학술논문

Plasma adenosine levels and platelet activation in patients with atrial fibrillation.
Document Type
Journal Article
Source
American Journal of Cardiology. 01/15/99, Vol. 83 Issue 2, p194-198. 5p. 2 Charts, 4 Graphs.
Subject
*ATRIAL fibrillation
*ADENOSINES
*BLOOD platelet activation
*ANTIGENS
*CELL receptors
*COMPARATIVE studies
*RESEARCH methodology
*MEDICAL cooperation
*RESEARCH
*THEOPHYLLINE
*EVALUATION research
*CASE-control method
*PHARMACODYNAMICS
Language
ISSN
0002-9149
Abstract
Platelet activation is observed in patients with atrial fibrillation (AF). P-selectin, which is expressed on platelet activation, plays an important role in the formation of thromboemobli. Because adenosine is known to attenuate platelet activation, we evaluated adenosine levels and 2 indicators of platelet activation, i.e., expression of P-selectin on platelets and plasma levels of beta-thromboglobulin, in 28 patients with AF (20 men and 8 women, age range 64+/-2 years) with sex- and age-matched (+/-2 years) subjects with sinus rhythm. The incidence of risk factors for stroke except for coronary heart disease and in echocardiographic parameters did not differ between the 2 groups. Plasma adenosine levels were lower (p <0.05) in patients with AF than in controls (mean [interquartile range] 13.4 [19.3-9.3] vs 19.1 [30.8-11.9] nmol/L). The expression of P-selectin on platelets (6.8% [13.6-3.4] vs 4.0% [8.8-1.8]) and plasma levels of beta-thromboglobulin were higher (p <0.05) in patients with AF. Flow cytometric analysis revealed that an antagonist of adenosine receptors, 8-sulfophenyltheophylline, increased the expression of P-selectin on platelets in a dose-dependent manner in the in vitro study. These results suggest that decreased plasma levels of adenosine were associated with platelet activation in patients with AF. Substitution of adenosine may provide a strategy for preventing platelet activation in these patients. [ABSTRACT FROM AUTHOR]