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European Heart Journal 2002 23(12):953-959; doi:10.1053/euhj.2001.3034
Copyright © 2002 by the European Society of Cardiology.
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Acute rise of circulating vascular endothelial growth factor-A in patients with coronary artery disease following cardiothoracic surgery

J.M. Cottona, A. Mathurb, Y. Hongb, A.S. Browna, J.F. Martinb and J.D. Erusalimskyb,f1

a Department of Cardiology, King's College, GKT School of Medicine and Dentistry, London, U.K.
b Centre for Cardiovascular Biology and Medicine, Department of Medicine, University College London, London, U.K.

revised September 18, 2001; accepted September 21, 2001

Abstract

Aims Vascular endothelial growth factor-A (VEGF-A) is an angiogenic and vasoprotective molecule whose expression is modulated by hypoxia and inflammatory mediators. Here we have tested the hypothesis that plasma levels of VEGF-A are influenced by pre-existing coronary artery disease and by changes in circulating interleukin-6 (IL-6).

Methods and Results Plasma VEGF-A and IL-6 were measured prior to and at various time intervals following surgery in individuals with angiographically normal coronary arteries requiring cardiac valve replacement (N group) and in patients with coronary artery disease and stable angina undergoing coronary artery bypass grafting (CAD group). Baseline VEGF-A levels were not significantly different in CAD (22·3±2·6pg.ml–1) compared to the N group (14·9±2·9pg.ml–1). Following cardiac surgery there was a significant rise of VEGF-A in CAD (P<0·0005 vs baseline), but not in the N group, reaching a maximum (~2 fold increase) after 24h. Surgery caused a rapid increase of plasma IL-6 in both groups, but the rise was significantly larger in CAD patients (P<0·0005 vs N) where it preceded the increase in VEGF-A. Furthermore, in patients with CAD there was a significant correlation between the change in VEGF-A and the change in IL-6 (P<0·04).

Conclusion These findings demonstrate that in patients with coronary artery disease cardiothoracic surgery leads to an acute rise in VEGF-A. We suggest that this rise may result from an interaction between the pre-existing atheromatous process and a systemic increase of inflammatory mediators.

Key Words: Atherosclerosis, cytokines, growth factors, cardiovascular surgery, human

f1 Correspondence: Dr Jorge D. Erusalimsky, Centre for Cardiovascular Biology and Medicine, Department of Medicine, University College London, The Rayne Institute, 5 University Street, London WC1E 6JJ, U.K.


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