Buchwald H, Hunter D W, Tuna N, Williams S E, Boen J R, Hansen B J, Titus J L, Campos C T
Department of Surgery, University of Minnesota, St. Paul, USA.
Atherosclerosis. 1998 Jun;138(2):391-401. doi: 10.1016/s0021-9150(98)00049-5.
The objective of this study was to assess the percent stenosis of the culprit lesion responsible for subsequent myocardial infarction in the Program on the Surgical Control of the Hyperlipidemias (POSCH). It is unknown if the susceptible coronary artery culprit lesion responsible for an acute myocardial infarction is relatively large ( > or = 50% arteriographic stenosis) and hemodynamically significant ( > or = 70% stenosis), or small ( < 50%, stenosis) and asymptomatic. Certain necropsy and arteriography studies support the large progenitor lesion concept, and other arteriography studies support the small lesion hypothesis. We analyzed the coronary arteriogram immediately preceding a Q wave (transmural) myocardial infarction for the degree of stenosis of the suspected culprit lesion, which was selected by visual inspection of the coronary circulation supplying the electrocardiogram-defined area of myocardial infarction. There was no perceptible difference with respect to vessel segment distribution of culprit lesions or time to infarction between the 52 control-group patients and the 27 intervention-group patients. For the two groups combined (n=79), the predominantly involved segments were the middle right coronary artery and the proximal left anterior descending coronary artery. The time interval from the preceding coronary arteriogram closest to the index myocardial infarction ranged from 0 days to 10 years; however, 64.6% of the arteriograms were performed 2 years or less prior to the myocardial infarction. Only 5.1% of the patients in both groups combined had a culprit lesion stenosis < 50%, while 88.6% of the patients in both groups combined had a culprit lesion stenosis > or = 70%. The results strongly favor the large lesion hypothesis of causation for myocardial infarction. It is premature, however, to state that the relative size of the culprit lesion has been indisputably determined. The resolution of this problem has exceedingly important practical implications for the management of patients with known atherosclerotic coronary heart disease and for those asymptomatic individuals with silent atherosclerotic coronary heart disease.
本研究的目的是评估在高脂血症外科治疗计划（POSCH）中导致后续心肌梗死的罪犯病变的狭窄百分比。目前尚不清楚导致急性心肌梗死的易损冠状动脉罪犯病变是相对较大（血管造影狭窄≥50%）且具有血流动力学意义（狭窄≥70%），还是较小（狭窄<50%）且无症状。某些尸检和血管造影研究支持大的原发病变概念，而其他血管造影研究支持小病变假说。我们分析了Q波（透壁）心肌梗死前即刻的冠状动脉造影，以确定可疑罪犯病变的狭窄程度，该病变是通过目视检查供应心电图定义的心肌梗死区域的冠状动脉循环来选择的。52例对照组患者和27例干预组患者在罪犯病变的血管段分布或梗死时间方面没有明显差异。对于合并的两组（n = 79），主要受累节段是右冠状动脉中段和左冠状动脉前降支近端。距最接近索引心肌梗死的前一次冠状动脉造影的时间间隔为0天至10年；然而，64.6%的血管造影是在心肌梗死前2年或更短时间进行的。两组合并患者中只有5.1%的罪犯病变狭窄<50%，而两组合并患者中88.6%的罪犯病变狭窄≥70%。结果强烈支持心肌梗死病因的大病变假说。然而，断言罪犯病变的相对大小已被无可争议地确定还为时过早。解决这个问题对于已知动脉粥样硬化性冠心病患者和无症状的隐匿性动脉粥样硬化性冠心病患者的管理具有极其重要的实际意义。
