Komamura K, Kitakaze M, Nishida K, Naka M, Tamai J, Uematsu M, Koretsune Y, Nanto S, Hori M, Inoue M
Cardiovascular Division, Osaka Police Hospital, Honshu, Japan.
J Am Coll Cardiol. 1994 Aug;24(2):370-7. doi: 10.1016/0735-1097(94)90290-9.
This study was undertaken to examine the effects of coronary flow dynamics after thrombolysis on infarct size limitation.
It has been commonly accepted that early thrombolysis does not necessarily salvage infarcted myocardium. Plausible causes for myocardial necrosis include such factors as elapsed time to reperfusion, residual stenosis, collateral vessels, hemodynamic loads, preconditioning and reperfusion injury. Recently, the no reflow phenomenon has been elucidated to be associated with infarct extension in clinical studies employing contrast echocardiography or thallium scintigraphy.
Nineteen patients with early reperfusion in acute anterior myocardial infarction and comparable clinical background were studied. The patients were classified into two groups on the basis of pattern of thermodilution measurements of great cardiac vein flow after reperfusion: group A, 9 patients with a progressive decrease in great cardiac vein flow during the 1st 24 h of the onset of infarction; and group B, 10 patients without this observation. Left ventricular ejection fraction and thallium perfusion defect were compared between the two groups at follow-up.
There were no significant differences in systemic hemodynamic variables between groups A and B, and neither group had recurrent ischemic events suggesting reocclusion or restenosis during the study. In group A, both great cardiac vein flow (mean +/- SD 44 +/- 17% reduction) and oxygen extraction (38 +/- 15% reduction) were progressively decreased after the onset of reperfusion. Compared with group B, this group showed a lower left ventricular ejection fraction (36 +/- 7% vs. 63 +/- 15%, p < 0.01) and a larger thallium-201 defect severity index (1,091 +/- 366 U vs. 247 +/- 261 U, p < 0.01) at follow-up. Although other patient characteristics were comparable between the two groups, antecedent angina occurred in 90% of group B patients in contrast to only 33% of group A patients.
Salvage of myocardium from infarction by successful thrombolysis was not observed in the patients demonstrating progressive decreases in great cardiac vein flow (group A). In those patients, inadequate myocardial reperfusion on a microvascular basis might be associated with a much larger myocardial infarction. Antecedent angina may protect against a progressive decrease in coronary flow and may have beneficial effects on infarct size limitation.
本研究旨在探讨溶栓后冠状动脉血流动力学对梗死面积限制的影响。
普遍认为早期溶栓不一定能挽救梗死心肌。心肌坏死的可能原因包括再灌注时间、残余狭窄、侧支血管、血流动力学负荷、预处理和再灌注损伤等因素。最近,在采用对比超声心动图或铊闪烁显像的临床研究中,无复流现象已被阐明与梗死扩展有关。
对19例急性前壁心肌梗死早期再灌注且临床背景相似的患者进行研究。根据再灌注后心大静脉血流热稀释测量模式将患者分为两组:A组,9例在梗死发作后最初24小时内心大静脉血流逐渐减少;B组,10例未观察到这种情况。随访时比较两组的左心室射血分数和铊灌注缺损。
A组和B组之间全身血流动力学变量无显著差异,且两组在研究期间均无提示再闭塞或再狭窄的复发性缺血事件。在A组中,再灌注开始后心大静脉血流(平均±标准差减少44±17%)和氧摄取(减少38±15%)均逐渐降低。与B组相比,该组在随访时左心室射血分数较低(36±7%对63±15%,p<0.01),铊-201缺损严重指数较大(1091±366 U对247±261 U,p<0.01)。尽管两组其他患者特征相似,但B组90%的患者有既往心绞痛,而A组仅33%。
在显示心大静脉血流逐渐减少的患者(A组)中未观察到成功溶栓挽救梗死心肌的情况。在这些患者中,微血管水平的心肌再灌注不足可能与更大面积的心肌梗死有关。既往心绞痛可能防止冠状动脉血流逐渐减少,并可能对梗死面积限制产生有益影响。