Does Aspirin Effectively Inhibit Platelet Activation During Left Ventricular Assist Device Support?

Purpose: To evaluate the efficacy of aspirin (ASA) in inhibiting ex vivo thrombin generation in patients with durable Left Ventricular Assist Device (LVAD) and to compare the thrombin generation profile of patients administered low (100mg/day) vs high (300mg/day) ASA dose. Methods: The Thrombin Generation Test was performed on a cohort patients implanted with LVAD who did not suffer any thrombotic event (n= 14). Thrombin generation was triggered by 0.5 pmol/L Tissue Factor in normal platelet poor plasma with the addition of the patients’ purified platelets, to account for the role played by platelets in mediating thrombin generation and to exclude any influence of anticoagulation therapy (Warfarin) on the test. Patients were on different ASA dose, according to the pump model: a) HeartMate II (Thoratec Corp., USA): 100mg/day (n= 3, 21%); b) HeartMate III (St. Jude Medical Inc., USA): 100mg/day (n= 4, 29%); c) Heartware HVAD (Heartware Corp., USA): 300mg/day (n= 7, 50%). In addition, one patient with HVAD who was not on ASA because of allergy was also profiled. Results were compared with those obtained from ASA-free volunteers (controls, n= 14). Results: Following a median time of LVAD support of 210 (IQR: 138-477) days, platelet-mediated thrombin generation was comparable in ASA-treated LVAD recipients and in controls (Fig. 1A,B). Notably, the patient not on ASA (491 days of support) showed higher thrombin generation as compared to the rest of the population (Fig. 1A,B). Comparison of low vs high ASA dose revealed no differences in terms of platelet-mediated thrombin generation (Fig. 1C). Conclusion: We report that ASA inhibits ex vivo platelet-mediated thrombin generation in LVAD recipients and may eventually mitigate the risk of thrombotic complications. The thrombin generation profile of ASA-treated LVAD patients was similar to controls. Moreover, we suggest that high dose ASA does not add any significant effect in blunting platelet activation and the associated thrombin generation pattern.