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Calcium channel blocker (CCB) has been widely used in the administration of hypertension. It remains unclear whether CCB can improve the coronary artery remodeling in patients with coronary artery disease and hypertension.
We examined the influence of CCB on subsequent coronary artery remodeling in patients with hypertension.
IVUS examinations at baseline and 12-month were performed in 148 coronary lesions from 93 patients at baseline (CCB group=46; non-CCB group=47). Serial IVUS images from baseline and follow-up were analyzed side-by-side. External elastic membrane (EEM) area, lumen area, and plaque areas were measured at 1-mm intervals. 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 between the two groups.
Among CCB and non-CCB groups, there were no differences in age (57.1±10.7 vs. 55.3±7.6 yrs; P=0.247), statin treatment (P=0.085),insulin administration (P=0.863), beta blocker (P=0.180) and lipid profiles. Most of patients were discharged on statin, and the treatment was continued during 12-month follow-up. Lipid values significantly decreased from baseline to 12 months in both groups. Between CCB and non-CCB groups, there was no difference in baseline remodeling index (0.99±0.12 vs. 0.99±0.13; P=0.687) and in baseline plaque burden (64.1±9.9% vs.62.8±9.58; P=0.390). From baseline to follow up, no difference was noted in the changes of mean lumen areas (-0.29±1.0 vs. -0.41±1.1mm2;P=0.525), mean plaque area (-0.30±1.2 vs. -0.26±0.90mm2; P=0.805), and mean EEM areas (-0.59±1.57 vs. -0.69±1.41mm2; P=0.708). The change in EEM area for each 1 mm2 change in plaque area (i.e., the slope of the regression line) was similar between CCB group and non-CCB group (slopes = 0.97 vs. 0.99mm2, P= 0.473).
The current study has demonstrated that serial coronary remodeling is not related to the administration of CCB. Our results indicate that the vascular protective effects of CCB do not derived from the influence of CCB on vascular remodeling.