Chronic myocardial infarction is a substrate for bradycardia-induced spontaneous tachyarrhythmias and sudden death in conscious animals.

Chronic myocardial infarction is a substrate for bradycardia-induced spontaneous tachyarrhythmias and sudden death in conscious animals.
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慢性心肌梗塞是心动过缓引起的自发性快速心律失常和意识动物猝死的基础。

DOI:
10.1111/j.1540-8167.2005.00336.x
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发表时间:
2006
期刊:
Journal of cardiovascular electrophysiology.
影响因子:
--
通讯作者:
Ideker,RaymondE
Ideker,RaymondE
中科院分区:
--
文献类型:
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作者:
Killingsworth,CherylR;Walcott,GregoryP;Gamblin,TracyL;Girouard,StevenD;Smith,WilliamM;Ideker,RaymondE

文献摘要

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引言:心动过缓患者可能发生严重的快速性心律失常,但尚不清楚心动过缓是否单独会诱发心律失常或是否需要额外的底物。虽然存在室性心动过速(VT)的几种动物模型,但尚未报道在不操纵自主神经系统的情况下,在存在心动过缓和慢性心肌梗死(MI)的大型动物中模拟自发性VT和心脏性猝死(SCD)的临床状况的模型。我们测试的假设,心肌梗死和心动过缓引起更多的自发持续VT比心动过缓along.Methods和结果:绵羊(42-56公斤)进行房室(AV)结导管消融单独(n = 5)或AV结消融和150分钟的血管成形术球囊闭塞的左前降支冠状动脉(n = 9)。植入式心律转复除颤器在第一周以每分钟90次的频率提供急救电击和按需起搏,此后以每分钟40次的频率提供。连续无线电遥测和记录6周的电描记图。急性MI后VT在第4天消失。第8天的突然心动过缓引发了大量室性早搏(PVC)和在接下来的5周内持续>30秒的持续VT发作。有43次持续性VT发作,无自发性室颤(VF)伴心动过缓。然而,在同时存在MI和心动过缓的情况下,在第13、15和34天有970次VT/VF发作(P < 0.05)和3例死亡。第7天,两组之间的平均24小时PVC计数相似,但到第11天和第40天,与单纯心动过缓相比,存在心动过缓和慢性MI时的PVC计数分别高出35倍和4倍。由于两组间个体差异较大,因此未检测到PVC发生率的显著差异(P = 0.21)。高PVC计数并没有出现预测SCD。结论:合并MI和心动过缓继发于AV结消融术在绵羊产生较高的发病率VT比心动过缓单独,这表明,这种制备可以作为一种模型,用于研究VT和心源性猝死。
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 the first 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.