Increased activity of oxygen free radicals during reperfusion in patients with peripheral arterial disease undergoing percutaneous peripheral artery balloon angioplasty

Abstract

Modern balloon angioplasty plays an important role in the treatment of localised arterial lesions in patients with peripheral vascular disease (PVD). However, the process of angioplasty produces a situation of acute ischaemia followed by reperfusion and animal studies have shown such situation to be associated with an increase in free radical (FR) generation. FRs cause tissue damage and may be prothrombotic and may therefore contribute to the occurrence of restenosis. Release of FRs during reperfusion has not been fully investigated in humans. We studied the FR activity in 44 patients with PVD in the superficial or popliteal arteries receiving angioplasty treatmemt. Thirty patients had stenotic lesions and 14 had totally occlusive disease. Baseline blood samples were taken from the arterial catheter for the assay of malondialdehyde (MDA) (spectrophotometric thiobarbituric acid assay) immediately before and after balloon inflation. MDA is a measure of lipid peroxidation which is an indicator of FR activity. MDA levels during reperfusion were significantly higher than those immediately prior to balloon inflation {8.4 (0.29) vs 8.1 (0.24) μmol/l, respectively: mean increase-0.34 (0.13) μmol/l; [mean (sem)] p < 0.01 (paired Wilcoxon rank test) } in the stenotic lesions. Such changes were not observed in the totally occlusive lesions [7.26 (0.39) vs 7.26 (0.48) μmol/l, respectively; p = 0.75]. Our study has shown increased FR release following angioplasty in patients with stenotic, but not occlusive, peripheral vascular lesions. Angioplasty of the stenotic lesions creats a situation of acute ischaemia and reperfusion whereas that of the occlusive lesions leads to the reperfusion of a chronically ischaemic area. Thus, our study has confirmed previous animal studies of increased FR activity during reperfusion following acute ischaemia. Although the mechanism of this phenomenon is not clearly understood, it may be responsible for the development of restenosis and contribute to tissue damage during treatment with thrombolytic agents. Furthermore, the above situation may be used as a model to assess the effects of antioxidative agents.