Transcatheter aortic valve implantation (TAVI) has emerged as an important alternative to surgical aortic valve repair (SAVR) for patients with severe aortic stenosis. This rapidly advancing field has produced new-generation devices being delivered with small delivery sheaths, embolic protection devices and improved retrieval features. Despite efforts to reduce the rate of thrombotic complications associated with TAVI, valve thrombosis and cerebral ischaemic events post-TAVI continue to be a significant issue. However, the antithrombotic treatments utilised to prevent these dreaded complications are based on weak evidence and are associated with high rates of bleeding, which in itself is associated with adverse clinical outcomes. Recently, experimental data has shed light on the unique mechanisms, particularly the complex haemodynamic changes at sites of TAVI, that underpin the development of post-TAVI thrombosis. These new insights regarding the drivers of TAVI-associated thrombosis, coupled with the ongoing development of novel antithrombotics which do not cause bleeding, hold the potential to deliver newer, safer therapeutic paradigms to prevent post-TAVI thrombotic and bleeding complications. This review highlights the major challenge of post-TAVI thrombosis and bleeding, and the significant issues surrounding current antithrombotic approaches. Moreover, a detailed discussion regarding the mechanisms of post-TAVI thrombosis is provided, in addition to an appraisal of current antithrombotic guidelines, past and ongoing clinical trials, and how novel therapeutics offer the hope of optimizing antithrombotic strategies and ultimately improving patient outcomes.
164 Early haemodynamic changes and myocardial injury after transfemoral transcatheter aortic valve implantation (TAVI)