111 FRAIL-AF RANDOMISED CONTROLLED TRIAL: RESULTS analysis, this time was assumed to be part of ‘the switch to a NOAC treatment strategy’ and therefore any outcome events observed during this period were included in the analyses. The primary outcome was compared between the trial arms (switching to a NOAC versus continuing with a VKA) using a cause-specific Cox regression analysis with death from causes other than major bleeding considered a competing event. The renal function stratum used to stratify randomisation was included as an independent variable in the Cox model. Thrombosis services were included as stratification factor, allowing a separate baseline hazard function for each service. Patients without major or CRNM bleeding complications who did not experience the competing event were censored at the last day of follow-up. The proportional hazard assumption was assessed visually using log-log survival plots, and a time-dependent coefficient for treatment arm would be added into the model in case of non-proportionality. HRs are reported as effect sizes with 95% confidence intervals (CI). The Aalen-Johansen cumulative incidence estimator was used for visualisation of the time to the first major or CRNM bleeding complication. The following subgroup analyses were proposed a posteriori: sex, age, type of prescribed NOAC in the intervention arm, different levels of GFI, and the strata of renal function. The primary analysis was followed for each subgroup. Analyses of secondary outcomes followed the primary analysis. RESULTS From 10 January 2018 through 25 April 2022, a total of 2,621 patients were screened for eligibility. Most of these patients were not included because they were considered non-frail. A total of 1,396 patients provided informed consent. In these patients renal function was assessed before randomisation, and an additional 66 patients were excluded from randomisation because of an eGFR <30 mL/min/1.73 m2. Thus, a total of 1,330 underwent randomisation (see Figure 1). After randomisation, 7 patients (0.5% of the trial population) were excluded from analysis because they met a priori defined exclusion criteria for participating in our trial: 5 patients were in hindsight wrongly registered as having AF by the participating thrombosis services, 1 patient had an eGFR <30 mL/min/1.73 m2, and 1 patient had valvular AF. Thus, the ITT population included 662 patients that switched from a VKA to a NOAC and 661 patients that continued with INR guided VKA management. This ITT population was used for all further analyses, both for our primary and secondary outcomes. Of note, all ITT analyses were also repeated including these 7 excluded patients yielding similar findings (data not shown). The mean age was 83±5.1 years and the median score of the GFI was 4. Other characteristics of the ITT population, such as comorbidities and renal function, are presented in Table 1. The median duration from randomisation to the start with a NOAC in the intervention arm was 52 days (interquartile range, 35–72 days). A total of 22 patients did not switch to a NOAC despite being allocated to switching (3.3%), 57 patients (8.6%) switched to dabigatran, 332 (50.2%) to rivaroxaban, 115 (17.4%) to 7
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