Von Willebrand factor activity predicts outcome after transcatheter edge-to-edge mitral valve repair

V. Bienert (Regensburg)1, M. Wester (Regensburg)2, F. Grewe (Regensburg)2, M. Haus (Regensburg)2, C. Schach (Regensburg)2, A. Luchner (Regensburg)3, C. Birner (Amberg)4, B. Unsöld (Gießen)5, L. S. Maier (Regensburg)2, M. Paulus (Regensburg)2, C. Meindl (Regensburg)2, K. Debl (Regensburg)2
1UKR Innere Medizin 2 Regensburg, Deutschland; 2Universitätsklinikum Regensburg Klinik und Poliklinik für Innere Med. II, Kardiologie Regensburg, Deutschland; 3Krankenhaus Barmherzige Brüder Regensburg Klinik für Kardiologie Regensburg, Deutschland; 4Klinikum St. Marien Klinik für Innere Medizin I Amberg, Deutschland; 5Universitätsklinikum Gießen und Marburg GmbH Medizinische Klinik I - Kardiologie und Angiologie Gießen, Deutschland
Von Willebrand factor activity predicts outcome after transcatheter edge-to-edge mitral valve repair
Background
Acquired von Willebrand syndrome (AvWS) is frequently associated with valvular heart disease due to shear-stress–induced degradation of high-molecular-weight multimers. While prior data demonstrated alterations in von Willebrand factor (vWF) parameters following transcatheter edge-to-edge mitral valve repair (M-TEER), their prognostic value regarding cardiovascular outcome remains unclear.
Methods and Results
We enrolled 254 consecutive patients undergoing M-TEER for symptomatic mitral regurgitation in a single-center observational study. vWF activity (vWF:Act) and vWF antigen (vWF:Ag) were measured before and four weeks after M-TEER. AvWS was defined as vWF:Act/vWF:Ag ratio <0.7. MR was of secondary etiology in 63.9% of the study population. MR reduction to grade II or less was achieved in 94.1% of patients. To assess clinical outcome, participants were followed up for a median of 12 months on the incidence of a combined endpoint of death or hospitalization for heart failure, which occurred in 30.3% of the study population. At baseline, AvWS was present in 13.4% of patients. Four weeks after M-TEER, vWF:Ag decreased from 222±93 to 214±89 IU/dL (p=0.019), while vWF:Act remained unchanged. In consequence, vWF:Act/vWF:Ag ratio increased from 0.83±0.14 to 0.86±0.15 (p=0.002). However, neither baseline vWF:Act/vWF:Ag ratio nor its improvement after M-TEER was associated with clinical outcome during follow-up. Instead, high baseline levels of vWF:Act emerged as a strong predictor of death or hospitalization for heart failure after the procedure, remaining independent from other clinical and echocardiographic risk factors in multivariate analysis (HR 1.65 [95% CI 1.22–2.24] per 100 IU/dL, p=0.001). Accordingly, patients with baseline vWF:Act ≥147 IU/dL had a remarkably increased risk for the occurrence of the combined endpoint during follow-up (log-rank HR 3.11, p<0.0001), driven both by mortality (HR 3.28, p=0.001) and heart failure hospitalization (HR 2.50, p=0.004). Furthermore, a trend towards increased risk of major bleeding was observed in these patients (HR 3.06, p=0.06).
Conclusions
vWF activity is a strong baseline predictor of death and hospitalization for heart failure after successful M-TEER and may be a useful prognostic biomarker for identifying patients at high risk for adverse outcomes.