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Angiotensin-converting enzyme inhibitors (ACEIs) have been extensively used in the treatment of coronary artery disease. They have various vascular protective effects, but the relevant mechanisms of action in these areas remain to be fully understood. We examined the influence of ACEI on subsequent vascular remodeling in response to changes in plaque size.
IVUS examinations were performed in 248 coronary lesions from 157 patients at baseline. Lesions were matched to the 12-month follow-up IVUS.Serial IVUS images from baseline and follow-up were analyzed side-by-side, and pullbacks were compared frame-by-frame to identify and match corresponding vessel segments. Identifiable anatomic structures were used as landmarks and included the carina of LAD and LCX, the ostium of RCA, stents, and large side branches. External elastic membrane (EEM), lumen, and plaque areas were measured at 1-mm intervals in each coronary target segment for each IVUS time point. Mean lumen, plaque, and EEM areas of lesions at each time point and changes from baseline to the 12-month follow-up evaluation were calculated. The change in EEM area for each 1 mm2 change in plaque area (i.e., the slope of the regression line) was calculated as a measure of vascular remodeling capacity. The extent of arterial remodeling was compared in plaque with and without ACEI.
The mean age was 57.0±8.9, 109 (69%) were male, 64 (41%) had diabetes mellitus, 80 (51%) had history of hyperlipidemia and 92 (59%) had hypertension. With regards to concomitant baseline medication,72 (46%) of patients were discharged on an ACEI and continued this treatment during the subsequent 12-month follow-up period. Lipid profiles improved on follow-up measurement, compared to baseline. In ACEI group, a slightly decrease in EEM (14.2± 4.7 vs. 13.7±4.8mm2; P=0.009), plaque (7.6±3.1 vs. 7.5± 3.1mm2; P=0.166), and lumen (6.6±2.4 vs. 6.3±2.4mm2; P=0.020)areas were observed during follow-up. The trend was the same in non-ACEI group, a slightly decrease in EEM (13.4± 4.5 vs. 13.0±4.5mm2; P=0.010), plaque (7.2±2.9 vs. 6.9±2.8mm2; P=0.001), and lumen (6.2±2.3 vs. 6.1±2.3mm2; P =0.425)areas were observed during follow-up. The change in EEM area for each 1 mm2 change in plaque area (i.e., the slope of the regression line) was greater for ACEI group compared to non-ACEI group but did not reach statistical significance (slopes = 1.15 vs. 1.12mm2, p = 0.147).
Serial IVUS examinations have demonstrates that serial coronary remodeling is not related to the administration of ACEI. The vascular protective effects of ACEI cannot be explained by the influence of ACEI on vascular remodeling.