Atrial platelet reactivity in patients with atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) is associated with an increased risk of thrombus formation in the left but not the right atrium. The mechanisms underlying this differential effect on the atria are unknown. OBJECTIVE: The purpose of this study was to examine whether atrial-specific differences in platelet activation are present in patients with AF. METHODS: Nineteen patients (13 men and 6 women; age 60 +/- 2 years) with AF undergoing ablation in sinus rhythm were studied. Blood samples from the left atrium, right atrium, and femoral vein were obtained at the start of the procedure and analyzed by whole-blood flow cytometry for expression of platelet P-selectin (CD62P), vitronectin receptor (CD51/61), and active glycoprotein IIb/IIIa receptor (PAC-1). Platelet aggregation was evaluated using adenosine diphosphate (ADP)-induced whole-blood impedance aggregometry. Seven patients with left-sided accessory pathway also were studies as a reference group for the effect of transseptal puncture on platelet reactivity. RESULTS: Platelet P-selectin levels were significantly elevated in the left atrium compared to the right atrium (10.2% +/- 2.5% vs 8.6% +/- 2.3%, P <.05). CD51/61 and PAC-1 levels did not differ between sampling sites. ADP-induced platelet aggregation was significantly higher in the left atrium compared to the right atrium and femoral vein (P <.05 for both). Platelet P-selectin levels and ADP-induced platelet aggregation did not differ between sampling site in the reference group. CONCLUSION: In patients with AF, left atrial platelet reactivity is increased compared to the right atria and peripheral circulation. The study data suggest that the presence of chamber-specific platelet activation may explain, in part, the propensity for left atrial thrombus formation in patients with AF.

Detrimental effects of energy drink consumption on platelet and endothelial function.

BACKGROUND: Energy drink consumption has been anecdotally linked with sudden cardiac death and, more recently, myocardial infarction. As myocardial infarction is strongly associated with both platelet and endothelial dysfunction, we tested the hypothesis that energy drink consumption alters platelet and endothelial function. METHODS: Fifty healthy volunteers (34 male, aged 22+/-2 years) participated in the study. Platelet aggregation and endothelial function were tested before, and 1 hour after, the consumption of 250 mL (1 can) of a sugar-free energy drink. Platelet function was assessed by adenosine diphosphate-induced (1 micromol/L) optical aggregometry in platelet-rich plasma. Endothelial function was assessed via changes in peripheral arterial tonometry and expressed as the reactive hyperemia index (RHI). RESULTS: Compared with baseline values, there was a significant increase in platelet aggregation following energy drink consumption, while no change was observed with control (13.7+/-3.7% vs 0.3+/-0.8% aggregation, respectively, P <.01). Similarly, RHI decreased following energy drink consumption (-0.33+/-0.13 vs 0.07+/-0.12 RHI [control], P <.05). Mean arterial pressure significantly increased following energy drink consumption, compared with control (P <.05). Heart rate was unaffected by energy drink consumption. CONCLUSION: Energy drink consumption acutely increases platelet aggregation and decreases endothelial function in healthy young adults.