Acquired Thrombocytopenia in Contemporary Transcatheter Aortic Valve Prosthesis

Abstract

Background: Postprocedural thrombocytopenia is a known phenomenon following transcatheter aortic valve implantations (TAVI). The aim of this study is to evaluate whether postinterventional platelet kinetics differ when comparing the current generation of balloon-expandable (BEV) and self-expanding valve prostheses (SEV). Methods: We performed a retrospective analysis of patients undergoing TAVI at our facility between 2017 and 2019. Patients were stratified according to the type of prosthesis used – BEV or SEV. Hematocrit-corrected platelet counts were calculated to account for dilution. Nadir platelet counts (lowest recorded platelet count), drop platelet counts (DPC – highest relative platelet drop from baseline) and severity of thrombocytopenia during the discourse and at discharge were assessed. Results: Of the 277 included patients, 212 received SEV and 65 BEV. BEV patients were younger (81.8 ± 4.4 years vs 79.7 ± 6.8 years, p=0.03). Further demographic characteristics were similar between groups. Implanted SEV were larger (p<0.001) and had shorter procedural times (p<0.01). There were no significant differences in postprocedural discourse. Postinterventional platelet drop was more pronounced in BEV patients in several evaluated metrics – mean DPC (24.3 ± 10.9% vs 18.8 ± 14.8%, p<0.01), patients with DPC>30% (n=19, 29.2% vs n=33, 15.6%, p=0.02) and also when comparing platelet kinetics. Conclusion: Despite improvements in outcome, the current generation of balloon-expandable TAVI prosthesis carry a predisposition for postprocedural thrombocytopenia even when the effects of dilution are accounted for.

Subclinical leaflet thrombus in patients with severe aortic stenosis and atrial fibrillation -ENRICH-AF TAVI study

“…2 . In particular, postprocedural thrombocytopenia is a well-known phenomenon following TAVI 18 , 19 . This condition can be attributed to several mechanisms, such as inflammation, drug toxicity (e.g., heparin, aspirin or other antiplatelet drugs, warfarin, and direct oral anticoagulants), mechanical damage caused by shear stress (e.g., in the event of a paravalvular leak), activation of the coagulation cascade, a decrease in platelet production and impaired platelet renewal 18 .…”