Homans D C, Pavek T, Laxson D D, Bache R J
Department of Medicine, University of Minnesota Medical School, Minneapolis.
J Am Coll Cardiol. 1994 Oct;24(4):1109-16. doi: 10.1016/0735-1097(94)90877-x.
This study tested the hypothesis that there is preferential recovery of subepicardial wall thickening after nontransmural myocardial infarction.
Previous studies have demonstrated gradual recovery of mechanical function after reperfusion in acute myocardial infarction. Because myocardial necrosis is primarily subendocardial, it was hypothesized that recovery of mechanical function would occur primarily in the subepicardial layers.
Eleven mongrel dogs were instrumented with ultrasonic crystals to measure transmural and outer wall thickening. Animals performed treadmill exercise before and 8 days after nontransmural infarction produced by coronary occlusion for 90 min.
Coronary artery occlusion reduced myocardial blood flow to inner layers more than that to outer wall layers (mean [+/- SD] 0.19 +/- 0.35 vs. 0.38 +/- 0.38 ml/g per min, p < 0.05). Infarct size (% of risk region) was also greater in subendocardial layers (33.3 +/- 24.3% inner vs. 8.3 +/- 9.7% outer). Rest transmural wall thickening was 22.4 +/- 7.5% versus 14.4 +/- 6.3% for outer wall layers. During coronary artery occlusion, transmural and outer wall thickening decreased similarly (3.2 +/- 7.7% vs. 0.2 +/- 5.9%). Eight days after reperfusion, thickening of the entire wall recovered to 7.5 +/- 4.7%; however, outer wall thickening had only recovered to 0.0 +/- 5.8%. Myocardial blood flow was abnormal during exercise 8 days after reperfusion, with markedly reduced subendocardial perfusion. However, thickening of the inner and outer layers was similar, with transmural thickening of 8.5 +/- 9.3% and outer wall thickening of 1.6 +/- 6.2%.
Despite preferential blood flow and less necrosis, thickening of the outer layer is not preserved 8 days after subendocardial infarction. The severity of subendocardial injury appears to be the major determinant of regional function after nontransmural infarction.
本研究检验了非透壁性心肌梗死后心外膜下心肌壁增厚存在优先恢复这一假设。
既往研究已证实急性心肌梗死后再灌注时机械功能会逐渐恢复。由于心肌坏死主要发生在心内膜下,因此推测机械功能的恢复主要发生在心外膜层。
对11只杂种犬植入超声晶体以测量透壁和外层心肌增厚情况。在冠状动脉闭塞90分钟造成非透壁性心肌梗死之前及之后8天,让动物进行跑步机运动。
冠状动脉闭塞使内层心肌血流减少程度大于外层(平均[±标准差]0.19±0.35对0.38±0.38毫升/克每分钟,p<0.05)。心内膜下层梗死面积(危险区域的百分比)也更大(内层为33.3±24.3%,外层为8.3±9.7%)。静息时透壁心肌增厚为22.4±7.5%,而外层为14.4±6.3%。冠状动脉闭塞期间,透壁和外层心肌增厚下降情况相似(3.2±7.7%对0.2±5.9%)。再灌注8天后,整个心肌壁增厚恢复至7.5±4.7%;然而,外层心肌增厚仅恢复至0.0±5.8%。再灌注8天后运动期间心肌血流异常,心内膜下灌注明显减少。然而,内层和外层增厚情况相似,透壁增厚为8.5±9.3%,外层增厚为1.6±6.2%。
尽管存在血流优先供应且坏死较少,但心内膜下梗死后8天外层心肌增厚并未保留。心内膜下损伤的严重程度似乎是非透壁性梗死后局部功能的主要决定因素。