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.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Serebruany, VL; Murugesan, SR; Pothula, A; Atar, D; Lowry, DR; O'Connor, CM; Gurbel, PA

Published Date

  • August 1999

Published In

Volume / Issue

  • 1 / 3

Start / End Page

  • 243 - 249

PubMed ID

  • 10935670

International Standard Serial Number (ISSN)

  • 1388-9842

Digital Object Identifier (DOI)

  • 10.1016/s1388-9842(99)00029-x


  • eng

Conference Location

  • England