INCOMPLETE LYSIS OF THROMBUS IN THE MODERATE UNDERLYING ATHEROSCLEROTIC LESION DURING INTRACORONARY INFUSION OF STREPTOKINASE FOR ACUTE MYOCARDIAL-INFARCTION - QUANTITATIVE ANGIOGRAPHIC OBSERVATIONS
INCOMPLETE LYSIS OF THROMBUS IN THE MODERATE UNDERLYING ATHEROSCLEROTIC LESION DURING INTRACORONARY INFUSION OF STREPTOKINASE FOR ACUTE MYOCARDIAL-INFARCTION - QUANTITATIVE ANGIOGRAPHIC OBSERVATIONS
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DOI：
10.1161/01.cir.73.4.653
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发表时间：
1986-04-01
期刊：
影响因子：
37.8
通讯作者：
DODGE, HT
中科院分区：
文献类型：
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作者：
BROWN, BG;GALLERY, CA;DODGE, HT
对32例急性心肌梗死患者冠脉内应用链激酶溶栓60 ~ 90分钟，观察其冠脉再通情况。在高动脉造影放大率下观察该过程，并通过计算机辅助测量从重复的单平面视图进行量化。根据最小直径估计值，该应用方法的变异性为0.15至0.18 mm。在常规放大倍数下通常看不到的结构细节。再通的管腔似乎沿着血栓和血管壁之间的界面形成，逐渐将其最小动脉造影直径扩大到0.65 ± 0.05。0.24 mm（±）。1 SD），反映最终狭窄百分比为77 ± 0.1%。百分之十在9个梗塞病灶中发现专利5 .+-。3周后，再通管腔的最小直径平均改善了0.34 mm（p <0.005），狭窄率平均改善了13%（p <0.01）。 除了两个病例外，所有病例中阻塞血栓周围的造影剂薄膜模糊地界定了原始动脉粥样硬化管腔的边界。“原始狭窄”测量值为1.25 ±。0.32最小直径为56 . ±.首次可视化时狭窄14%;在链激酶输注过程中无变化。在5例导管插入患者中，10 .+-。在梗塞前12周，原始狭窄平均为1.15 ± 1.15。0.22梗塞前血管造影时为1.17 ± 0.01mm。0.23溶栓治疗期间，以模糊的形式存在的直径为1.5mm（p = NS）。在10例病例中，该原始病变小于50%狭窄，在21例病例中小于60%狭窄。这些测量允许的溶栓过程的客观评价，他们表明，轻度至中度动脉粥样硬化冠状动脉病变是急性血栓闭塞和冠状动脉内链激酶给药超过60至90分钟，只有部分溶解阻塞血栓。
Thrombolytic recanalization of the obstructed coronary lumen was studied in 32 patients receiving intracoronary streptokinase for 60 to 90 min during acute myocardial infarction. The process was viewed at high arteriographic magnification and was quantified with computer-assisted measurements from repeated single-plane views. The variability of the method for this application was 0.15 to 0.18 mm on minimum diameter estimates. Structural details were seen that are not commonly appreciated at conventional magnification. The recanalized lumen appears to form along an interface between the thrombus and the vessel wall, progressively enlarging its minimum arteriographic diameter to 0.65 .+-. 0.24 mm (.+-. 1 SD) at the end of the short-term infusion of streptokinase reflecting a final percent stenosis of 77 .+-. 10%. In nine infarct lesions found patent 5 .+-. 3 weeks later, the recanalized lumen further improved an average of 0.34 mm in minimum diameter (p < .005) and 13% stenosis (p < .01). A thin film of contrast medium surrounding the obstructing thrombus faintly defined the boundaries of the original atherosclerotic lumen in all but two cases. The "original stenosis" measured 1.25 .+-. 0.32 mm in minimum diameter and 56 .+-. 14% stenosis when first visualized; it was unchanged throughout the course of infusion of streptokinase. In five patients catheterized 10 .+-. 12 weeks before their infarction, the original stenosis averaged 1.15 .+-. 0.22 mm in the preinfarct angiogram, as compared with 1.17 .+-. 0.23 mm in its faintly defined form during thrombolytic therapy (p = NS). In 10 cases, this original lesion was less than a 50% stenosis, and in 21 cases less than 60%. These measurements permit an objective evaluation of the thrombolytic process; they demonstrate that mild-to-moderate atherosclerotic coronary lesions are subject to acute thrombotic occlusion and that intracoronary streptokinase administered over 60 to 90 min only partially lyses the obstructing thrombus.