Management of hypoattenuated leaftlet thickening and bioprosthetic valve thrombosis following interventional tricuspid valve replacement

https://doi.org/10.1007/s00392-025-02625-4

Steffen Kriechbaum (Bad Nauheim)1, C. Unbehaun (Bad Nauheim)1, S. Knebelkamp (Bad Nauheim)1, M. Rademann (Bad Nauheim)1, A. Rieth (Bad Nauheim)1, M. Renker (Bad Nauheim)1, J.-M. Treiber (Bad Nauheim)1, J. S. Wolter (Bad Nauheim)1, S. J. Backhaus (Bad Nauheim)1, A. Rolf (Bad Nauheim)1, S. T. Sossalla (Gießen)2, T. Seidler (Bad Nauheim)1

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.
 
Diese Seite teilen