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. 2025 Jun 27;6(9):1467–1470. doi: 10.1016/j.hroo.2025.06.014

Comparative thromboelastography with platelet mapping assessment of coagulation profiles in postablation vs nonablated patients with paroxysmal atrial fibrillation and peripheral artery disease: Implications for thrombotic risk

Isabella Ferlini Cieri 1,9, Adriana Araceli Rodriguez 1,9, Shiv Patel 1, Mounika Boya 1, Andrea Nurko 1, Qun Sha 2, Eric A Secemsky 3,4,5, Aneesh C Bapat 6,7, Theofanie Mela 8, Anahita Dua 1,∗
PMCID: PMC12635713  PMID: 41280523

Key Findings.

  • ▪

    Persistent platelet hyperreactivity after ablation: Catheter ablation for atrial fibrillation induced significant platelet hyperreactivity that persisted 2–3 months after the procedure, with adenosine diphosphate (ADP) aggregation nearly doubling (81.55% vs 36.75%, P = .02) compared with nonablated controls despite more intensive antiplatelet therapy in the ablated group.

  • ▪

    Enhanced clot strength despite anticoagulation: Maximum clot strength parameters were significantly elevated in postablation patients, with ADP maximum amplitude increasing by 90% (56.48 mm vs 29.68 mm, P = .03) and kaolin-heparinase maximum amplitude rising by 18% (64.36 mm vs 54.46 mm, P = .04).

  • ▪

    Thromboelastography with platelet mapping reveals hidden thrombotic risk: Thromboelastography with platelet mapping detected significant coagulation abnormalities in postablation patients that would be missed by conventional coagulation tests, suggesting a potential role for advanced hemostatic monitoring in personalizing postablation anticoagulation strategies.

  • ▪

    Extended vulnerable period: The prothrombotic state after catheter ablation extends well beyond the traditionally recognized acute phase, persisting for months and potentially explaining the temporal disconnect between ablation procedures and subsequent unexpected thrombotic events.

Despite catheter ablation’s established efficacy for atrial fibrillation (AF), recent reports of unexpected thrombotic events—including rare strokes with pulsed field ablation (PFA)—have raised critical questions about postprocedural coagulation dynamics.1 Current guidelines recommend standard anticoagulation protocols based primarily on clinical experience, yet specific hemostatic alterations after ablation remain poorly characterized. We hypothesized that ablation-induced myocardial injury creates a persistent prothrombotic state detectable by advanced coagulation testing.

Traditional coagulation monitoring fails to capture the complex interplay among ablation-induced inflammation, platelet activation, and thrombotic risk. Thromboelastography with platelet mapping (TEG-PM) offers unprecedented insight into whole blood hemostasis, providing real-time assessment of clot formation dynamics that conventional tests cannot detect.2 This new technology enables precise quantification of platelet function and contribution to overall clot strength, critical factors in postablation thrombotic risk.

A prospective observational study was conducted at Massachusetts General Hospital between March 2022 and June 2024. The study protocol was approved by the institutional review board (IRB 2022P002264), and all participants provided a written informed consent. The research was conducted in accordance with the Declaration of Helsinki and adhered to relevant ethical guidelines for human subjects research. From 105 patients with peripheral artery disease with cardiovascular comorbidities, we rigorously matched 10 patients with paroxysmal AF: 5 who underwent catheter ablation 30–90 days earlier vs 5 nonablated controls. Matching criteria included age (±5 years), gender, body mass index (±2 kg/m2), cardiovascular comorbidities, and anticoagulation regimens.

Blood samples underwent TEG-PM analysis using the TEG 6s hemostasis analyzer (Haemonetics Corporation, Boston, MA) within 2 hours of collection. We focused on adenosine diphosphate (ADP)-mediated platelet function—the primary target of standard antiplatelet therapy—measuring ADP inhibition percentage, ADP aggregation percentage, ADP maximum amplitude, and kaolin-heparinase maximum amplitude.

Our results revealed a remarkable hemostatic paradox. Despite 40% of ablated patients receiving dual antiplatelet therapy vs 0% of controls, ablated patients demonstrated profound platelet hyperreactivity persisting 2 to 3 months after the procedure. ADP inhibition was dramatically reduced in ablated patients (20.95% vs 61.85%, P = .03) (Figure 1A), whereas ADP aggregation nearly doubled (81.55% vs 36.75%, P = .02) (Figure 1B). Maximum clot strength parameters were significantly elevated: ADP maximum amplitude increased by 90% (56.48 mm vs 29.68 mm, P = .03) (Figure 1C), and kaolin-heparinase maximum amplitude increased by 18% (64.36 mm vs 54.46 mm, P = .04) (Figure 1D).

Figure 1.

Figure 1

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TEG-PM parameters in ablated vs nonablated patients with AF. A: Adenosine diphosphate (ADP) % inhibition shows significantly higher values in nonablated patients with AF than ablated patients (P < .05). This increased platelet inhibition in nonablated patients indicates a stronger suppression of platelet aggregation when exposed to ADP, suggesting that these patients may be in a more hypocoagulable state that could help prevent thrombotic events. B: ADP % aggregation displays significantly higher values in ablated patients with AF than nonablated patients (P < .05). This indicates that ablated patients maintain stronger platelet aggregation responses to ADP stimulation, suggesting that their platelets retain greater reactivity than nonablated patients. C: ADPMA shows significantly higher values in ablated patients with AF than nonablated patients (P < .05). This indicates that ablated patients exhibit greater clot strength from platelet contributions in response to ADP stimulation. D: HKHMA is significantly higher in ablated patients with AF than nonablated patients (P < .05). This indicates increased overall clot strength in ablated patients even after heparinase treatment, reflecting a more hypercoagulable profile. ADPMA = adenosine diphosphate maximum amplitude; AF = atrial fibrillation; HKHMA = kaolin-heparinase maximum amplitude; TEG-PM = thromboelastography with platelet mapping.

These findings align with an emerging understanding of ablation-induced pathophysiology. Catheter ablation creates controlled myocardial lesions that trigger sustained inflammatory cascades, elevating proinflammatory cytokines.3 This inflammatory milieu directly activates platelets while upregulating prothrombotic pathways. Thermal or minimally thermal electrical energy delivery also causes endothelial disruption and direct platelet activation through mechanical trauma. This prothrombotic state persists far longer than previously recognized, potentially explaining the temporal disconnect between ablation procedures and subsequent thrombotic events.

These findings challenge current anticoagulation paradigms by demonstrating that standard antiplatelet therapy may be insufficient to counteract ablation-induced platelet hyperreactivity, conventional coagulation monitoring provides false reassurance about thrombotic risk, and the vulnerable period after ablation extends well beyond the traditionally recognized acute phase. The enhanced ADP aggregation parallels landmark research in percutaneous coronary intervention, where high platelet reactivity independently predicts thrombotic events.4

Although our cohort included primarily radiofrequency and cryoballoon ablation, these findings gain particular relevance given recent concerns about PFA-associated complications. PFA’s unique mechanism may trigger distinct coagulation responses, including hemolysis-induced platelet activation.5 Our methodology provides a framework for systematically evaluating these emerging technologies’ hemostatic effects.

Study limitations include a small sample size and a cross-sectional design, preventing the assessment of temporal evolution. Future studies should include larger cohorts with longitudinal sampling, incorporating PFA patients and correlating TEG-PM findings with clinical outcomes. These findings suggest potential roles for TEG-PM in personalizing postablation anticoagulation strategies. Patients with AF demonstrating persistent platelet hyperreactivity might benefit from intensified antithrombotic therapy, whereas those with preserved platelet inhibition could undergo earlier therapy de-escalation.

Catheter ablation for AF induces persistent platelet hyperreactivity that overcomes standard antiplatelet therapy and persists months after the procedure. TEG-PM reveals hidden thrombotic risk invisible to conventional coagulation tests, potentially explaining unexpected postablation thrombotic events. These findings support incorporating advanced hemostatic assessment into postablation care protocols and developing personalized anticoagulation strategies based on individual coagulation profiles.

Conclusion

Catheter ablation for AF induces persistent platelet hyperreactivity that persists months after the procedure and overcomes standard antiplatelet therapy. TEG-PM reveals hidden thrombotic risk invisible to conventional coagulation tests, supporting the incorporation of advanced hemostatic assessment into postablation care protocols.

Disclosures

The authors have no conflicts of interest to disclose.

Acknowledgments

Funding Sources

This work was supported by the National Institutes of Health (R21 Federal Grant R1 AG077310).

Authorship

All authors attest they meet the current ICMJE criteria for authorship.

Patient Consent

All participants provided a written informed consent.

Ethics Statement

The study protocol was approved by the institutional review board (IRB 2022P002264). The research was conducted in accordance with the Declaration of Helsinki and adhered to relevant ethical guidelines for human subjects research.

References

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