Quinaprilat-eluting stents do not attenuate intimal thickening following stenting in porcine coronary arteries
Objective: Vascular injury increases angiotensin-converting enzyme (ACE) activity in the vessel wall, and experimental evidence suggests that high-dose oral ACE inhibition reduces intimal hyperplasia following balloon angioplasty. Local drug delivery can achieve high local concentrations which may be especially efficacious in inhibiting tissue growth following stent implantation. The aim of this study was to evaluate the angiographic and histomorphologic effects of quinaprilat-eluting stents in normal porcine coronary arteries. Methods: Ten pigs received phosphorylcholine-coated stents in each of the three major coronary arteries: one loaded with 780 μg quinaprilat, one with the solvent and one non-loaded control. Quantitative angiography was performed before and after stenting and at 4 weeks follow-up. At this time point the stented arteries were also analyzed using histology and morphometry. Results: Repeated measures ANOVA yielded significantly smaller angiographic lumen in both quinaprilat and solvent groups: 2.62 ± 0.31 and 2.65 ± 0.31 mm, respectively versus control: 2.70 ± 0.32 mm at follow-up, p < 0.05. Histology confirmed this finding with an increment in intimal area (2.5 ± 0.86 mm2) and thickness (0.57 ± 0.29 mm) in the quinaprilat group; versus solvent (1.98 ± 0.57 mm20.4 ± 0.26 mm) and controls (1.92 ± 0.50 mm2and 0.41 ± 0.18 mm). Conclusion: Quinaprilat-eluting stents do not attenuate neointimal thickening following implantation in normal porcine coronary arteries, but rather show a tendency towards the opposite.
|Keywords||ACE-inhibitor, Drug eluting stent, Experimental angioplasty, Restenosis|
|Persistent URL||dx.doi.org/10.1016/j.atherosclerosis.2008.11.029, hdl.handle.net/1765/24277|
van Beusekom, H.M.M, Ferrero, V, Ribichini, F, & van der Giessen, W.J. (2009). Quinaprilat-eluting stents do not attenuate intimal thickening following stenting in porcine coronary arteries. Atherosclerosis, 205(1), 120–125. doi:10.1016/j.atherosclerosis.2008.11.029