Coronary Arterial Remodeling in Athersclerotic Disease: An Intravascular Ultrasonic Study in vivo

Background:Adaptive remodeling of the wall of diseased arterial segments occurs to compensate for the accumulation of atherosclerotic plaque. Histopathologic studies and intraoperative high-frequency epicardial coronary ultrasound imaging as well as intracoronary ultrasound imaging have shown that human coronary arteries enlarge in parallel with the formation of atherosclerotic plaque. Therefore, the lumen area is preserved until the progressive accumulation of plaque exceeds the compensatory mechanisms of the vessel. In 1995, however, Pastercamp et al. reported that arterial wall constriction (shrinkage) or inadequate enlargement may be a different mechanism associated with the development of severe arterial lumen narrowing in addition to plaque proliferation. The aim of this study is to examine what extent of de novo native coronary arterial stenosis is accompanied by compensatory enlargement and to find the predictors of inadequate remodeling with intravascualr ultrasound. Methods:Fifty eight patients were enrolled from February 1997 through October 1997. Patients who had the lesion of more than 50% stenosis of minimal luminal diameter in coronary angiography were indicated. The lesion which was located in the ostium or was very tortuous or angulated was excluded. The lesion which had the history of balloon angioplasty or stent insertion was also excluded. We used 20 MHz endosonic intravascular ultrasound catheter. We measured EEM area (External Elastic Membrane area), lumen area and plaque plus media area and analysed plaque characteristics. Results:1) Fifty-eight consecutive patients (43 men, 15 women;mean age 55.4 years, range 33 to 78)who had not undergone previous catheter intervention were studied with a single intravascular ultrasound system. 2) Among 58 patients, 20 patients (35%) had acute myocardial infarction, 30 patients (52%) unstable angina, 6 patients (10%) stable angina and 2 patients (3%) old myocardial infarction. Lesions were located at the left anterior descending arteries in 29 patients (50%), right coronary arteries in 21 patients (36%) and left circumflex coronary artery in 8 patients (14%). 3) Compensatory enlargement was observed in 19 (32%) of 58 lesions and inadequate compensatory enlargement in 39 (68%). 4) EEM and plaque areas at lesion site of compensatory enlargement group were significantly larger than those of inadequate enlargement group (p