MORPHOLOGICAL AND QUANTITATIVE ANGIOGRAPHIC ANALYSES OF PROGRESSION OF CORONARY STENOSES - A COMPARISON OF Q-WAVE AND NON-Q-WAVE MYOCARDIAL-INFARCTION

Background The purpose of this study was to determine differences in c oronary stenosis severity and morphology and time course of progressio n between Q-wave and non-Q-wave myocardial infarction (MI). Methods an d Results We studied 32 patients with new Q-wave MI and 38 patients wi th new non-Q-wave MI who underwent coronary angiography both before an d after MI without interval revascularization procedures. Quantitative coronary angiographic analysis was performed by the caliper method, a nd morphological analysis of coronary angiograms was obtained before a nd soon after acute MI. Before infarction, the stenosis severity at th e site of future MI was worse in Q-wave (44+/-25%) versus non-Q-wave ( 23+/-35%) MI patients (P<.01). Eccentric and irregular plaques were mo re common in Q-wave MI patients (18 of 32, 56%, versus 5 of 38, 13%; P <.001). Non-Q-wave MI patients were more frequently found to have sign ificant collaterals after MI compared with Q-wave MI patients (18 of 3 8, 47%, versus 1 of 32, 3%; P<.001) despite no difference in post-MI s tenosis severity. Analysis according to time interval after pre-MI ang iography showed that 9 of 11 patients (82%) with Q-wave MI <18 months later had a stenosis of greater than or equal to 50% versus 7 of 21 (3 3%) with an interval >18 months (P<.05). By comparison, non-Q-wave MI patients tended to fall into two categories regardless of time of prog ression: Either minimal or no stenosis (<20%) or else a severe stenosi s (>70%) was typically present. Conclusions The atheromatous plaque su bstrate is different in Q-wave and non-Q-wave MI. Non-Q-wave MI occurs typically at a site shown by pre-MI angiography to involve either min imal luminal narrowing or a severe stenosis before MI, which is usuall y nonulcerated. By comparison, Q-wave MI follows a moderate stenosis i n which the plaque is eccentric and ulcerated. Such differences culmin ate in differences in thrombus lability and collateral development and consequently in different clinical profiles.