Kerin N Z, Rubenfire M, Naini M, Wajszczuk W J, Rao P
J Electrocardiol. 1982 Oct;15(4):365-80. doi: 10.1016/s0022-0736(82)81010-8.
Thirty patients with variant angina pectoris (VAP) were analyzed for electrocardiographic features during episodes of VAP. Twenty-nine of these patients had cardiac catheterization, and an autopsy study was performed in one. The patients showed predominantly concave upright T-waves during pain. An increase of R wave amplitude (expressed as delta R) of more than 10% was seen in 17/30 patients (57%). The primary ST-T changes produced by the VAP episodes were conspicuous in two patients with pre-existent complete left and right bundle branch block. Serious dysrhythmias, including ventricular fibrillation (VF), ventricular tachycardia (VT), ventricular premature beats (VPBs) (more than five/min, multifocal and R on T phenomenon), and 2 degrees atrioventricular block were found in thirteen patients (43%). The development of dysrhythmias was related to the duration of VAP episodes. The average time to onset of dysrhythmias was 3.54 min. The dysrhythmias were not contingent upon pre-existing coronary artery anatomy (defined by Friesinger's coronary score), left ventricular ejection fraction or left ventricular segmental abnormalities. The location of the ST-segment elevation and the presence of dysrhythmias during the episodes of VAP (A-V blocks, ventricular tachycardia and fibrillation) were not predictive factors of the coronary anatomy. Eight patients (27%) developed myocardial infarction (MI). Five of them had nontransmural MIs and three developed transmural MIs. The development of MI was not related to the severity of the VAP attacks (appreciated by the magnitude of ST-segment elevation and R wave changes) but showed a relation to the development of an unstable pattern which preceded the infarction. Sixteen patients underwent exercise testing. In eight of them, the coronary arteriograms were normal (Group I); in the remaining eight, significant proximal coronary artery obstructive disease was found (Group II). Group I patients displayed a normal ST-segment response and functional aerobic capacity (FAI = 4.4 +/- 14) as well as normal heart rate (HR) and double product (SBP X HR) responses (HR = 154 +/- 21; SBP X 21; SBP X HR = 290 +/- 71). During exercise, a normal delta R was observed. With one exception, Group II patients showed an abnormal ST-segment response with an overall low exercise capacity (FAI = 57 +/- 17) and decreased hemodynamic response (HR = 27; SBP X HR = 130 +/- 40). FAI, HR, SBP X HR Group I vs. Group II = P less than .005/less than .02/less than .005. The abnormal ST-segment response included elevation in four patients and depression in three. During exercise, Group I with ST-elevation displayed a normal (negative) delta R response; while Group II with ST-depression displayed an abnormal delta R response (positive or no change). There was no difference in the coronary score between Group II patients with ST-segment elevation or depression.
对30例变异型心绞痛(VAP)患者发作时的心电图特征进行了分析。其中29例患者进行了心导管检查,1例进行了尸检研究。患者疼痛发作时主要表现为T波凹面向上。30例患者中有17例(57%)R波振幅增加(以ΔR表示)超过10%。VAP发作引起的原发性ST-T改变在2例原有完全性左、右束支传导阻滞的患者中较为明显。13例患者(43%)出现严重心律失常,包括心室颤动(VF)、室性心动过速(VT)、室性早搏(VPB,每分钟超过5次,多灶性及R波落在T波现象)以及二度房室传导阻滞。心律失常的发生与VAP发作持续时间有关。心律失常发作的平均时间为3.54分钟。心律失常并非取决于原有冠状动脉解剖结构(由弗里辛格冠状动脉评分定义)、左心室射血分数或左心室节段性异常。VAP发作时ST段抬高的部位以及心律失常(房室传导阻滞、室性心动过速和颤动)的出现并非冠状动脉解剖结构的预测因素。8例患者(27%)发生了心肌梗死(MI)。其中5例为非透壁性心肌梗死,3例为透壁性心肌梗死。心肌梗死的发生与VAP发作的严重程度(通过ST段抬高幅度和R波变化来评估)无关,但与梗死前不稳定模式的发展有关。16例患者进行了运动试验。其中8例冠状动脉造影正常(I组);其余8例发现有明显的近端冠状动脉阻塞性疾病(II组)。I组患者表现出正常的ST段反应和功能性有氧能力(FAI = 4.4±14)以及正常的心率(HR)和双乘积(收缩压×心率)反应(HR = 154±21;收缩压×心率 = 290±71)。运动期间,观察到正常的ΔR。除1例例外,II组患者表现出异常的ST段反应,总体运动能力较低(FAI = 57±17)且血流动力学反应降低(HR = 27;收缩压×心率 = 130±40)。I组与II组的FAI、HR、收缩压×心率比较 = P<0.005/<0.02/<0.005。异常的ST段反应包括4例ST段抬高和3例ST段压低。运动期间,ST段抬高的I组表现出正常(负性)的ΔR反应;而ST段压低的II组表现出异常的ΔR反应(正性或无变化)。ST段抬高或压低的II组患者冠状动脉评分无差异。