Objectives Macrophages play an important role in the pathogenesis of atherosclerosis. Captopril is one kind of the effictive drugs to the atherosclerosis besides statins. However, how does macrophage change in the therapeutic process of captopril has not been described in detail. The study was designed to investigate the effects of captopril (angiotensin converting enzyme inhibitor) on the development of atherosclerosis in rabbit model.
Methods Sixteen rabbits were fed with a high-cholesterol diet for 20 weeks. At week 4, all rabbits underwent ballom injury of the right common carotid artery. At week 12, 18F-fluorodeoxyglucose positron emissiontomography computed tomography (FDG-PET-CT) was performed in the right commoncarotid artery to detect macrophages and intravascular ultrasound (IVUS) was performed to evaluated the degree of plaque. Then all rabbits receives either placebo (n = 8) or 0.5 mg/kg/day of captopril (n = 8). And FDG-PET-CT and IVUS were repeatedly performed at week 20. At week 20, each 4 rabbits were sacrificed histologic evaluation.
Results At week 12 and 20, the FDG-PET-CT imaging detected an increase inaverage standardised uptake value in the placebo group (from 0.41 ± 0.12 and 0.59 ± 0.07, p = 0.05), indicating progressive inflammation, whereas not in the captopril-treated group (from 0.39 ± 0.13 to 0.35 ± 0.06, p = 0.56). Atweek 12 and 20, IVUS-derived volumetric parameters showed no significantdifferences between the two groups (all p > 0.05). The volumes of the twogroups were similar in histomorphology analysis. But the macrophage content wassignificant lower in captopril-treated group (p = 0.03).
Conclusions These results indicate that ACE-inhibitor has suppressed the degree of atherosclerotic inflammation but not modified the plaque size.