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Clin. Cardiol. 24, 301–304 (2001)
Dimitris Tousoulis, M.D., Ph.D., FACC, Graham J. Davies, M.D., George Asimakopoulos, M.D., Homeyra Homaei, M.B., Emmanouil Zouridakis, M.D., Nabeel Ahmed, M.B., Juan Carlos Kaski, M.D., FACC
Cardiology Units, Hammersmith Hospital, Imperial College School of Medicine, and St George's Hospital Medical School, London, U.K.
Summary
Background: Plasma levels of soluble vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) mediators of leukocyte adhesion to vascular endothelium may implicate in the pathogenesis of the syndrome of chest pain with normal coronary arteries.
Hypothesis: We attempted to determine whether markers of endothelial activation are raised in patients with chest pain and normal coronary arteries.
Methods: We measured plasma VCAM-1, ICAM-1 (ng/ml) in 36 patients (34 men, 2 women, aged 62 ± 9 years) with stable angina, coronary artery disease (CAD), and a positive response to exercise test; in 21 patients (6 men, 15 women, aged 56 ± 9 years) with chest pain and normal coronary arteriograms (syndrome X); and in 11 healthy control subjects (8 men, 3 women, aged 49 ± 14 years).
Results: Plasma ICAM-1 levels were significantly higher both in patients with CAD (mean ± standard error of the mean) (328 ± 26, p<0.05), and in syndrome X (362 ± 22, p<0.01) than in controls (225 ± 29). VCAM-1 levels were also higher in syndrome X (656 ± 42 ng/ml) and in patients with CAD (626 ± 42 ng/ml) than in controls (551 ± 60, p = 0.09).
Conclusions: ICAM-1 and VCAM-1 levels are increased both in patients with CAD and with syndrome X compared with control individuals. These findings may suggest the presence of chronic inflammation with involvement of the endothelium in patients with anginal chest pain and normal coronary angiograms.
Key words: endothelium, coronary artery disease, adhesion molecules, syndrome X
Address for reprints:
Juan Carlos Kaski, M.D., FESC, FACC
Cardiology Unit
St George's Hospital Medical School
Cranmer Terrace
London SW 17 ORE, England
Received: November 29, 1999
Accepted: July 31, 2000