4.6 Article

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

Journal

JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
Volume 134, Issue 2, Pages 335-341

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/j.jtcvs.2006.12.064

Keywords

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Funding

  1. Medical Research Council [G0601215] Funding Source: Medline
  2. MRC [G0601215] Funding Source: UKRI
  3. Medical Research Council [G0601215] Funding Source: researchfish

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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-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.

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