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European Journal of Heart Failure 1999 1(3):243-249; doi:10.1016/S1388-9842(99)00029-X
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© 1999 European Society of Cardiology

Increased soluble platelet / endothelial cellular adhesion molecule-1 and osteonectin levels in patients with severe congestive heart failure. Independence of disease etiology, and antecedent aspirin therapy

Victor L. Serebruanya,*, Selva R. Murugesana, Anitha Pothulaa, Dan Atarb, David R. Lowrya, Christopher M. O'Connorc and Paul A. Gurbela

a Sinai Hospital Baltimore, MD, USA
b University of Zurich Hospital Zurich, Switzerland
c Duke Clinical Research Institute Durham, NC, USA

* Corresponding author. Center for Thrombosis Research, Sinai Hospital of Baltimore, 2401 West Belvedere Avenue, Schapiro Research Building-R 202, Baltimore, MD 21215, USA. Tel.: +1-410-601-5266; fax: +1-410-601-9061. E-mail address: heartdrug{at}aol.com (V.L. Serebruany)


  Abstract

Background: Platelet–endothelial interactions modulated by adhesion molecules, may play an important role in the pathogenesis of congestive heart failure (CHF). Soluble levels of these molecules and platelet-derived substances are reportedly elevated in patients with CHF. However, no data are available on the plasma levels of Platelet / Endothelial Cell Adhesion Molecule-1 (PECAM-1), and platelet-derived osteonectin in this growing population.

Methods and Results: Soluble levels by ELISA were prospectively determined in patients with severe CHF (n = 37) and correlated to etiology and antecedent aspirin use, and compared with 14 healthy control subjects. Left ventricular dysfunction was attributed to idiopathic dilated cardiomyopathy in 18 and coronary artery disease in 19 patients. Twenty-one patients were aspirin-free and 16 patients were using aspirin (81–500 mg daily). Elevated soluble PECAM-1 (51.31 ± 2.44 ng/ml, P = 0.0001), and osteonectin (826.27 ± 22.37 ng/ml, P = 0.0001) were observed in patients with CHF, as compared to healthy controls (32.56 ± 1.21 ng/ml, and 478.02 ± 31.32 ng/ml, respectively). Neither etiology of CHF, nor antecedent aspirin therapy significantly affects the levels of PECAM-1 or osteonectin.

Conclusions: Despite long-term aspirin therapy and independently of the etiology of the disease, soluble PECAM-1 and osteonectin were elevated in the majority of patients with severe CHF, suggesting platelet–endothelial activation. The present data provide additional evidence that more potent anti-platelet and endothelial preservation regimens deserve further study in the heart failure population.

Key Words: PECAM- 1 • Osteonectin • Aspirin • Congestive heart failure

Accepted June 23, 1999


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