Prospective evaluation of hydroperoxide plasma levels and stable nitric oxide end products in patients subjected to angioplasty for coronary artery disease

Abstract Background: Oxidative stress appears to be involved in several processes that contribute to atherogenesis and restenosis following vascular intervention. Methods: The aim of our study was to evaluate prospectively the plasma concentrations of a hydroperoxide (ROOH) and nitric oxide end product (NO x ) in patients subjected to coronary angioplasty (PTCA) and routine control angiography 6 months after the initial procedure. We prospectively studied 48 consecutive patients (39 men, nine women, mean age 52 years) with stable angina who underwent successful elective angioplasty. A vascular segment was considered successfully treated when the residual luminal narrowing in the dilated segment immediately after angioplasty was 3 reductase. The Griess reagent was used for the measurement of NO 2 . Results: The overall angiographic restenosis rate was 35%. There were no significant differences in clinical variables between the patients with or without restenosis. The baseline levels (0.8±0.09 vs. 0.6±0.2 μmol/l) as well as the concentrations of authentic lipid hydroperoxide in plasma after 1 month (0.7±0.09 vs. 1.0±0.2 μmol/l) and 6 months (0.8±0.1 vs. 1.0±0.2 μmol/l) were similar in both groups. Three months after the angioplasty a significant increase in the ROOH level was noticed in the patients with restenosis (0.9±0.1 vs. 1.4±0.2, P =0.04). Plasma levels of NO x were similar in both groups at baseline (23.6±2.1 vs. 22.7±2.6 μmol/l) and 1 month after procedure (24.4±2.2 vs. 23.4±3.3 μmol/l). However, in patients with restenosis significant decreases in stable NO end products were observed 3 and 6 months after PTCA (18.1±1.5 vs. 13.3±1.7, P =0.04; 14.2±1.0 vs. 8.7±1.3, P =0.02, respectively). Conclusions: In patients with angiographic restenosis a significant increase in lipid peroxidation accompanied by a reduction in the stable end products of nitric oxide in plasma is observed several months after PTCA.