Pozzati A, Pancaldi L G, Di Pasquale G, Pinelli G, Bugiardini R
Cardiology Section, Bentivoglio Hospital, Bologna, Italy.
J Am Coll Cardiol. 1996 Mar 15;27(4):847-52. doi: 10.1016/0735-1097(96)00033-2.
The aim of this study was to investigate the relation between "ischemic" sudden death (arrhythmic death preceded by ST segment shift) and autonomic nervous system activity. Background. Mechanisms precipitating sudden death are poorly known despite the importance of detecting functional factors that may contribute to such a fatal event.
We analyzed the tapes of eight patients (seven men and one woman with a mean age of 66 +/- 8 years) who had ischemic sudden death during ambulatory electrocardiographic (Holter) monitoring. Four patients had unstable and four had stable angina; none was taking antiarrhythmic drugs. Twenty patients with angina and transient myocardial ischemia during Holter monitoring served as control subjects. Arrhythmias, ST segment changes and heart rate variability were analyzed by a computerized interactive Holter system.
Five patients had ventricular tachyarrhythmias (ventricular fibrillation in three, ventricular tachycardia in two), and three had bradyarrhythmias (atrioventricular block in two, sinus arrest in one) as the terminal event; all eight patients showed ST segment shift (maximal change 0.46 +/- 0.16 mV; with ST elevation in two) that occurred 41 +/- 34 min (mean +/- SD) before sudden death. The standard deviation of normal RR intervals (SDNN) was 89 +/- 33 ms during the 10 +/- 6 h of Holter monitoring; 5 min before the onset of the fatal ST shift, SDNN measurements were significantly lower than during the initial 5-min period (48 +/- 10 vs. 29 +/- 9 ms; p=0.002). In control patients, the SDNN was 102 +/- 39 ms during Holter monitoring, whereas it measured 56 +/- 30 ms 5 min before the most significant episode of ST shift (p<0.01 vs. 29 +/- 9 ms [corrected] in the group with sudden death).
Autonomic dysfunction, as detected by a marked decrease in heart rate variability, is present in the period (5 min) immediately preceding the onset of the ST shift precipitating ischemic sudden death. These data suggest that sympathovagal imbalance may trigger fatal arrhythmias during acute myocardial ischemia, thus resulting in sudden death.
本研究旨在探讨“缺血性”猝死（ST段移位前发生的心律失常性死亡）与自主神经系统活动之间的关系。背景。尽管检测可能导致此类致命事件的功能因素很重要，但引发猝死的机制仍知之甚少。
我们分析了8例患者（7名男性和1名女性，平均年龄66±8岁）的动态心电图（Holter）监测磁带，这些患者在监测期间发生了缺血性猝死。4例患者患有不稳定型心绞痛，4例患有稳定型心绞痛；均未服用抗心律失常药物。20例在Holter监测期间患有心绞痛和短暂性心肌缺血的患者作为对照。通过计算机交互式Holter系统分析心律失常、ST段变化和心率变异性。
5例患者发生室性快速心律失常（3例为心室颤动，2例为室性心动过速），3例患者发生缓慢性心律失常（2例为房室传导阻滞，1例为窦性停搏）作为终末事件；所有8例患者均出现ST段移位（最大变化0.46±0.16mV；2例为ST段抬高），发生在猝死前41±34分钟（平均±标准差）。在Holter监测的10±6小时内，正常RR间期标准差（SDNN）为89±33ms；在致命性ST段移位发作前5分钟，SDNN测量值显著低于最初5分钟期间（48±10对29±9ms；p=0.002）。在对照患者中，Holter监测期间SDNN为102±39ms，而在最显著的ST段移位发作前5分钟测量值为56±30ms（与猝死组中29±9ms[校正后]相比，p<0.01）。
在引发缺血性猝死的ST段移位发作前（5分钟），存在通过心率变异性显著降低检测到的自主神经功能障碍。这些数据表明，交感迷走神经失衡可能在急性心肌缺血期间触发致命性心律失常，从而导致猝死。
