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Published on: March 5, 2020
Assessment of Platelet Response to Aspirin Therapy and Hemocompatibility-Related Adverse Events in HeartMate 3 Left
Hebe Al Asadi1, Theodor Abart1, Caroline Schwarz1
1Department of Cardiac Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Background: Patients with a HeartMate 3 (HM3) left ventricular assist device (LVAD) typically receive anticoagulation and antiplatelet therapy. The HM3 has shown a marked reduction in hemocompatibility-related adverse events (HRAEs) like stroke, bleeding, and pump thrombosis. This study evaluated whether aspirin (ASA) response influences HRAE incidence and if ASA sensitivity changes over time in HM3 recipients. Methods: This single-center, cross-sectional study included 32 HM3 patients (age: 59.0 ± 10.0 years, 15.6% female). ASA sensitivity was assessed twice using the VerifyNow assay, with ASA resistance defined by ASA reactivity units (ARU) > 550. The primary endpoint was HRAE incidence in ASA responders vs. non-responders over two consecutive follow-ups; the secondary endpoint was temporal changes in ASA resistance. Results: At the first follow-up, 13 (40.6%) patients were ASA-resistant, and 8 (28.6%) were resistant at the second follow-up, without significant change (p = 0.22). ASA non-responders and responders had similar ASA doses and baseline characteristics. No significant difference in HRAE incidence was found between ASA non-responders and responders (0.0% vs. 15.8%, p = 0.14), and no additional HRAEs occurred during follow-up. Conclusions: ASA resistance varied considerably among HM3 patients without significant temporal changes, and the demonstrated excellent hemocompatibility supports recent evidence that ASA may have a limited role in the antithrombotic regimen for HM3 recipients.
Background: Patients with a HeartMate 3 (HM3) left ventricular assist device (LVAD) typically receive anticoagulation and antiplatelet therapy. The HM3 has shown a marked reduction in hemocompatibility-related adverse events (HRAEs) like stroke, bleeding, and pump thrombosis. This study evaluated whether aspirin (ASA) response influences HRAE incidence and if ASA sensitivity changes over time in HM3 recipients. Methods: This single-center, cross-sectional study included 32 HM3 patients (age: 59.0 ± 10.0 years, 15.6% female). ASA sensitivity was assessed twice using the VerifyNow assay, with ASA resistance defined by ASA reactivity units (ARU) > 550. The primary endpoint was HRAE incidence in ASA responders vs. non-responders over two consecutive follow-ups; the secondary endpoint was temporal changes in ASA resistance. Results: At the first follow-up, 13 (40.6%) patients were ASA-resistant, and 8 (28.6%) were resistant at the second follow-up, without significant change (p = 0.22). ASA non-responders and responders had similar ASA doses and baseline characteristics. No significant difference in HRAE incidence was found between ASA non-responders and responders (0.0% vs. 15.8%, p = 0.14), and no additional HRAEs occurred during follow-up. Conclusions: ASA resistance varied considerably among HM3 patients without significant temporal changes, and the demonstrated excellent hemocompatibility supports recent evidence that ASA may have a limited role in the antithrombotic regimen for HM3 recipients.
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