BACKGROUND: Thrombocytopenia after transcatheter aortic valve implantation (TAVI) has been evaluated in several studies, but the pathomechanisms behind this phenomenon are not well described. Here, we assess the influence of TAVI on hemostasis-related biomarkers and their potential role in post-TAVI thrombocytopenia. METHODS AND RESULTS: We assessed perioperative platelet counts in 307 patients undergoing transfemoral TAVI. Additionally, hemostasis-related biomarkers including thrombin-anti-thrombin complex (TAT), prothrombin activation fragment 1+2 (F1+2), plasmin-α₂-antiplasmin complex (PAP), and d-dimer were assessed in a subcohort of 35 patients. The course of these parameters was correlated with platelet counts and compared in patients with and without a relevant thrombocytopenia, i.e., a decline in platelet count of ≥50% compared to baseline. Levels of TAT (8.6±8.7μg/l), PAP (992±597μg/l), and d-dimer (1.43±1.66mg/l) were elevated above normal range before TAVI. TAT, F1+2, and d-dimer significantly increased after TAVI, and d-dimer as well as PAP remained elevated until day 7, indicating TAVI-induced increased thrombin formation associated with secondary fibrinolysis. Post-TAVI thrombocytopenia occurred in 17.9% of patients and was associated with a significantly higher incidence of post-TAVI complications, e.g. acute kidney injury and vascular complications. No impact of activated coagulation on thrombocytopenia was observed. CONCLUSIONS: TAVI induces an increase in hemostasis-related biomarkers, which persists until 1week after the procedure. The frequent finding of post-TAVI thrombocytopenia appears not to be linked to increased thrombin formation.
BACKGROUND:Thrombocytopenia after transcatheter aortic valve implantation (TAVI) has been evaluated in several studies, but the pathomechanisms behind this phenomenon are not well described. Here, we assess the influence of TAVI on hemostasis-related biomarkers and their potential role in post-TAVI thrombocytopenia. METHODS AND RESULTS: We assessed perioperative platelet counts in 307 patients undergoing transfemoral TAVI. Additionally, hemostasis-related biomarkers including thrombin-anti-thrombin complex (TAT), prothrombin activation fragment 1+2 (F1+2), plasmin-α₂-antiplasmin complex (PAP), and d-dimer were assessed in a subcohort of 35 patients. The course of these parameters was correlated with platelet counts and compared in patients with and without a relevant thrombocytopenia, i.e., a decline in platelet count of ≥50% compared to baseline. Levels of TAT (8.6±8.7μg/l), PAP (992±597μg/l), and d-dimer (1.43±1.66mg/l) were elevated above normal range before TAVI. TAT, F1+2, and d-dimer significantly increased after TAVI, and d-dimer as well as PAP remained elevated until day 7, indicating TAVI-induced increased thrombin formation associated with secondary fibrinolysis. Post-TAVI thrombocytopenia occurred in 17.9% of patients and was associated with a significantly higher incidence of post-TAVI complications, e.g. acute kidney injury and vascular complications. No impact of activated coagulation on thrombocytopenia was observed. CONCLUSIONS: TAVI induces an increase in hemostasis-related biomarkers, which persists until 1week after the procedure. The frequent finding of post-TAVI thrombocytopenia appears not to be linked to increased thrombin formation.