"Research shows that acute atrial fibrillation (AF) causes local activation of platelets and other prothrombotic markers in the heart within minutes of onset.
"This study provides a mechanism that may explain why such short episodes of AF predispose to stroke, especially in patients with underlying vascular disease," such as patient with diabetes and hypertension, Dr. Joseph G. Akar, from the division of cardiovascular medicine at Loyola University Medical Center, Maywood, Illinois, noted in an e-mail to Reuters Health.
The study findings, reported in the May 6th issue of the
Journal of the American College of Cardiology, "support the practice of anticoagulating patients with AF and stroke risk factors even if they are predominantly in sinus rhythm," Dr. Akar said.
In the study, 22 patients with a history of paroxysmal AF but who were in sinus rhythm at the beginning of the study underwent radiofrequency catheter ablation. AF was induced by burst atrial pacing in 14 patients, while eight control subjects underwent atrial pacing at 120 beats per minute.
The study team obtained blood samples simultaneously from the femoral vein and the coronary sinus during baseline sinus rhythm and after 15 minutes of pacing. They used enzyme-linked immunosorbent assays to measure markers of thrombin generation, inflammation and nitric oxide.
They found that local cardiac platelet activation (per cent P-selectin (+) platelets) increased significantly (p = 0.007), whereas systemic platelet activation did not change. Neither local nor systemic platelet activation changed in the control group.
Results of this, "the first study to examine the effect of a precisely known duration of acute AF on human platelet activation," Dr. Akar noted, "demonstrates that very brief episodes of AF can lead to local cardiac platelet activation."
The AF group also experienced increased local thrombin generation and decreased nitric oxide production, but no change in inflammatory markers.
"The results demonstrate how AF alone, independent of other risk factors, may contribute to the hypercoagulable state," the investigators write.
J Am Coll Cardiol 2008;51:1790-1793."
