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首页> 外文期刊>Journal of cardiovascular electrophysiology >Chronic Myocardial Infarction is a Substrate for Bradycardia-Induced Spontaneous Tachyarrhythmias and Sudden Death in Conscious Animals.
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Chronic Myocardial Infarction is a Substrate for Bradycardia-Induced Spontaneous Tachyarrhythmias and Sudden Death in Conscious Animals.

机译:慢性心肌梗塞是心律失常引起的心动过缓引起的自发性心律失常和猝死的基质。

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MI and Bradycardia-Induced Spontaneous Arrhythmia. Introduction: Patients with bradycardia can have severe tachyarrhythmias but it is unclear whether bradycardia alone can induce arrhythmias or whether an additional substrate is necessary. While several animal models of ventricular tachycardia (VT) exist, no model has been reported to mimic the clinical condition of spontaneous VT and sudden cardiac death (SCD) in the presence of bradycardia and chronic myocardial infarction (MI) in large animals without manipulation of the autonomic nervous system. We tested the hypothesis that MI and bradycardia cause more spontaneous sustained VT than does bradycardia alone. Methods and Results: Sheep (42-56 kg) underwent atrioventricular (AV) node catheter ablation alone (n = 5) or AV node ablation and 150 minutes of angioplasty balloon occlusion of the left anterior descending coronary artery (n = 9). An implantable cardioverter defibrillator delivered rescue shocks and demand pacing at 90 beats per minute for thefirst week and at 40 beats per minute thereafter. Electrograms were continuously radiotelemetered and recorded for 6 weeks. Acute post-MI VT disappeared by day 4. The sudden bradycardia on day 8 triggered numerous premature ventricular contractions (PVCs) and episodes of sustained VT lasting >30 seconds during the next 5 weeks. There were 43 episodes of sustained VT and no spontaneous ventricular fibrillation (VF) with bradycardia alone. However, in the presence of both MI and bradycardia there were 970 episodes of VT/VF (P < 0.05) and three deaths at days 13, 15, and 34. The average 24-hour count of PVCs was similar at day 7 between the two groups but by days 11 and 40, the PVC counts were 35 times and 4 times greater, respectively, in the presence of bradycardia and chronic MI compared to bradycardia alone. No significant difference in the incidence of PVCs was detected because of large individual variation between the two groups (P = 0.21). A high PVC count did not appear to predict SCD. Conclusion: The combination of MI and bradycardia secondary to AV node ablation in sheep produces a higher incidence of VT than bradycardia alone, suggesting that this preparation can serve as a model for the study of VT and sudden cardiac death.
机译:MI和心动过缓引起的自发性心律不齐。简介:心动过缓患者可出现严重的快速性心律失常,但尚不清楚单独的心动过缓是否会诱发心律不齐或是否需要其他底物。尽管存在几种室性心动过速(VT)的动物模型,但尚无模型可以在没有操作心动过缓和慢性心肌梗死(MI)的情况下模拟自发性VT和心源性猝死(SCD)的临床状况。自主神经系统。我们检验了以下假设:MI和心动过缓比单独的心动过缓引起更多的自发持续性VT。方法和结果:绵羊(42-56 kg)单独进行房室结(AV)消融(n = 5)或进行AV结消融,并行冠状动脉左前降支的血管成形术球囊闭塞(n = 9)150分钟。植入式心脏复律除颤器在第一周以每分钟90次的搏动发出抢救电击,并在之后以每分钟40次的搏动起搏。将电描记图连续进行无线电遥测并记录6周。急性心肌梗死后VT在第4天消失。第8天突然心动过缓引发了许多室性早搏(PVC),并且在接下来的5周中持续的VT发作持续> 30秒。仅伴有心动过缓,有43次持续性VT发作且无自发性心室纤颤(VF)。然而,如果同时存在心律失常和心动过缓,则VT / VF发作970次(P <0.05),在第13、15和34天有3例死亡。在第7天,PVC之间的平均24小时计数相似。两组,但在第11天和第40天时,存在心动过缓和慢性MI的患者的PVC计数分别比单独的心动过缓分别高35倍和4倍。由于两组之间的个体差异较大,因此未检测到PVC发生率的显着差异(P = 0.21)。较高的PVC计数似乎不能预测SCD。结论:与单纯心动过缓相比,MI与房室结消融继发的心动过缓相结合产生的VT发生率更高,表明该制剂可作为研究VT和心源性猝死的模型。

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