Key result
Continuing VKA during S-ICD implantation is linked to a ~23% absolute increase in pocket hematomas.
Why the study?
Little data exists regarding the optimal antithrombotic strategy during S-ICD implantation to prevent pocket hematomas.
Does continuation of antithrombotic therapy increase the risk of pocket hematoma in patients undergoing subcutaneous implantable cardioverter-defibrillator (S-ICD) implantation?
Observational (n=347)
No
Does continuation of antithrombotic therapy increase the risk of pocket hematoma in patients undergoing subcutaneous implantable cardioverter-defibrillator (S-ICD) implantation?
Continuation of vitamin K antagonists or dual antiplatelet therapy with ticagrelor during S-ICD implantation is associated with a significantly increased risk of pocket hematoma compared to interruption or clopidogrel use.
Answers are grounded in this paper and cite their sources.
May warrant interrupting VKA during S-ICD implantation; leaves open need for randomized confirmation.
BACKGROUND: Little data exists regarding the optimal antithrombotic strategy during S-ICD implantation to prevent pocket hematomas. This study explores the association between perioperative antithrombotic management and the occurrence of pocket hematoma following S-ICD implantation. METHODS: All patients who underwent de novo S-ICD implantation between February 2009 and January 2023 at Amsterdam UMC were included. Data was collected retrospectively from electronic patient records. Clinically significant pocket hematomas were defined as an accumulation of blood at the pocket site within 30 days after implantation. RESULTS: A total of 347 patients were included of which 224 (64.6%) patients used antithrombotic therapy pre-implantation. The median age at implantation was 50 years (IQR 36-61 years), 33.4% of the patients were female, and the majority of implants were intermuscular (90.2%). A total of 18 patients (5.2%) developed a clinically significant pocket hematoma. There were significantly more pocket hematomas in patients with continued vitamin K antagonists (VKA) compared to patients with interrupted VKA (27.3% (6/22) vs. 4.3% (2/47), respectively, p = 0.01), and continuation of VKA was an independent predictor for pocket hematoma formation in the VKA group (p = 0.04). Moreover, continuation of dual antiplatelet therapy (DAPT) with ticagrelor was associated with significantly more pocket hematomas post-implantation compared to continuation of DAPT with clopidogrel (4/12 vs. 1/28, respectively, p = 0.02). CONCLUSION: Continuation of VKA during S-ICD implantation was associated with an increased risk of pocket hematoma formation compared to interruption of VKA. This supports the need for specific perioperative antithrombotic therapy guidelines for S-ICD implantations to reduce the risk of pocket hematomas.
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Pepplinkhuizen et al. (2025) conducted an observational in High risk of ventricular arrhythmias requiring S-ICD implantation (n=347). Continuation of vitamin K antagonists (VKA) vs. Interruption of VKA was evaluated on Clinically significant pocket hematoma within 30 days after implantation (p=0.01). Continuation of vitamin K antagonists during S-ICD implantation was associated with a higher rate of pocket hematomas compared to interruption of VKA.
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