Boden W E, Bough E W, Benham I, Shulman R S
J Am Coll Cardiol. 1983 Jul;2(1):11-20. doi: 10.1016/s0735-1097(83)80371-4.
The syndrome of episodic angina at rest, recurrent ST segment elevation (mean = 9 mV) and nontransmural infarction characterized by minimal serum creatine kinase (CK) (mean 243 IU; upper normal limit 132 IU) was studied in 15 patients who presented with these findings. All were initially managed with intensive nitrate and beta-receptor blocker therapy. Eleven patients underwent intraaortic balloon counterpulsation for refractory angina and 13 underwent cardiac catheterization. High grade (greater than or equal to 90%) stenosis of the proximal left anterior descending coronary artery was demonstrated in 11 patients, and coronary spasm without significant, fixed occlusive disease was noted in 2 patients. Urgent aortocoronary bypass surgery was performed in seven patients with recurrent pain or electrocardiographic injury, or both, unresponsive to maximal medical therapy. The initial mean ST segment elevation and CK elevation for this group was 10 mV and 232 IU, respectively. No surgical patient developed recurrent infarction; there was one late death after reoperation. Eight patients whose condition stabilized initially on medical therapy did not undergo urgent surgery. However, five subsequently developed large transmural anterior reinfarction despite intensive medical therapy, and three died from pump failure. These patients on medical therapy did not differ from the surgical group in magnitude of ST segment elevation or increase in serum CK. Their initial mean ST segment elevation and CK elevation were 8 mV and 254 IU, respectively (difference not significant). Thus, repetitive episodes of rest angina with marked anterior wall ST segment elevation and mild CK elevations may define a subset of patients who appear to progress rapidly from minimal nontransmural necrosis to massive transmural infarction. Prompt recognition of this syndrome, followed by cardiac catheterization and urgent aortocoronary bypass surgery, may prevent extensive cardiac muscle loss.
对15例出现静息时发作性心绞痛、反复ST段抬高（平均9mV）以及非透壁性梗死（其特征为血清肌酸激酶[CK]水平最低，平均243IU；正常上限为132IU）的患者进行了研究。所有患者最初均采用强化硝酸酯类和β受体阻滞剂治疗。11例患者因顽固性心绞痛接受了主动脉内球囊反搏治疗，13例患者接受了心导管检查。11例患者显示左前降支近端冠状动脉存在高度（大于或等于90%）狭窄，2例患者发现无明显固定性闭塞性病变的冠状动脉痉挛。7例对最大程度的药物治疗无反应的反复疼痛或心电图损伤（或两者皆有）患者接受了紧急主动脉冠状动脉搭桥手术。该组患者最初的平均ST段抬高和CK升高分别为10mV和232IU。没有手术患者发生反复梗死；再次手术后有1例晚期死亡。8例最初病情在药物治疗下稳定的患者未接受紧急手术。然而，5例患者随后尽管接受了强化药物治疗仍发生了大面积透壁性前壁再梗死，3例死于泵衰竭。这些接受药物治疗的患者在ST段抬高幅度或血清CK升高方面与手术组并无差异。他们最初的平均ST段抬高和CK升高分别为8mV和254IU（差异无统计学意义）。因此，伴有明显前壁ST段抬高和轻度CK升高的反复静息心绞痛发作可能界定了一部分患者，这些患者似乎从最小程度的非透壁性坏死迅速进展为大面积透壁性梗死。及时识别该综合征，随后进行心导管检查和紧急主动脉冠状动脉搭桥手术，可能预防广泛的心肌损失。
