Patients with paroxysmal atrial fibrillation but not paroxysmal supraventricular tachycardia display evidence of platelet activation during arrhythmia.

It is well known that chronic atrial fibrillation (CAF) and paroxysmal atrial fibrillation (PAF) are associated with hypercoagulable state. However, pathological hemostatic changes during the paroxysmal supraventricular tachycardia (PSVT) have not yet been elucidated. To determine platelet activity in patients with PSVT, PAF and CAF, we examined the levels of beta-thromboglobulin (BTG) and platelet factor 4 (PF4) during tachyarrhythmia attacks. We measured the levels of BTG and PF4, as an index of platelet activation in 15 patients with PAF (9 men, mean age 45+/-11), and 14 patients with PSVT (8 men, mean age 40+/-10). Levels were compared to 22 age and sex matched healthy controls in sinus rhythm and with 25 patients with CAF (16 men, mean age 51+/-12). Blood samples were taken during arrhythmia and 24 hours after conversion to sinus rhythm. Patients taking medications or have clinical conditions that may affect the BTG and PF4 levels were excluded. In patients with PAF, BTG and PF4 levels were significantly higher than in controls (p<0.009, and p=0.002, respectively), and in patients with PSVT (p<0.004, and p=0.009, respectively), however, BTG and PF4 levels were significantly lower than CAF patients (p=0.002, and p=0.02, respectively). Moreover, BTG and PF4 levels were significantly decreased 24 hours after conversion to sinus rhythm (p<0.0001), and p=0.004, respectively). Although BTG and PF4 levels in patients with PSVT were significantly lower than in patients with PAF (p=0.04, and p=0.009, respectively) and CAF (p=0.0001, and p=0.0001, respectively), BTG and PF4 levels were similar to controls and did not change significantly after recovery to sinus rhythm (p=NS for all). These results indicate that there was no platelet activation in patients with PSVT during tachyarrhythmia but significantly increased platelet activity in PAF and CAF patients. There was a significant decrement of the platelet activity to a level of control subjects twenty-four hours after cardioversion of PAF.