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.