The association between saphenous vein endothelial function, systemic inflammation, and statin therapy in patients undergoing coronary artery bypass surgery

2007 
Objectives Endothelial dysfunction and C-reactive protein play a pivotal role in development of atherosclerosis and act as markers for future adverse cardiac events. Statins reduce C-reactive protein levels and improve endothelial function. However, little information is available on endothelial function and its determinants in veins. We investigated the association between saphenous vein endothelial function and C-reactive protein levels in patients treated with statins undergoing coronary artery bypass surgery. Methods Seventy-six patients with optimal low-density lipoprotein cholesterol levels (≤1.6 mmol/L) secondary to regular treatment with a minimum of simvastatin 40 mg were recruited. Each subject underwent detailed characterization according to anthropomorphic data, saphenous vein endothelial function (assessed ex vivo by measuring acetylcholine-induced relaxation of venous rings), and markers of systemic inflammation (C-reactive protein and tumor necrosis factor-α). Results Despite regular treatment with statins, 26% of patients had C-reactive protein levels in the "high-risk" range (>3.0 mg/L). There was a negative linear correlation between acetylcholine-induced venous relaxation and C-reactive protein ( r = −.30, P = .02) and waist circumference ( r = −0.21, P = .03). In a multivariate regression model, C-reactive protein ( P = .02) was the only independent predictor of acetylcholine-induced venous relaxation. In turn, correlates of C-reactive protein were assessed. There was a correlation between C-reactive protein and coronary atherosclerotic burden ( r = .46, P r = .26, P = .03), fasting glucose levels ( r = .31, P = .01), and waist circumference ( r = .29, P = .01). Using multivariate analysis, coronary atherosclerotic burden ( P Conclusions In our cohort of patients with coronary artery disease, C-reactive protein level was the only independent predictor of saphenous vein endothelial function. In turn, its levels were independently influenced by the extent of coronary atherosclerotic burden.
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