Vaitkus P T, Miller J M, Buxton A E, Josephson M E, Laskey W K
Division of Cardiology, Hospital of the University of Pennsylvania, Philadelphia.
Am Heart J. 1994 Jun;127(6):1481-90. doi: 10.1016/0002-8703(94)90374-3.
The electrophysiologic sequelae of acute reversible transmural myocardial ischemia in humans are poorly understood. Experimental models have demonstrated slowing of conduction in ischemic myocardium, but similar evidence in humans is lacking. We used percutaneous transluminal coronary angioplasty as a model for reversible ischemia to (1) analyze the regional endocardial electrogram response to ischemia and (2) determine whether an initial episode of ischemia may mitigate the effects of a subsequent bout of ischemia (preconditioning). We recorded bipolar left ventricular endocardial electrograms during elective angioplasty in 11 patients and examined changes in amplitude and duration on the electrogram. Each of the 11 patients underwent two to seven balloon inflations. The electrogram amplitude at 90 seconds of balloon occlusion fell to 86% +/- 17% of the control value, and the electrogram duration increased to 109% +/- 12% of the control value. These variables returned to baseline values by 30 and 120 seconds, respectively, after balloon deflation. Among the six patients in the preconditioning protocol, the electrogram duration at 90 seconds was less with the second inflation (106% +/- 7%) than with the first (115% +/- 17%, p < 0.05). The difference in electrogram amplitude between the first and the second inflation was not significant (88% +/- 17% vs 85% +/- 13%, p = NS). At 60 seconds of ischemia there was no difference between normal sinus rhythm and paced complexes in the magnitude of change in electrogram amplitude or duration. We conclude that acute transmural myocardial ischemia in humans is associated with a decrease in local bipolar endocardial electrogram amplitude and an increase in electrogram duration. These findings are consistent with slowed conduction in the ischemic zone and are in agreement with experimental findings in animals. Furthermore, a preconditioning effect on electrogram duration suggests a possible protective effect for repeated bouts of ischemia.
人类急性可逆性透壁心肌缺血的电生理后遗症目前了解甚少。实验模型已证明缺血心肌中传导减慢，但人类中缺乏类似证据。我们使用经皮腔内冠状动脉成形术作为可逆性缺血模型，以（1）分析局部心内膜电图对缺血的反应，以及（2）确定初次缺血发作是否可减轻随后缺血发作的影响（预处理）。我们在11例患者择期血管成形术期间记录双极左心室心内膜电图，并检查电图上振幅和持续时间的变化。11例患者中的每例均接受了两至七次球囊充盈。球囊闭塞90秒时的电图振幅降至对照值的86%±17%，电图持续时间增加至对照值的109%±12%。球囊放气后，这些变量分别在30秒和120秒时恢复至基线值。在预处理方案中的6例患者中，第二次充盈时90秒的电图持续时间（106%±7%）短于第一次（115%±17%，p<0.05）。第一次和第二次充盈之间电图振幅的差异不显著（88%±17%对85%±13%，p=无显著性差异）。在缺血60秒时，正常窦性心律和起搏复合波在电图振幅或持续时间变化幅度上无差异。我们得出结论，人类急性透壁心肌缺血与局部双极心内膜电图振幅降低和电图持续时间增加有关。这些发现与缺血区传导减慢一致，并且与动物实验结果相符。此外，对电图持续时间的预处理效应提示反复缺血发作可能具有保护作用。
