Marzullo P, Parodi O, Sambuceti G, Marcassa C, Gimelli A, Bartoli M, Neglia D, L'Abbate A
CNR Institute of Clinical Physiology, Pisa, Italy.
Am J Cardiol. 1993 May 1;71(12):1045-51. doi: 10.1016/0002-9149(93)90571-s.
To assess whether myocardial stunning occurs after brief periods of ischemia, global and regional ventricular function assessed by radionuclide angiography was studied in 52 patients. Patients were divided into 3 groups according to the type of ischemic episodes. Group 1 consisted of 15 patients studied before, during and after episodes of angina at rest. Seventeen patients studied immediately before and after coronary angioplasty constituted group 2. Group 3 consisted of 20 patients with stable angina studied before, during and after exercise-induced ischemia. Medical therapy was discontinued 48 hours before the study in all patients except those undergoing coronary angioplasty who were receiving diltiazem 180 mg/day. No difference in baseline ejection fraction was found between groups, whereas peak filling rate was statistically lower in group 3 patients. Evidence of left ventricular dysfunction during ischemia was seen in patients in groups 1 and 3, whereas transient ischemia was documented by ST-segment displacement and/or typical chest pain during balloon inflation in group 2. Persistence of systolic or diastolic dysfunction was not observed in any of the 3 groups in the recovery phase after ischemia. In conclusion, transient ischemia caused either by a primary reduction in oxygen supply (angina at rest, coronary angioplasty) or by an increase in oxygen demand (angina on effort) did not reproduce the phenomenon of systolic and diastolic stunning observed in animal experiments, although in all patients the ischemia was of sufficient duration and severity to induce marked ventricular dysfunction. The search for stunned myocardium should be extended to other different clinical models characterized by prolonged ischemia such as unstable angina or myocardial infarction.
为评估短暂缺血后是否会发生心肌顿抑，我们对52例患者进行了研究，通过放射性核素血管造影评估整体和局部心室功能。根据缺血发作类型将患者分为3组。第1组由15例在静息性心绞痛发作前、发作期间及发作后进行研究的患者组成。第2组由17例在冠状动脉血管成形术前及术后立即进行研究的患者组成。第3组由20例稳定性心绞痛患者组成，在运动诱发缺血前、缺血期间及缺血后进行研究。除接受冠状动脉血管成形术且每日服用地尔硫卓180 mg的患者外，所有患者在研究前48小时停用药物治疗。各组间基线射血分数无差异，而第3组患者的峰值充盈率在统计学上较低。第1组和第3组患者在缺血期间可见左心室功能障碍的证据，而第2组患者在球囊扩张期间通过ST段移位和/或典型胸痛记录到短暂缺血。在缺血后的恢复阶段，3组患者均未观察到收缩或舒张功能障碍的持续存在。总之，无论是由氧供应原发性减少（静息性心绞痛、冠状动脉血管成形术）还是由氧需求增加（劳力性心绞痛）引起的短暂缺血，均未重现动物实验中观察到的收缩和舒张期顿抑现象，尽管所有患者的缺血持续时间和严重程度足以诱发明显的心室功能障碍。对顿抑心肌的研究应扩展到以长时间缺血为特征的其他不同临床模型，如不稳定型心绞痛或心肌梗死。
