Effect of sinus rhythm restoration on platelet function in patients with lone atrial fibrillation

Abstract

Atrial fibrillation (AF) is associated with increased risk of thrombo- embolic complications. The aim of thestudywasto assessif arrhythmia, independent of other risk factors leads to increased platelet activation. The study involved 34 (mean age 50 +/� 9.03, range 21-59) male patients with lone persistent atrial fibrillation. The exclusion criteria were: age N60, coronary artery disease, left ventricular dysfunction (ejection fraction EF b 40%), congenital and acquired heart defects, artificial heart valve, diabetes, thyroid disease, inflammatory diseases, cancer, renal disease, and active smoking. The exclusion criteria precluded more than 95.4% of patients with AF hospitalized in our Department within the last 6 years. The AF patients underwent cardioversion to restore sinus rhythm and remained subsequently under observation for 1 month. Echocardi- ography, ECG and blood collection was performed before cardioversion (T0) and 4 weeks after successful cardioversion (T1). During the study period, patients were contacted and examined weekly along with 24-hour ECG monitoring. In all patients sinus rhythm was maintained at the end of the study period, however in 12 patients recurrence of AF was observed, confirmed by 24-hour ECG monitoring (atrial fibrillation recurrence group — AFR). In 10 patients the episodes of arrhythmia were asymp- tomatic, while only 2 patients complained of arrhythmia symptoms. In 22 patients no recurrence of AF in 24-hour ECG monitoring was observed (sinus rhythm group — SR). Parameters of resting platelets collected from peripheral blood activation was measured using flow cytometry. Platelet activation was assessed by expression of p-selectin (CD62) on platelets (CD61 positive cells). The platelet aggregate number was presented as a percentage of CD61+ blood elements bigger than platelets. The platelet derived microparticles (PDMPs) were assessed based on FSC histogram profile as CD61+ particles smaller than platelets. The leukocyte-platelet aggregates were detected based on coexpression of CD11b and CD62