Restenosis after stenting of matched occluded and non-occluded coronary arteries. Should there be a difference?

Abstract

It is not known whether the higher restenosis rates reported after balloon angioplasty of occluded as opposed to non-occluded coronary arteries are still found after placement of coronary stents in lesions matched for factors known to affect late angiographic outcome. In a retrospective analysis of 1276 patients who had undergone coronary stent placement and in whom 6-month angiographic follow-up was available, we identified 144 patients with a total coronary occlusion which matched a non-occluded coronary lesion in another 144 patients. Matching lesion pairs were of the same type (de novo or restenotic), were supplied with the same type of stent, had reference vessel diameters identical within 0.3 mm and stented vessel segment lengths identical within 8 mm, and were located in corresponding target vessels. After stenting, statistically identical minimal lumen diameters had been achieved in both groups (occluded: 2.74+/-0.35 mm, non-occluded: 2. 77+/-0.32 mm, P = 0.45). At follow-up, minimal lumen diameters were not different (occluded: 1.65+/-0.77 mm, non-occluded: 1.76+/-0.76 mm, P = 0.24), reflecting an identical late lumen loss for occlusions (1.09+/-0.76 mm) and non-occluded lesions (1.01+/-0.70 mm, P = 0.38). Because of the significantly larger acute gain, the loss index was significantly lower for occluded vessels (0.40+/-0.27 vs 0. 51+/-0.35, P = 0.003). Corresponding restenosis rates were 33% (occluded) and 28% (non-occluded;P = 0.44). For stented vessel segment lengths >18 mm, restenosis rates were markedly higher (occluded: 42%, non-occluded: 36%) than for stented vessel segment lengths </=18 mm (occluded: 25%, non-occluded: 22%). In occluded and non-occluded coronary lesions matched for factors known to affect the angiographic outcome, no difference between the respective restenosis rates was observed within 6 months of coronary stenting. Thus, either type of coronary lesion appears to exhibit the same propensity for neointimal hyperplasia.