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首页> 外文期刊>American Journal of Physiology >Mechanism of sudden cardiac death in pigs with viable chronically dysfunctional myocardium and ischemic cardiomyopathy.
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Mechanism of sudden cardiac death in pigs with viable chronically dysfunctional myocardium and ischemic cardiomyopathy.

机译：患有慢性慢性功能障碍和缺血性心肌病的猪突然心源性死亡的机制。

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摘要

Pigs with viable chronically dysfunctional myocardium and ischemic cardiomyopathy are at high risk of sudden cardiac death (SCD). We sought to identify the arrhythmic mechanism of SCD, the relation to changes in left ventricular (LV) function, and inducibility of malignant arrhythmias before SCD. Juvenile pigs (n = 72) were instrumented with chronic stenoses on proximal left anterior descending and circumflex arteries. Survival was only 29% 3 mo after instrumentation, and all deaths were sudden and without prodromal symptoms of heart failure. Triphenyltetrazolium chloride staining demonstrated necrosis in only nine animals averaging 2.3 +/- 0.9% of the LV, with no difference between SCD animals and survivors. Implantable loop recorders (n = 13) documented both ventricular fibrillation (n = 6) and bradyasystole (n = 2) as the arrhythmic mechanism of death. Although regional and global function were depressed [anteroseptal wall thickening 1.8 +/- 0.2 vs. 4.2 +/- 0.2 mm in Sham animals (P < 0.001); fractional shortening 21 +/- 2 vs. 31 +/- 1% in Sham animals (P < 0.01)], there were no differences between SCD animals and survivors. LV mass increased in animals with ischemic cardiomyopathy and was greater in animals with SCD (4.0 +/- 0.2 vs. 3.1 +/- 0.1 g/kg in survivors; P < 0.001). Serial programmed ventricular stimulation failed to induce any sustained arrhythmias. We conclude that pigs with viable dysfunctional myocardium and globally reduced LV function have a high rate of SCD with a spectrum of arrhythmias similar to patients with ischemic cardiomyopathy. The risk is independent of necrosis but appears to increase with LV hypertrophy. Like patients with ischemic cardiomyopathy, programmed stimulation is insensitive to predict SCD when viable dysfunctional myocardium is the pathological substrate.
机译：具有生存力的慢性心肌功能不全和缺血性心肌病的猪极有可能发生心脏猝死（SCD）。我们试图确定SCD的心律失常机制，与左心室（LV）功能变化的关系以及SCD之前恶性心律失常的可诱导性。幼猪（n = 72）在左侧近前降支和回旋支动脉上装有慢性狭窄。仪器安装后3个月的存活率仅为29％，所有死亡都是猝死的，无前驱性心力衰竭症状。氯化三苯四唑鎓染色仅在9只动物中显示出坏死，平均占LV的2.3 +/- 0.9％，SCD动物和幸存者之间无差异。植入式循环记录仪（n = 13）记录了室颤（n = 6）和Bradyasystole（n = 2）作为死亡的心律失常机制。尽管区域和整体功能受到抑制[假手术动物的前腹壁壁增厚1.8 +/- 0.2相对于4.2 +/- 0.2 mm（P <0.001）;假动物的分数缩短了21 +/- 2与31 +/- 1％（P <0.01）]，SCD动物和幸存者之间没有差异。在患有缺血性心肌病的动物中，LV质量增加，而在患有SCD的动物中，LV质量增加（幸存者为4.0 +/- 0.2对3.1 +/- 0.1 g / kg; P <0.001）。连续程序性心室刺激未能引起任何持续的心律不齐。我们得出的结论是，存活的心肌功能障碍和左室功能全面降低的猪与缺血性心肌病患者相似，其心律失常的发生率较高。风险与坏死无关，但随着左室肥大而增加。像缺血性心肌病患者一样，当可行的功能障碍性心肌病是病理性基质时，程序性刺激对预测SCD不敏感。

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