SAT0597 RISK OF HEART FAILURE FOLLOWING EXPOSURE TO NON-TNFI COMPARED TO TNFI BIOLOGICS IN US PATIENTS WITH RHEUMATOID ARTHRITIS
Authors: Thomas Bo Jensen, Nicole Tsao, Ajinkya Pawar, Rishi J. Desai, Seoyoung Kim
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Biologic disease modifying drugs including TNF-inhibitors (TNFi) and non-TNFi agents have become cornerstone of rheumatoid arthritis (RA) management. Case reports on new-onset heart failure (HF) following TNFi initiation led to an FDA black box warning released in October 2001. Subsequent observational studies have shown no association or even a protective effect of TNFi for HF, but the black box warning is still in place. There is a lack of knowledge regarding the risk of HF following exposure to the newer non-TNFi biologics. <h3>Objectives</h3> We aimed to assess the risk of incident HF following exposure to non-TNFi compared to TNFi biologics. <h3>Methods</h3> Using US claims data from Truven MarketScan (2004-2016), we conducted a cohort study of RA patients who initiated a 'TNFi' (adalimumab, certolizumab pegol, etanercept, golimumab, infliximab), or 'non-TNFi' biologic or targeted synthetic DMARD (abatacept, anakinra, tocilizumab, tofacitinib). Patients were excluded if they were &lt;18 years old, had previous HF, an implantable cardiologic device, or a loop-diuretics prescription. Patients were followed from the day after treatment initiation until the earliest event of the following: death, insurance disenrollment, treatment switching or discontinuation. The primary outcome of incident HF was defined based on primary inpatient diagnosis. Cox proportional hazards regression compared risk of HF among new users of non-TNFi compared to TNFi. To control for confounding, we used multivariable adjustment as well as propensity score (PS) adjustment by decile with trimming. <h3>Results</h3> A total of 13,290 non-TNFi patients were included, primarily consisting of abatacept (65%), tocilizumab (17%), and tofacitinib (15%). For the TNFi group, we identified 67,892 patients, primarily consisting of etanercept (42%), adalimumab (37%), and infliximab (15%). More patients treated with non-TNFi were female, older, had higher proportion of co-morbidities and number of rheumatologist visits; but lower proportion of NSAID/Coxib use, Table 1. The crude hazard ratio (HR) of HF after initiating a non-TNFi was 1.28 (95%CI 0.75-2.18) versus TNFi. After confounding adjustment in a multivariable model, the HR was attenuated to 1.08 (95%CI 0.57-2.05). The PS adjusted analysis showed consistent results (Table 2). <h3>Conclusion</h3> In this large US-based cohort of 81,182 RA patients, we found no difference in the risk of incident HF after initiation of non-TNFi biologic or targeted synthetic DMARD versus TNFi. Covariates included in adjusted and PS models: year of cohort entry, age, gender, region, comorbidities, prior drug-use, and health utilization. <h3>Disclosure of Interests</h3> Thomas Bo Jensen: None declared, Nicole Tsao: None declared, Ajinkya Pawar: None declared, Rishi J Desai Grant/research support from: RJD has received research grants to the Brigham and Women's Hospital from Merck, Bayer and Vertex for unrelated projects., Seoyoung Kim Grant/research support from: Pfizer, Bristol-Myers Squibb, Roche/Genentech and AbbVie.