LAUSR

Objective: The purpose of this study was to investigate the roles of the kallikrein‐kinin system and matrix metalloproteinases (MMPs) in the development of arterial restenosis attributable to intimal hyperplasia in the femoropopliteal arteries. Methods: This report describes a single‐center prospective study of 27 patients with peripheral artery disease who required percutaneous transluminal angioplasty and stenting of the femoropopliteal segment using covered stent grafts. The blood concentrations of total and kininogen fractions were evaluated using immunoenzymatic methods. Plasma kallikrein was evaluated by the colorimetric method. Tissue kallikrein was evaluated by the spectrophotometric method. The activity of kininase II was measured by fluorometric analysis. Quantification of MMPs was performed by zymography, and tissue inhibitors of metalloproteinases were measured by enzyme‐linked immunosorbent assay. Results: Four (15%) of the treated patients developed restenosis at the 6‐month follow‐up evaluation. These patients had significantly lower levels of high‐molecular‐weight kininogens (24 hours; P < .05) and low‐molecular‐weight kininogens (before, P < .05; 24 hours, P < .01; 6 months, P < .05) and lower levels of tissue inhibitor of metalloproteinases‐2 (6 months; P < .05) than the patients without restenosis. The activity levels of plasma and tissue kallikrein, kininase II, and MMPs did not differ significantly between the patients with and without restenosis. Conclusions: This study demonstrates an involvement of the kallikrein‐kinin system in in‐stent restenosis, although we could not confirm the participation of metalloproteinases in the restenosis process.