Abstract 12499: Risk of Venous Thromboembolism in Autoimmune Connective Tissue Diseases: A Population-Based Retrospective Study
Abstract
Introduction: Autoimmune Connective tissue diseases (CTD) are known to induce systemic and intravascular inflammation, endothelial damage, and the resulting surge in the prothrombotic milieu. However, the literature describing the correlation between various CTD and risk of Venous thromboembolism (VTE) is limited.
Objective: We sought to assess the association of VTE and CTD in a nationwide larger population-based database.
Methods: We conducted a retrospective analysis on all adults (aged >=18 years) admitted with an index diagnosis of either acute Pulmonary Embolism (PE) or deep venous thrombosis (DVT) from the National Inpatient Sample (NIS) database (2017) using ICD 10 codes. Logistic regression models were used to adjust for the potential confounders of VTE including factors related to admission, hospital, and patients’ comorbidities.
Results: Out of more than 30 million hospital admissions, a total of 285,650 patients (mean age 63±17 vs 57±20 yrs, p<0.01; Females 51% vs 57%, p<0.01) were identified with a primary diagnosis of VTE. Advancing age and black race (OR 1.38, 95% CI 1.35-1.42, p<0.001) had a higher risk of VTE, whereas females had a lower risk of VTE compared to men (OR 0.82, 95% CI 0.8-0.83, p<0.001). Out of twenty-one, autoimmune CTD evaluated in this study, eight diseases [antiphospholipid antibody syndrome (APS), ANCA vasculitis, dermatopolymyositis, giant cell arteritis (GCA), Polymyalgia rheumatica (PMR), Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and sarcoidosis] were independently associated with risk of VTE. APS (OR 4.4, 95% CI 3.8-5.1, p<0.001), GCA (OR 1.8, 95% CI 1.4-2.3, p<0.001), and SLE (OR 1.6, 95% 1.4-1.7, p<0.001) had the highest risk of VTE based on their odds ratio.
Conclusions: In our study, various autoimmune connective tissue diseases were significantly associated with the risk of VTE. Further studies are warranted to identify the underlying mechanism and preventive strategies in this population.
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© 2021 by American Heart Association, Inc.
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Published online: 8 November 2021
Published in print: 16 November 2021
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