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Soluble E-selectin levels in acute human myocardial infarction
F Squadrito1, D Altavilla, M Ioculano
1Institute of Pharmacology, School of Medicine, University of Messina, Italy.
International Journal of Microcirculation, Clinical and Experimental
|March 1, 1995
Summary
Elevated soluble E-selectin levels indicate endothelial dysfunction in acute myocardial infarction patients. Treatment with urokinase reduced these markers, suggesting leukocyte adhesion plays a role in human heart attacks.
Area of Science:
- Cardiology
- Immunology
- Vascular Biology
Background:
- Leukocyte adhesion mechanisms are implicated in experimental myocardial infarction.
- E-selectin, a selectin family adhesion molecule, is involved in myocardial ischemia pathogenesis.
Purpose of the Study:
- To investigate circulating levels of soluble E-selectin as a marker of endothelial dysfunction in acute myocardial infarction.
- To assess the impact of thrombolytic therapy on soluble E-selectin levels.
Main Methods:
- Serum soluble E-selectin levels were measured in 60 subjects: 20 with acute myocardial infarction, 20 with angina pectoris, and 20 healthy controls.
- Patients with acute myocardial infarction received thrombolytic therapy with urokinase.
Main Results:
- Patients with acute myocardial infarction exhibited significantly higher serum soluble E-selectin levels (255 +/- 12 ng/ml) compared to angina pectoris patients (51 +/- 14 ng/ml) and controls.
- Thrombolytic therapy with urokinase reduced serum soluble E-selectin levels in acute myocardial infarction patients (71 +/- 19 ng/ml).
Conclusions:
- Circulating soluble E-selectin is elevated in acute myocardial infarction, serving as a marker for endothelial dysfunction.
- Adhesion mechanisms involving leukocyte-endothelium interactions are likely operative in human acute myocardial infarction.
- Thrombolytic therapy may modulate these adhesion mechanisms.