MYOCARDIAL-INFARCTION AND PERCENT ARTERIOGRAPHIC STENOSIS OF CULPRIT LESION - REPORT FROM THE PROGRAM ON THE SURGICAL CONTROL OF THE HYPERLIPIDEMIAS (POSCH)

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 (greater than or equal to 50% arteriographic stenosis) and hemodynamically significa nt (greater than or equal to 70% stenosis), or small (< 50% stenosis) and asymptomatic. Certain necropsy and arteriography studies support t he large progenitor lesion concept, and other arteriography studies su pport the small lesion hypothesis. We analyzed the coronary arteriogra m immediately preceding a Q wave (transmural) myocardial infarction fo r the degree of stenosis of the suspected culprit lesion, which was se lected 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 pat ients and the 27 intervention-group patients. For the two groups combi ned (n = 79), the predominantly involved segments were the middle righ t coronary artery and the proximal left anterior descending coronary a rtery. The time interval from the preceding coronary arteriogram close st to the index myocardial infarction ranged from 0 days to 10 years; however, 64.6% of the arteriograms were performed 2 years or less prio r to the myocardial infarction. Only 5.1% of the patients in both grou ps combined had a culprit lesion stenosis < 50%, while 88.6% of the pa tients in both groups combined had a culprit lesion stenosis greater t han or equal to 70%. The results strongly favor the large lesion hypot hesis of causation far myocardial infarction. It is premature, however , to state that the relative size of the culprit lesion has been indis putably determined. The resolution of this problem has exceedingly imp ortant practical implications for the management of patients with know n atherosclerotic coronary heart disease and for those asymptomatic in dividuals with silent atherosclerotic coronary heart disease. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.