Impaired forearm reactive hyperemia is related to late restenosis after coronary stenting

To investigate whether systemic endothelial function on forearm resistance vessels is related to angiographic restenosis after coronary stenting, 47 m en who underwent elective coronary stenting were divided into 2 groups acco rding to the presence (n = 20) or absence (n = 27) of in-stent restenosis 6 months after the procedure. Another 19 risk factor-matched men with normal coronary angiograms served as the control group. Forearm blood flow was as sessed by venous occlusive plethysmography. Basal forearm blood flow was si milar between restenosis, nonrestenosis, and control groups (2.63 +/- 0.19, 2.58 +/- 0.14, and 3.23 +/- 0.13 ml/100 mi forearm tissue per minute, resp ectively). In all 3 groups, forearm blood flow increased significantly duri ng reactive hyperemia (5.75 +/- 0.7, 11.32 +/- 1.23, and 14.52 +/- 1.36 ml/ 100 mi forearm tissue per minute, p <0.05, respectively) and remained uncha nged after sublingual administration of nitroglycerin. The percentage chang e of forearm blood flow during reactive hyperemia was significantly lower i n the restenosis group (117.3 +/- 18.3%) than in the nonrestenosis group (3 54.2 +/- 46.5%, p <0.01). This difference was still present after sublingua l nitroglycerin (37.6 +/- 21.2% vs 226.4 +/- 40.5%, p <0.01). In contrast, percentage change of hyperemic forearm blood flow was significantly lower i n patients with angina (117.5 +/- 49.5%) than in those without angina (290. 1 +/- 37.4%, p <0.05) at follow-up. In all patients, the angiographic loss index was correlated negatively to the percentage change of hyperemic forea rm blood flow (r = -0.33, p <0.01) and positively to the percentage change of forearm vascular resistance during reactive hyperemia (r = 0.33, p <0.01 ). In patients with angiographic restenosis after coronary stenting, forear m reactive hyperemia was more impaired compared with those without angiogra phic restenosis. Systemic endothelial dysfunction might be either a marker or one of the confounding factors in the development of late restenosis aft er coronary stenting. (C) 2000 by Excerpta Medica, Inc.