DOR比32‐单独组增加（84±7 ms比40±7 ms， P<0.05），而32‐Amio组CV减慢。在36°C缺血时，胺碘酮不影响CV、DOR或动作电位持续时间。传导阻滞仅在36°C时观察到（5/8 36‐Amio vs 6/7 36‐Alone, 0/8 32‐Amio vs 0/7 32‐Alone）。在体内：QTc在缺血再灌注后降低，并通过靶向温度管理改善。胺碘酮未使DOR或CV恶化。胺碘酮抑制室颤引起的再骤停（7/8不使用胺碘酮，2/7使用胺碘酮，P=0.041），但无脉性电活动（2/8不使用胺碘酮，5/7使用胺碘酮，P=0.13）。虽然胺碘酮消除了治疗性低温对缺血诱导的DOR和CV的有益作用，但它并没有加重复苏期间室性心动过速/心室颤动的易感性。
Amiodarone is administered during resuscitation, but its antiarrhythmic effects during targeted temperature management are unknown. The purpose of this study was to determine the effect of both therapeutic hypothermia and amiodarone on arrhythmia substrates during resuscitation from cardiac arrest. We utilized 2 complementary models: (1) In vitro no‐flow global ischemia canine left ventricular transmural wedge preparation. Wedges at different temperatures (36°C or 32°C) were given 5 µmol/L amiodarone (36‐Amio or 32‐Amio, each n=8) and subsequently underwent ischemia and reperfusion. Results were compared with previous controls. Optical mapping was used to measure action potential duration, dispersion of repolarization (DOR), and conduction velocity (CV). (2) In vivo pig model of resuscitation. Pigs (control or targeted temperature management, 32–34°C) underwent ischemic cardiac arrest and were administered amiodarone (or not) after 8 minutes of ventricular fibrillation. In vitro: therapeutic hypothermia but not amiodarone prolonged action potential duration. During ischemia, DOR increased in the 32‐Amio group versus 32‐Alone (84±7 ms versus 40±7 ms, P<0.05) while CV slowed in the 32‐Amio group. Amiodarone did not affect CV, DOR, or action potential duration during ischemia at 36°C. Conduction block was only observed at 36°C (5/8 36‐Amio versus 6/7 36‐Alone, 0/8 32‐Amio, versus 0/7 32‐Alone). In vivo: QTc decreased upon reperfusion from ischemia that was ameliorated by targeted temperature management. Amiodarone did not worsen DOR or CV. Amiodarone suppressed rearrest caused by ventricular fibrillation (7/8 without amiodarone, 2/7 with amiodarone, P=0.041), but not pulseless electrical activity (2/8 without amiodarone, 5/7 with amiodarone, P=0.13). Although amiodarone abolishes a beneficial effect of therapeutic hypothermia on ischemia‐induced DOR and CV, it did not worsen susceptibility to ventricular tachycardia/ventricular fibrillation during resuscitation.