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Updated: Jun 15, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Atrial platelet reactivity in patients with atrial fibrillation
Scott R Willoughby1, Ross L Roberts-Thomson, Han S Lim
1Cardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital, Adelaide, Australia.
Insights
In atrial fibrillation (AF), platelets show increased activation in the left atrium compared to the right. This chamber-specific platelet reactivity may explain the higher risk of left atrial thrombus formation in AF patients.
Area of Science:
- Cardiology
- Hematology
- Thrombosis Research
Background:
- Atrial fibrillation (AF) increases thrombus risk in the left atrium, but not the right.
- Mechanisms for this chamber-specific risk in AF remain unclear.
Purpose of the Study:
- To investigate potential atrial-specific differences in platelet activation in patients with AF.
- To determine if platelet reactivity varies between the left and right atria.
Main Methods:
- Whole-blood flow cytometry analyzed platelet markers (P-selectin, CD51/61, PAC-1) from left atrial, right atrial, and femoral vein samples.
- Adenosine diphosphate (ADP)-induced platelet aggregation was measured using impedance aggregometry.
- A reference group controlled for transseptal puncture effects.
Main Results:
- Left atrial platelet P-selectin levels were significantly higher than in the right atrium.
- Adenosine diphosphate (ADP)-induced platelet aggregation was significantly greater in the left atrium versus the right atrium and femoral vein.
- No significant differences in platelet markers or aggregation were observed in the reference group.
Conclusions:
- Platelet reactivity is elevated in the left atrium compared to the right atrium and peripheral circulation in AF patients.
- Chamber-specific platelet activation in the left atrium may contribute to thrombus formation.
- Findings suggest a mechanism for increased left atrial thrombosis in 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.
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