Previtali M, Klersy C, Salerno J A, Chimienti M, Panciroli C, Marangoni E, Specchia G, Comolli M, Bobba P
Am J Cardiol. 1983 Jul;52(1):19-25. doi: 10.1016/0002-9149(83)90062-0.
Fifty-six patients with active Prinzmetal's variant angina were studied to determine the incidence and clinical significance of ventricular tachyarrhythmias and the correlation between arrhythmias and degree and time course of S-T segment changes during the ischemic attacks. Twenty-nine patients (Group I) had no ventricular arrhythmias in any of the 1,083 recorded episodes, while 27 patients (Group II) developed arrhythmias in 18% of the attacks. No significant differences in clinical, electrocardiographic, angiographic, or hemodynamic findings could be found between the 2 groups. In 23 of the 27 Group II patients, ventricular arrhythmias developed during maximal S-T segment elevation (occlusion arrhythmias), while in 10 they occurred during resolution of S-T segment changes (reperfusion arrhythmias); 6 of the latter patients also had occlusion arrhythmias. Eight of the 23 patients with occlusion arrhythmias and 6 of the 10 with reperfusion arrhythmias had ventricular fibrillation or ventricular tachycardia. Maximal S-T segment elevation was significantly greater (p less than 0.001) in patients with occlusion arrhythmias than in those without arrhythmias. The episodes with reperfusion arrhythmias were significantly longer (p less than 0.001) and showed a significantly greater S-T segment elevation (p less than 0.001) than those without arrhythmias in Group I patients. This study shows that significant ventricular tachyarrhythmias develop during ischemic attacks in about 50% of patients with active variant angina; clinical and angiographic features are not useful in distinguishing patients with arrhythmias from the others. Our findings suggest that in variant angina ventricular arrhythmias may be due to the effects of both coronary artery occlusion and reperfusion; both types of arrhythmias are correlated with the severity of ischemia, as measured by the degree of S-T segment elevation. Reperfusion arrhythmias also appear to be correlated with the duration of ischemia.
对56例活动性变异型心绞痛患者进行了研究,以确定室性快速心律失常的发生率和临床意义,以及心律失常与缺血发作期间ST段改变的程度和时程之间的相关性。29例患者(第一组)在记录的1083次发作中均未出现室性心律失常,而27例患者(第二组)在18%的发作中出现了心律失常。两组在临床、心电图、血管造影或血流动力学检查结果方面均未发现显著差异。在第二组的27例患者中,23例在ST段最大抬高时出现室性心律失常(闭塞性心律失常),10例在ST段改变恢复时出现室性心律失常(再灌注性心律失常);后一组中有6例患者也有闭塞性心律失常。23例有闭塞性心律失常的患者中有8例,10例有再灌注性心律失常的患者中有6例发生了心室颤动或室性心动过速。有闭塞性心律失常的患者ST段最大抬高显著高于无心律失常的患者(p<0.001)。与第一组无心律失常的发作相比,有再灌注性心律失常的发作持续时间显著更长(p<0.001),且ST段抬高显著更大(p<0.001)。本研究表明,约50%的活动性变异型心绞痛患者在缺血发作期间会出现显著的室性快速心律失常;临床和血管造影特征无助于区分有心律失常的患者和其他患者。我们的研究结果表明,在变异型心绞痛中,室性心律失常可能是冠状动脉闭塞和再灌注共同作用的结果;两种类型的心律失常均与缺血严重程度相关,缺血严重程度通过ST段抬高程度来衡量。再灌注性心律失常似乎也与缺血持续时间相关。