Abstract

Objectives We studied the safety and efficacy of warfarin compared to direct acting oral anticoagulant use in patients with IPF. Methods We conducted a retrospective cohort study of all patients with IPF who were prescribed warfarin or direct acting oral anticoagulants (DOACs) for cardiac or thromboembolic indications and followed at our institute for their care. Univariate tests and multivariable logistic regression analyses were used for assessing association of variables with outcomes. Results A total of 73 patients were included in the study with 28 and 45 patients in the warfarin and DOAC groups, respectively. Univariable analysis revealed a significant difference in mortality in one year between warfarin and DOAC groups (7/28 vs. 3/45, p value 0.027). Significantly more patients in the warfarin group suffered an exacerbation that required hospitalization within one year (9/28 vs. 5/45, p value 0.026). Multivariate logistic regression analysis showed that anticoagulation with warfarin was independently associated with mortality at one-year follow-up (OR: 77.4, 95% CI: 5.94–409.3, p value: 0.007). Conclusion In our study of patients with IPF requiring anticoagulants, we noted statistically significant higher mortality with warfarin anticoagulation when compared to DOAC use. Further larger prospective studies are needed to confirm these findings.

Highlights

  • Idiopathic pulmonary fibrosis (IPF) is a pulmonary disease of unknown etiology that is characterized by interstitial fibrotic change in lung parenchyma [1,2,3]

  • IPF is associated with an increase in thromboembolic and acute coronary syndromes [9,10,11], with a recent metaanalysis showing a twofold increase in the risk of VTE in this

  • Patients with IPF who were initiated on anticoagulation with warfarin or direct acting oral anticoagulants (DOACs) including apixaban, rivaroxaban, or dabigatran were identified using our electronic health record system, and their charts were reviewed by two study authors

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Summary

Introduction

Idiopathic pulmonary fibrosis (IPF) is a pulmonary disease of unknown etiology that is characterized by interstitial fibrotic change in lung parenchyma [1,2,3]. Prior studies have demonstrated a role of the coagulation cascade in the pathogenesis of this disease [4, 5]. Based on this premise, its role as a therapeutic target was explored by a placebo-controlled trial of warfarin therapy for the treatment of IPF [6]. Its role as a therapeutic target was explored by a placebo-controlled trial of warfarin therapy for the treatment of IPF [6] This trial was discontinued early due to excess mortality in the warfarin group. The ACE-IPF trial mentioned above studied the role of warfarin for treatment of IPF in patients with no indications for anticoagulation. IPF is associated with an increase in thromboembolic and acute coronary syndromes [9,10,11], with a recent metaanalysis showing a twofold increase in the risk of VTE in this

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