INFLUENCE OF CORONARY COLLATERAL VESSELS ON MYOCARDIAL INFARCT SIZE IN HUMANS - RESULTS OF PHASE-I THROMBOLYSIS IN MYOCARDIAL-INFARCTION (TIMI) TRIAL
INFLUENCE OF CORONARY COLLATERAL VESSELS ON MYOCARDIAL INFARCT SIZE IN HUMANS - RESULTS OF PHASE-I THROMBOLYSIS IN MYOCARDIAL-INFARCTION (TIMI) TRIAL
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DOI：
10.1161/01.cir.83.3.739
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发表时间：
1991-03-01
期刊：
影响因子：
37.8
通讯作者：
BOLLI, R
中科院分区：
文献类型：
--
作者：
HABIB, GB;HEIBIG, J;BOLLI, R
背景资料。冠脉侧支血管对人类梗死范围的影响仍然存在争议，部分原因是之前没有研究检查急性心肌梗死发病时存在的侧支血管对梗死范围的影响。本研究使用心肌梗死溶栓治疗(TIMI)I期试验的数据库，通过连续测量血清肌酸激酶(CK)来评估在心肌梗死演变的最初几个小时是否有血管造影记录的侧支的存在与心肌梗死的大小相关。为了避免再灌注对心肌梗塞大小的酶学估计的混淆影响，本报告仅限于125名在给予组织型纤溶酶原激活剂或链激酶剂后90分钟未能再通的患者。有侧支病变组(A组，n=51)血清CK峰值显著低于无侧支病变组(B组，n=74)，分别为1,877+/-216IU/L和2,661+/-212IU/L，P=0.004。类似地，A组CK来源的梗塞面积估计值显著低于B组(20.6±-2.5vs31.4+/-2.8CK克当量，p=0.001)。在有侧支的患者中，观察到的前壁和其他部位的梗塞面积较小；因此，络脉的有益作用与梗塞部位无关。在125例再通失败的患者中，65例在首次心导管置入术(溶栓治疗前)和出院时用对比心动图测定了左心室射血分数(LVEF)。在两项研究的患者中，A组的整体LVEF从治疗前到出院时呈上升趋势(从50.6+/-1.8%上升到53.4+/-1.8%，P=0.10)，而B组则下降(从50.3+/-1.8%下降到47.8+/-1.7%，P=0.02)。在出院时，冠脉侧支患者的整体左心室射血分数更大(53.5+/-1.7%比49.6+/-1.7%，p=0.01)。结果表明，在溶栓治疗不能诱导再通的患者中，心肌梗死发作时冠脉侧支血管的存在与心肌梗塞范围的限制有关，与出院时的左心室功能改善有关。
Background. The influence of coronary collateral vessels on infarct size in humans remains controversial, partly because no previous study has examined the impact of collaterals present at the onset of acute myocardial infarction on infarct size.Methods and Results. The present study used the data base of the Thrombolysis in Myocardial Infarction (TIMI) Phase I trial to correlate the presence or absence of angiographically documented collaterals in the initial hours of myocardial infarct evolution with the size of the infarct as assessed by serial measurements of serum creatine kinase (CK). To avoid the confounding effects of reperfusion on enzymatic estimates of infarct size, this report is limited to those 125 patients who failed to recanalize at 90 minutes after administration of tissue plasminogen activator or streptokinase. Patients with angiographically documented collaterals (group A, n = 51) had significantly lower values of peak serum CK than patients without collaterals (group B, n = 74) (1,877 +/- 216 versus 2,661 +/- 212 IU/l, respectively [mean +/- SEM], p = 0.004). Similarly, CK-derived infarct size estimates were significantly lower in group A than in group B (20.6 +/- 2.5 versus 31.4 +/- 2.8 CK gram equivalents, p = 0.001). The infarct size observed in patients with collaterals was less for anterior infarctions as well as for infarctions of other locations; thus, the beneficial effects of collaterals were independent of the site of the infarct. In 65 of the 125 patients who failed to reperfuse, left ventricular ejection fraction (LVEF) was assessed by contrast ventriculography both at initial cardiac catheterization (before thrombolytic therapy) and at hospital discharge. Among the patients who had both studies, global LVEF tended to increase from pretreatment to hospital discharge in group A (from 50.6 +/- 1.8% to 53.4 +/- 1.8%, p = 0.10) but decreased in group B patients (from 50.3 +/- 1.8% to 47.8 +/- 1.7%, p = 0.02). At hospital discharge, global LVEF was greater in patients with coronary collaterals (53.5 +/- 1.7% versus 49.6 +/- 1.7%, p = 0.01).Conclusions. The results demonstrate that, in patients in whom thrombolytic therapy fails to induce reperfusion, the presence of coronary collateral vessels at the onset of myocardial infarction is associated with limitation of infarct size as assessed enzymatically and with improved ventricular function on discharge as assessed by LVEF.