Of Lipidlowering Drugs that may Benefit PAD Patients

Statins exert pleiotropic effects, which may be independent of LDL-C lowering. These effects may appear even before a change in lipid level occurs [26, 35].

Statins increase nitric oxide (NO) production and improve endothelial function (e.g. increased flow-mediated dilatation). They have antioxidant properties and they inhibit the migration of macrophages and smooth muscle cell proliferation, leading to an antiproliferative effect and the stabilization of atherosclerotic plaques. Statins have anti-inflammatory effects including a reduction in the circulating levels of CRP, inflammatory and proinflammatory cytokines [e.g. interleukin-6 (IL-6), IL-8], adhesion molecules [e.g. intercellular adhesion mol-ecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1)] and other acute phase proteins. They reduce tissue factor expression and platelet activity, whereas fi-brinolysis can be enhanced. Statins improve microalbu-minuria, renal function, hypertension and arterial wall stiffness. A significant reduction of the carotid and femoral intima-media thickness was also reported early after statin treatment.

In the GREACE trial, the effect [3, 4] of atorvastatin on serum creatinine and uric acid in patients with CHD was rapid and it was reversed equally rapidly if patients happened to discontinue atorvastatin. The fall in creati-nine was greater in both those with higher baseline serum levels of this indicator of the glomerular filtration rate and at the higher doses of atorvastatin. Simvastatin can also significantly reduce serum creatinine and serum uric acid (p < 0.0001) in patients with PAD treated for 3-4 months [38]. The difference in the creatinine levels was more pronounced in the tertile of patients with the highest baseline creatinine levels.

Statins can reduce circulating CRP levels [6, 20]. Other lipid-lowering drugs (e.g. ciprofibrate [33], fenofibrate [36] and ezetimibe [7, 34]) can also decrease circulating CRP levels. However, the potential relevance of lowering CRP levels to a greater or lesser extent remains unclear. Furthermore, recent evidence suggests that circulating CRP levels may only be a moderate predictor of CHD risk.

Patients with the metabolic syndrome have a clustering of many risk factors, such as hypertension, insulin resistance/type 2 diabetes mellitus, dyslipidaemia and obesity [11]. Therefore, it not surprising that these patients are at increased risk of developing PAD [15, 28]. The prevalence of the metabolic syndrome in PAD patients in a cross-sectional survey [15] was 58%.

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