Thanyasiri Panuratn, Kathir Krishna, Celermajer David S, Adams Mark R
Department of Cardiology, Royal Prince Alfred Hospital, Missenden Rd, Camperdown 2050, Sydney, Australia.
Int J Cardiol. 2007 Jul 31;119(3):362-7. doi: 10.1016/j.ijcard.2006.08.015. Epub 2006 Nov 7.
Restenosis remains an important limitation of PCI. Although local factors such as small vessel diameter and systemic factors such as diabetes explain some of its incidence, it nevertheless also occurs in low-risk patients. We hypothesize that endothelial dysfunction may be an independent risk factor in some of these cases.
20 patients who had previously undergone PCI were studied at cardiac catheterization (10 with restenotic lesions were matched to 10 without restenosis). Infusion of multiple concentrations of acetylcholine (ACh) and nitroglycerine (GTN) were made via a 3F infusion catheter into the target artery. Following infusion, changes in diameter of segments proximal and distal to the PCI site were measured.
There was a significant impairment in endothelium-dependent dilatation at the maximal dose of acetylcholine in those with restenosis compared to those without restenosis, both proximal and distal to the stented area (proximal; 11.5+/-7.0% versus -20.9+/-9.0% p<0.001, distal; 12.0+/-3.1% versus -17.8+/-8.1% p<0.001), but there was no difference in the response to GTN. There was a significant correlation between the endothelium-dependent dilatation response and the percent restenosis (r=-0.65, p=0.003).
Coronary endothelium-dependent dilatation is reduced in subjects with restenosis in arterial segments separate from the stented lesion. This supports a hypothesis that endothelial dysfunction contributes to the development of restenosis, following percutaneous coronary intervention.
