The one-year bleeding risk for patients with atrial fibrillation (AF) who undergo transcatheter aortic valve implantation (TAVI) is the same whether they are receiving vitamin K antagonist therapy or a non-vitamin K antagonist (NOAC). However, the risk of all-cause mortality, myocardial infarction, or any cerebrovascular event is higher with NOAC use, a registry study, published in JACC: Cardiovascular Interventions has found, although the researchers admit that the statistical significance of this increased risk is “borderline”.
David Jochheim (Ludwig-Maximilians University, Munich, Germany) et al note that the “higher ischaemic event rate observed with NOACs needs to be evaluated in large randomised trials”.
They say that, although NOACs are superior to vitamin K antagonists (VKAs) in nonvalvular atrial fibrillation (AF), the “comparative performance among patients in need of OAC [oral anticoagulation] undergoing TAVI is underinvestigated”. The study aimed to assess the impact of the type of oral anticoagulant on clinical outcomes one year after TAVI.
Jochheim et al enrolled 962 consecutive patients who underwent TAVI in four tertiary centres in Europe and who were discharged on either NOACs (326) or VKAs (636). Of the patients on NOAC therapy, 54% received rivaroxaban and 39% were taking apixaban. In order to compare the two therapy groups, potential confounders were adjusted for using propensity scores for inverse probability of treatment weighting (IPTW).
The mean age of participants was 81.3±6.3 years, and 52.5% of the study population were women. The mean Society of Thoracic Surgeons (STS) score was 4.5% (interquartile range [IQR] 3–7.3%), and 62.7% of patients received a balloon-expandable valve.
The primary outcome was a combined incidence of all-cause mortality, myocardial infarction, and any cerebrovascular event at one-year after TAVR, and was 21.2% with NOACs versus 15% for patients treated with VKAs (hazard ratio [HR] 1.44, 95% confidence interval [CI] 1–2.07, p=0.05, IPTW-adjusted). The one-year incidence of any Bleeding Academic Research Consortium bleeds and all-cause mortality were comparable between both treatment arms, 33.9% for NOACs versus 34.1% for non-vitamin K antagonists (HR 0.97, 95% CI 0.74–1.26, p=0.838, IPTW-adjusted) and 16.5% versus 12.2% (HR 1.36, 95% CI 0.90–2.06, p=0.136, IPTW-adjusted), respectively.
The investigators conclude: “Chronic use of both NOACs and VKAs among patients in need of OAC after TAVI are comparable regarding one-year bleeding risk.”
But, an accompanying editorial urges caution when interpreting the findings. Dominick J Angiolillo and Andreas Pineda point out: “Despite antithrombotic agents being one of the most broadly studied therapeutic agents, important knowledge gaps persist with regard to understanding the optimal antithrombotic regimen following TAVI. This includes antithrombotic approaches for patients with concomitant comorbidities, such as AF, who have an indication for oral anticoagulant therapy.”
Current advice is conflicting, with US guidelines favouring the use of a VKA for three months after TAVI among patients at low bleeding risk, and with no specific advice given on NOAC therapy. European agencies stress the use of a VKA for the first three months after TAVI and then suggest that a NOAC can be considered as an alternative after this.
The editorial says that the nonrandomised nature of the study and its unbalanced baseline characteristics and unmeasurable confounders limit the applicability of its findings. They also point to a need for further randomised trials and, in the meantime, recommend: “NOACs should be used with caution, and the choice of antithrombotic therapy should be individualised, taking into account the patients’ bleeding and thrombotic risk profile.”