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Aziz Momin
Lindsay C. John
Michael T. Marrinan
Jatin B. Desai
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J Thorac Cardiovasc Surg 2007;134:335-341
© 2007 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

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

Aziz Momin, MBBS, MRCSa,*, Narbeh Melikian, BSc, MBBS, MRCPa,*, Stephen B. Wheatcroft, PhD, MB, BCh, MRCPb, David Grieve, PhDa, Lindsay C. John, MD, FRCSc, Ahmad El Gamel, MD, FRCSc, Michael T. Marrinan, MD, FRCSc, Jatin B. Desai, MD, FRCSc, Catherine Driver, BScd, Roy Sherwood, PhD, FRCPathd, Ajay M. Shah, MD, FRCP, FMedScia, Mark T. Kearney, MD, MRCPb,*

a Cardiovascular Division, King’s College London School of Medicine at Guy’s, King’s College and St Thomas’ Hospitals, London, United Kingdom
b Leeds Institute for Genetics Health and Therapeutics, University of Leeds, Leeds, United Kingdom
c Department of Cardiothoracic Surgery, King’s College Hospital, London, United Kingdom
d Department of Clinical Biochemistry, King’s College Hospital, London, United Kingdom.

Received for publication July 18, 2006; revisions received November 30, 2006; * Address for reprints: Professor Mark Kearney, Leeds Institute for Genetics Health and Therapeutics, The LIGHT Laboratories, University of Leeds, Clarendon Way, Leeds LS1 3EX, United Kingdom. (Email: m.t.kearney{at}leeds.ac.uk).

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.

Abbreviations and Acronyms ACE = angiotensin-converting enzyme; ACh = acetylcholine; BMI = body mass index; CABG = coronary artery bypass graft; CAD = coronary artery disease; CRP = C-reactive protein; HDL = high-density lipoprotein; LDL = low-density lipoprotein; L-NMMA = NG monomethyl-L-arginine; NO = nitric oxide; QCA = quantitative coronary angiography; SNP = sodium nitroprusside; TNF{alpha} = tumor necrosis factor-{alpha}


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