Akasaka T, Yoshikawa J, Yoshida K, Kato H, Okumachi F, Koizumi K, Shiratori K, Takao S, Asaka T, Shakudo M
Department of Cardiology, Kobe General Hospital, Japan.
J Cardiogr. 1986 Dec;16(4):819-30.
The detection of regional myocardial dysfunction due to acute ischemic event has been limited almost entirely to experimental animal models. In human subjects, it has been limited to the observations during spontaneously-occurring or exercise-induced ischemic events. Recently, percutaneous transluminal coronary angioplasty (PTCA) provides an opportunity to study such dysfunction as the result of repeated interruptions of coronary blood flow. Echocardiograms and electrocardiograms were simultaneously recorded immediately before, during, and after 21 episodes of complete interruptions of coronary blood flow by PTCA in 11 patients. No patient had asynergy of the left ventricle either by two-dimensional echocardiography (2DE) or angiography. All patients had isolated single coronary artery stenosis including the left anterior descending artery in nine, left circumflex artery in one and right coronary artery in one. Recordings of M-mode and 2DE were successfully obtained in 10 patients. After balloon inflation, regional asynergy in the distribution of the instrumented coronary artery appeared in all 10 patients. Hypokinesis developed 9 +/- 3 (means +/- SD) sec after balloon inflation and progressed rapidly to akinesis or dyskinesis. At the same time, decreased systolic thickening of the left ventricular wall appeared in some patients in relation to the development of regional asynergy. However, systolic thinning of the left ventricular wall was not noted in all. The regional asynergy preceded ischemic electrocardiographic changes and had no relation to chest pain. Left ventricular wall motion began to normalize 12 +/- 3 sec after balloon deflation. Thereafter, transient hyperkinesis of the left ventricle developed. The first ischemic electrocardiographic change was a negative U wave which appeared 13 +/- 7 sec after coronary occlusion and remained 3 to 4 sec. Tall T waves were recorded at 28 +/- 12 sec and significant ST elevations developed 31 +/- 11 sec, after balloon inflation. These electrocardiographic changes invariably occurred only after the onset of wall motion abnormalities. Normalization of T waves was recognized at 17 +/- 16 sec and ST segment deviation were no longer present at 18 +/- 10 sec, after reperfusion. These electrocardiographic changes also preceded normalization of regional myocardial dysfunction. In conclusion, left ventricular wall motion abnormalities after coronary occlusion invariably precede the electrocardiographic changes, and begin to normalize after reperfusion prior to the electrocardiographic recovery.
急性缺血事件所致局部心肌功能障碍的检测几乎完全局限于实验动物模型。在人体中,检测一直局限于对自然发生或运动诱发缺血事件的观察。最近,经皮腔内冠状动脉成形术(PTCA)为研究因冠状动脉血流反复中断导致的这种功能障碍提供了机会。对11例患者在PTCA导致冠状动脉血流完全中断的21个时段之前、期间和之后,同时记录了超声心动图和心电图。通过二维超声心动图(2DE)或血管造影检查,没有患者出现左心室运动失调。所有患者均为单一冠状动脉狭窄,其中9例为左前降支,1例为左旋支,1例为右冠状动脉。10例患者成功获得了M型和2DE记录。球囊充盈后,所有10例患者在置入导管的冠状动脉分布区域均出现局部运动失调。球囊充盈后9±3(均值±标准差)秒出现运动减弱,并迅速发展为运动不能或运动障碍。与此同时,部分患者左心室壁收缩期增厚减少与局部运动失调进展相关。然而,并非所有患者均出现左心室壁收缩期变薄。局部运动失调先于缺血性心电图改变出现,且与胸痛无关。球囊放气后12±3秒,左心室壁运动开始恢复正常。此后,左心室出现短暂的运动增强。首次缺血性心电图改变是负向U波,在冠状动脉闭塞后13±7秒出现,并持续3至4秒。球囊充盈后28±12秒记录到高尖T波,31±11秒出现明显的ST段抬高。这些心电图改变总是在壁运动异常发生之后才出现。再灌注后17±16秒T波恢复正常,18±10秒ST段偏移消失。这些心电图改变也先于局部心肌功能障碍恢复正常。总之,冠状动脉闭塞后左心室壁运动异常总是先于心电图改变出现,并在再灌注后先于心电图恢复而开始恢复正常。