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 (< or =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-alpha).
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 < .0001), body mass index (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 < .0001) was the only independent predictor of C-reactive protein.
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.