Acute onset atrial fibrillation induced by burst pacing significantly increased local cardiac platelet activation from 2.2% to 2.8% (p=0.007) within 15 minutes.
Does acute onset atrial fibrillation induce local cardiac platelet activation and endothelial dysfunction in patients with paroxysmal AF?
Acute onset atrial fibrillation causes local cardiac platelet activation and endothelial dysfunction within minutes, contributing to a hypercoagulable state independent of other risk factors.
p-value: p=0.007
OBJECTIVES: The purpose of this study was to determine whether acute onset atrial fibrillation (AF), independent of other risk factors, predisposes to an early prothrombotic state. BACKGROUND: Several risk factors predispose to the hypercoagulable state in human AF, but whether acute onset AF alone is prothrombotic remains unclear. METHODS: Patients with paroxysmal AF (n = 22) underwent radiofrequency catheter ablation. All patients presented in sinus rhythm. Baseline blood samples were obtained simultaneously from the femoral vein (systemic sample) and the coronary sinus (local cardiac sample). The AF was induced by burst atrial pacing in 14 patients (AF group). A control group (n = 8) underwent atrial pacing at 120 beats/min. Blood samples were recollected after 15 min. Platelet P-selectin expression (CD62) was measured using flow cytometry. Markers of thrombin generation (thrombin antithrombin complex, prothrombin fragment 1.2), inflammation (C-reactive protein, interleukin-6), and nitric oxide were measured using enzyme-linked immunosorbent assays. RESULTS: Neither local nor systemic platelet activation changed in the control group. In the AF group, local cardiac platelet activation (percent P-selectin + platelets) increased significantly (2.2 +/- 0.6% to 2.8 +/- 1.0%, p = 0.007); however, systemic platelet activation did not change. The AF group had increased local thrombin generation (thrombin antithrombin complex: 8.5 +/- 7.6 ng/ml to 33.2 +/- 17.4 ng/ml, p = 0.003; prothrombin fragment 1.2: 95.6 +/- 45.6 micromol/l to 243.8 +/- 120.1 micromol/l, p = 0.003), decreased nitric oxide production (25.2 +/- 10.8 micromol/l to 22.3 +/- 10.0 micromol/l, p < 0.02), and no change in inflammatory markers. CONCLUSIONS: Human AF causes local cardiac platelet activation within minutes of onset. The results demonstrate how AF alone, independent of other risk factors, may contribute to the hypercoagulable state.
Akar et al. (2008) studied Paroxysmal atrial fibrillation (n=22). Burst atrial pacing to induce atrial fibrillation vs. Atrial pacing at 120 beats/min was evaluated on Local cardiac platelet activation (percent P-selectin [+] platelets) (p=0.007). Acute onset atrial fibrillation induced by burst pacing significantly increased local cardiac platelet activation from 2.2% to 2.8% (p=0.007) within 15 minutes.
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