Platelet activation in acute atrial fibrillation

MAYWOOD, ILLINOIS. It is not known whether atrial fibrillation as such results in a hypercoagulable state that could increase the risk of ischemic stroke. A group of cardiovascular researchers at Loyola University Medical Center now provides an intriguing insight into this question. Their study involved 22 patients with paroxysmal afib who were scheduled to undergo radiofrequency catheter ablation. The patients did not have left ventricular dysfunction, rheumatic valve disease, mitral valve prolapse, or any significant valvular regurgitation; however, about 30% had hypertension and about 14% had diabetes. The study participants were divided into two groups of 14 (Group A) and 8 patients (Group B) respectively. The only statistically significant difference between the two groups was a greater preponderance of men (93%) in Group A than in Group B (50%).

All patients were in sinus rhythm when the study began and had sheaths (tubes) inserted in the femoral veins and coronary sinus (via the right internal jugular vein) for collection of blood samples. Atrial fibrillation was induced for 15 minutes by burst pacing (330 bpm or a cycle length of 180 ms) in Group A resulting in a ventricular rate (heart beat) of 121 bpm. In Group B atrial pacing to achieve a ventricular rate at 120 bpm without going into afib was applied for 15 minutes. Analysis of blood samples taken at the coronary sinus in Group A revealed increased platelet activation and thrombin generation as well as reduced nitrogen oxide production when compared with Group B. The blood sample (systemic) taken from the femoral vein did not change with pacing indicating that the effect is localized to the heart – at least for the first 15 minutes.

The researchers conclude that their findings may help explain why short episodes of atrial fibrillation predispose to stroke, especially in patients with underlying vascular disease such as diabetes and hypertension.

Akar, JG, et al. Acute onset human atrial fibrillation is associated with local cardiac platelet activation and endothelial dysfunction. Journal of the American College of Cardiology, Vol. 51, May 6, 2008, pp. 1790-93

Editor’s comment: Obviously, the question is “Do these findings apply to lone afibbers without hypertension and diabetes?” Unfortunately, the researchers did not separate out the effects due to hypertensive/diabetic subjects vs. those with no stroke risk factors, so it is impossible to say and, in all fairness, the study population really was not large enough to allow such a separation. However, the results of this study would certainly support the supplementation with natural antiplatelet agents such as vitamins C, E, B3 and B6, and fish oils, some of which would also have an inhibitory effect on the formation of prothrombin. Nattokinase would not have any effect on platelet activation or prothrombin or thrombin formation, but would be effective in increasing fibrinolytic actively and thereby prevent blood clots from forming.