Transcatheter Aortic Valve Implantation, Atrial Fibrillation, and Bleeding: A Surprisingly Fatal Attraction
- 18 October 2020
- journal article
- research article
- Published by Georg Thieme Verlag KG in Thrombosis and Haemostasis
- Vol. 120 (11), 1479-1482
- https://doi.org/10.1055/s-0040-1718533
Abstract
Bleeding Complications Drive In-Hospital Mortality of Patients with Atrial Fibrillation after Transcatheter Aortic Valve Replacement The treatment of severe aortic stenosis (AS) has been transformed by the advent and widespread adoption of transcatheter aortic valve implantation (TAVI). Initially indicated for the management of severe AS in patients considered an unacceptably high surgical risk, there is now growing evidence that TAVI has a role in the management of AS across a spectrum of patients ranging from low to high surgical risk.[1] [2] The clinical importance of AS is ever increasing with the aging of the population, since the prevalence of AS exponentially increases with age such that approximately 10% of the population aged 80 to 89 have AS.[3] This rapidly evolving field has already ushered in new improvements regarding the application of advanced imaging modalities for preprocedure planning, the development of new generation devices, in addition to greater operator experience.[4] These have led to improvements in TAVI safety and efficacy. Nevertheless, there remains an ongoing debate, and pressing clinical need, regarding the optimal antithrombotic strategy for patients undergoing TAVI given the Janus face of antithrombotic therapy helps prevent the high rates of ischemic stroke, yet endows a significant risk of bleeding complications.[5] Indeed, while the optimal antithrombotic strategy for patients undergoing TAVI remains to be defined, it is sobering that the 1 year incidence of stroke is approximately 8 to 10%, while the rate of bleeding approximates 30% at 5 years, with similar proportions of access site- and nonaccess site-related bleeding.[6] [7] [8] Current consensus guidelines (European Society of Cardiology and American College of Cardiology), recommend dual antiplatelet therapy (DAPT) with aspirin and clopidogrel for 3 to 6 months postprocedure, followed by long-term aspirin.[1] [9] However, the data supporting these recommendations remain limited, and are largely empiric, having been derived from recommendations for patients undergoing percutaneous coronary intervention (PCI). But notably, despite the larger extent of data available in the PCI population, the optimal antithrombotic strategy for elderly patients undergoing PCI similarly remains contentious given the elderly cohort represents a unique challenge given the association between advancing age and the heightened risk of both thrombosis and bleeding risk.[10] [11] [12] Pleasingly, this important knowledge gap has begun to be addressed with the just recently published POPular TAVI trial demonstrating that aspirin, compared with DAPT for 3 months, for patients undergoing TAVI was associated with a significant reduction in bleeding rates (all bleeding events over 1 year: aspirin 15.1%, aspirin + clopidogrel 26.6%, p = 0.001), without significant difference in the incidence of thromboembolic complications.[13] A critical aspect regarding antithrombotic therapy post-TAVI is the issue of patients with preexisting atrial fibrillation (AF). Indeed, up to 45% of high-risk patients undergoing TAVI have preexisting AF, and thus have a compelling indication for anticoagulation.[14] As such, defining the optimal antithrombotic strategy that threads the needle of antithrombotic efficacy and safety in the TAVI patient cohort with AF is fundamentally important. This represents a major challenge as risk prediction both for thromboembolic and bleeding events in patients with AF, independent of TAVI, remains a challenge.[15] [16] [17] In this context, the article in this issue by Lother et al sheds further light on the interplay between preexisting AF and outcomes in patients undergoing transfemoral TAVI (TF-TAVI).[18] Using extensive registry data from over 55,000 patients, the authors demonstrate that in patients with AF undergoing TF-TAVI, bleeding was the strongest predictor of in-hospital mortality after adjustment for EuroSCORE and age (odds ratio [OR] 18.00, 95% confidence interval [CI] 15.22–21.30, p < 0.001). These findings are particularly striking given these data demonstrated that while stroke was also associated with increased mortality (OR 3.35, 95% CI 2.61–4.30, p < 0.001), this risk was significantly outweighed by the adverse prognostic effects of bleeding. Moreover, it is noteworthy that this study highlights the adverse effects of preexisting AF on TF-TAVI outcomes with this patient group displaying a 1.35 increase of in-hospital mortality compared with patients without AF. While the data presented by Lother et al[18] should be interpreted with usual caveats associated with a retrospective analysis, the reported findings are consistent with previous data emphasizing the prognostic significance of TAVI-associated bleeding. Indeed, early (< 30 days) major bleeding complications occur in 10 to 15% of patients undergoing TAVI, and are associated with adverse cardiovascular outcomes and increased mortality.[19] Likewise, late bleeding complications are associated with a threefold increase in mortality.[20] Against this back drop, it is significant that several studies now implicate AF as an adverse prognostic factor for patients undergoing TAVI.[21] Although data regarding the specific antithrombotic therapy in the study by Lother et al was not available, it seems likely that more intense antithrombotic approaches incorporating anticoagulation in patients with AF is a central reason for the bleeding complications. However, whether AF, independent of antithrombotic regimen, confers an increased risk of bleeding in TAVI patients remains to be investigated. The association of AS and bleeding ([Fig. 1]) has been well appreciated for over 50 years since the initial description of the association of calcific AS and gastrointestinal bleeding by Dr. E.C. Heyde.[22] Indeed, Heyde's syndrome, as it became eponymously named, was later demonstrated to involve the intricate interplay between...Funding Information
- Department of Health, Australian Government
- National Health and Medical Research Council
- National Heart Foundation of Australia
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