Abstract
The various risk factors for peripheral arterial disease (PAD) are almost identical to those for atherosclerosis and include abnormal levels of lipids or lipoproteins. Lipid peroxidation parameters and total antioxidant capacity in the serum of male patients with PAD before surgery as well as 3–5 days and 7–10 days after surgery were measured. We also compared these parameters with those in a group of patients receiving simvastatin therapy. Concentrations of lipid hydroperoxides (LOOHs) and malondialdehyde, the total antioxidant capacity (assessed by ferric reducing antioxidant power assay), concentration of thiol (-SH) groups, and ceruloplasmin activity were determined spectrophotometrically in PAD patients treated surgically (Group I) or pharmacologically (Group II). The patients before surgical treatment had significantly higher concentrations of malondialdehyde but lower ceruloplasmin activity than those observed in Group II, treated with simvastatin. No significant differences before surgery in ferric reducing antioxidant power or thiol concentrations were found between the two groups. However, in Group I, both ferric reducing antioxidant power and thiol group concentrations decreased 3–5 days postoperatively, and ceruloplasmin activity increased 7–10 days after surgical treatment. The presented results demonstrate diverse oxidative stress responses to surgical treatment and confirm the beneficial effects of statin therapy in PAD.
Highlights
Peripheral arterial disease (PAD) commonly results from progressive narrowing of arteries in the lower extremities due to atherosclerosis [1]
The concentrations of total cholesterol and LDL cholesterol were found to be significantly higher in Group I before surgery than those in Group II on simvastatin therapy
A decrease was observed in ferric reducing antioxidant power (FRAP) level 3–5 days after surgery, and 7–10 days after surgery, it was significantly lower in comparison to the values before surgery and on simvastatin therapy
Summary
Peripheral arterial disease (PAD) commonly results from progressive narrowing of arteries in the lower extremities due to atherosclerosis [1]. It has become evident that PAD is an important predictor of substantial coronary and cerebral vascular risk [2, 3]. Several studies, using the anklebrachial index, have revealed that the presence of PAD, even when being asymptomatic and in patients with no history of other cardiovascular diseases, is a marker of greatly increased cardiovascular morbidity and mortality [7, 8]. Through the extra generation of reactive oxygen species (ROS), is involved in the development and progression of PAD [9]. Risk factors associated with PAD [10], similar to those for coronary heart disease [11], include high blood concentrations of total cholesterol and LDL-cholesterol. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, called statins, are well-known
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