Limitations
Our study has several limitations. First, we could not clearly identify the prevalence of provoked and unprovoked VTE in our VTE cohort. Several observational studies have reported that unprovoked VTE does not contribute to the same risk as provoked VTE in terms of clinical outcomes, including arterial thromboembolic events. However, a 20-year national observational cohort study reported no significant differences in arterial CV events between provoked and unprovoked VTE.11 In addition, the distinction between provoked/unprovoked PE is no longer supported by the 2019 ESC guidelines for the diagnosis and management of acute pulmonary embolism.34 Furthermore, clinical presentations/manifestations and laboratory data were not available in NHIRD and such information might affect the outcomes of VTE, especially those with PE.34 In order to reduce the bias, we excluded those died during hospitalization and within 3 months after discharge. Second, differentiating subtypes of AF (paroxysmal, sustained) cannot be performed because this information was not available in our national database. Although the incidence of ischemic stroke is considered to be generally lower in paroxysmal AF patients than in patients with sustained AF,35 it should not affect the outcomes between AF and VTE in such a large volume study. Third, the duration of anticoagulation therapy was different between AF versus VTE cohorts.2,34 We also did not compare the outcomes between AF and VTE cohorts in individual different scenarios with different durations of anticoagulation therapy.