Key result
Tachypacing-induced AF without atrial myopathy increases LA prothrombotic biomarkers in a duration-dependent manner.
Why the study?
Whether lone AF without underlying atrial myopathy directly exerts a thrombogenic effect is not well studied.
Does high-rate atrial tachypacing induced AF increase atrial thrombotic biomarkers in a healthy porcine model?
Does high-rate atrial tachypacing induced AF increase atrial thrombotic biomarkers in a healthy porcine model?
High-rate atrial tachypacing induced AF leads to significant prothrombotic activation in the left atrium of healthy pigs, suggesting lone AF itself has a thrombogenic effect independent of underlying atrial myopathy.
Lone AF may be intrinsically thrombogenic; leaves open translation from this porcine model to human stroke risk.
Background/Introduction Atrial fibrillation (AF) is known to significantly increase thrombo-embolic risk, including the risk of stroke. In recent years, it has been suggested that this risk is mainly driven by the underlying atrial myopathy rather than the active presence of the arrhythmia itself. The thrombogenic effect of lone AF (without underlying atrial myopathy) is not well studied. Purpose The present experimental study aims to assess the effect of short periods of high-rate atrial activation and subsequent AF on atrial thrombotic risk in otherwise healthy pigs. Methods A total of 26 Piétrain pigs underwent high-rate atrial tachypacing to induce paroxysmal AF (consisting of burst pacings of 50 Hz during 15 seconds with intervals of 10 seconds after AF termination, for a total of 15 minutes) using a decapolar catheter introduced into the right atrium through a femoral sheath. We used an equal number of healthy male and female pigs of sixteen weeks old with an average weight of 40 kg (n = 20). Some of the pigs (n = 6) were followed for 4 weeks and underwent another atrial tachypacing session (60 minutes). Blood samples before and after each pacing session were drawn directly from the left atrium with a 21G needle, for which all pigs received a sternotomy at the beginning of the experiment. To explore thrombotic pathway activation, we measured platelet indices, platelet aggregation (by using the VerifyNow platelet function test), intrinsic, extrinsic, and common coagulation pathways, as well as fibrinolysis. Results The mean cumulative AF duration after high rate atrial tachypacing was 82 ± 94 seconds in the short pacing group and 300 ± 379 seconds in the long pacing group. The effect on atrial thrombotic biomarkers is shown in Table 1. There was a significant increase in haemoglobin, as well as a significant decrease in leukocytes. Prothrombin time (PT) significantly decreased and fibrinogen and D-dimers significantly increased after tachypacing, indicating an increase in the local thrombotic environment. Most of the differences appear to be more pronounced after the long tachypacing sessions (Table 2). No differences were observed between female and male pigs. Conclusion Our data suggest high-rate atrial tachypacing induced AF, without underlying atrial myopathy, leads to a significant prothrombotic activation of the left atrium in a duration-dependent way.
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Laer et al. (2025) studied Atrial fibrillation (n=26). High-rate atrial tachypacing vs. Baseline (before pacing) was evaluated on Atrial thrombotic biomarkers (platelet indices, platelet aggregation, coagulation pathways, fibrinolysis). High-rate atrial tachypacing induced AF (mean duration 82±94s in short pacing, 300±379s in long pacing) led to significant prothrombotic activation of the left atrium in a duration-dependent way.
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