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Updated: Feb 1, 2026

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
Published on: February 26, 2013
Morphological determinators of platelet activation status in patients with atrial fibrillation
Jedrzej Kosiuk1, Tobias Uhe1, Clara Stegmann1
1Department of Electrophysiology, Heart Center Leipzig, Germany.
Insights
Platelet activation in atrial fibrillation (AF) patients is linked to left atrial appendage (LAA) volume. Larger LAA volumes and heart failure exacerbate platelet activation, increasing stroke risk.
Area of Science:
- Cardiology
- Hematology
- Thrombosis Research
Background:
- Platelet activation influences stroke risk in atrial fibrillation (AF).
- Factors affecting thrombocyte activation in AF patients remain understudied.
Purpose of the Study:
- To investigate the relationship between cardiac anatomy and platelet activation in AF patients.
- To identify determinants of platelet activation status in individuals with AF.
Main Methods:
- 83 AF patients undergoing catheter ablation provided blood samples from the left atrium.
- Platelet activation assessed via flow cytometry (P-selectin expression, microparticles, aggregates) and light transmission aggregometry (LTA).
- Cardiac anatomy evaluated using echocardiography and MRI, focusing on left atrial appendage (LAA) volume and morphology.
Main Results:
- Left atrial appendage (LAA) volume correlated with increased platelet pre-activation and reduced response to TRAP-6 stimulation.
- Larger LAA volume was associated with diminished platelet response in LTA.
- Heart failure also correlated with a reduced platelet response to TRAP-6 stimulation.
Conclusions:
- Left atrial appendage (LAA) volume is a significant correlate of platelet activation status in AF patients.
- The pro-thrombotic effect of LAA volume on platelet activation is amplified in patients with co-existing heart failure.
Background:
Stage of platelet activation is an important modulator of stroke risk associated with atrial fibrillation (AF). However, factors determining such activation status of thrombocytes in patients with AF are still not well studied.
Methods And Results:
We enrolled 83 patients (mean age 61 ± 10 years, 61% male, mean CHA2DS2-VASc 2.1 ± 1.4) with paroxysmal (75%) or persistent (25%) AF admitted for catheter ablation. Blood samples were collected directly from the left atrium (LA) and platelet activation status was measured by means of flow cytometric assessment in whole blood and light transmission aggregometry (LTA) in unstimulated and Thrombin-receptor-activated-peptide-6 (TRAP-6)-stimulated platelet rich plasma. In flow cytometry, we measured fractions of platelet microparticles and aggregates as well as P-selectin expression on platelets' surfaces. LTA findings are expressed as maximal aggregation (MA), primary slope (PS) and area under curve (AUC). Cardiac anatomy has been assessed by means of echocardiography and magnetic resonance imaging. Left atrial appendage (LAA) volume, but not LAA morphology nor morphological and functional parameters describing LA, was significantly correlated with increased pre-activation of platelets (R = 0.224, p = 0.043) and consecutive reduced response to TRAP-6 (R = 0.231, p = 0.037) measured by P-selectin expression in flow cytometry. Similarly, a reduced response to TRAP-6 in patients with larger LAA volume (PS: R = -0.240; p = 0.042; AUC: R = -0.244; p = 0.035; MA: R = -0.270; p = 0.019) as well as with heart failure (PS 54.75 vs 71.45, p = 0.026) was observed in LTA.
Conclusion:
In patients with AF, LAA volume correlates with extent of platelet activation status, this effect is aggravated in patients with heart failure.
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