https://doi.org/10.1007/s00392-025-02625-4
1Kerckhoff Klinik GmbH Abteilung für Kardiologie Bad Nauheim, Deutschland; 2Universitätsklinikum Gießen und Marburg GmbH Medizinische Klinik I - Kardiologie und Angiologie Gießen, Deutschland
Background: Recently, the first catheter-based orthotopic tricuspid valve replacement (ITVR) device became available. However, no standard recommendations currently exist regarding anticoagulation/antiplatelet therapy post-ITVR. Hyperattenuated leaflet thickening (HALT) or bioprosthetic valve thrombosis (PVT) can significantly impact prognosis following interventional valve replacement, presenting a challenge in clinical management. Various diagnostic protocols and treatment strategies combining anticoagulation and/or antiplatelet therapy have been described and limited data are available on incidence and managing HALT and PVT after this procedure.
Methods: Patients undergoing ITVR at the study center between March and October 2024 were included in a standardized diagnostic follow-up protocol, with echocardiography and computed tomography (CT) performed at four weeks and three months post-procedure to detect HALT/PVL. Patients with clinically significant HALT/PVT [defined by symptoms and an elevated transvalvular gradient (TVpmean)] received a standardized regimen, beginning with prolonged low-dose thrombolysis (rt-PA 25 mg over 25 hours), followed by anticoagulation with a vitamin K antagonist and aspirin.
Results: A total of 10 patients underwent ITVR for severe (n=4) or torrential (n=6) tricuspid regurgitation. Discharge echocardiograms performed one to three days post-ITVR showed a reduction of tricuspid regurgitation (TR) to grade 0 or 1 in all patients. The median TVpmean was 2.5 mmHg (IQR 2-3 mmHg). While no HALT/PVL was observed during the initial hospitalization, follow-up CT screening identified subclinical HALT in 7 patients (70%) with varying degrees of severity. Clinically significant PVT was detected in two patients at 4 and 6 weeks post-ITVR, respectively, accompanied by new-onset dyspnea (NYHA-class III) and an increase in TVpmean from 2 to 7 mmHg and 3 to 5 mmHg, respectively, between discharge and PVT detection. Both patients had been on consistent oral anticoagulation therapy post-ITVR. The thrombolysis-anticoagulation-antiplatelet regimen successfully resolved PVT in both cases.
Conclusion: HALT and PVT appear to be frequent occurrences after ITVR, likely exacerbated by low-flow conditions in the right heart cavities, with potentially significant clinical implications. A standardized screening and treatment protocol is essential to optimize complication management in this population.