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Abstract Number: 1242

Use of Anti-Tumor Necrosis Factor Therapy Is Associated with Reduced Cardiovascular Event Risk in Rheumatoid Arthritis

Mike Nurmohamed1, Yanjun Bao2, James Signorovitch3, Parvez M. Mulani4 and Daniel Furst5, 1VU University Medical Center & Jan van Breemen Research Institute, Amsterdam, Netherlands, 2AbbVie, North Chicago, IL, 3Analysis Group, Inc., Boston, MA, 4Abbott Laboratories, Abbott Park, IL, 5Div of Rheumatology, UCLA Medical School, Los Angeles, CA

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Adalimumab, Adverse events, cardiovascular disease and methotrexate (MTX), DMARDs

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Session Information

Title: Rheumatoid Arthritis - Clinical Aspects II: Clinical Features & Comorbidity/Cardiovascular Disease

Session Type: Abstract Submissions (ACR)

Background/Purpose: Rheumatoid arthritis (RA) is associated with increased risks for cardiovascular (CV) comorbidities because of an increased prevalence of traditional CV risk factors and the underlying chronic inflammatory process. We assessed the effects of treatment with anti–tumor necrosis factor (anti-TNF) therapy, methotrexate (MTX), or other nonbiologic DMARDs on CV event risk in patients with RA.

Methods: Adult patients with ≥2 RA diagnoses (ICD-9 CM: 714.xx) and ≥1 filled prescription of anti-TNF therapy, MTX, or other nonbiologic DMARD were identified in the Thomson Reuters MarketScan® database (2003–2010). Patients were assessed from index fill date to first inpatient CV diagnosis of myocardial infarction (MI), stroke, unstable angina, or congestive heart failure (CHF) to the end of health plan enrollment or to 6 months after the discontinuation of their index drug, whichever came first. Cox proportional-hazards models assessed the effect of cumulative exposure to anti-TNF therapy, MTX, and other nonbiologic DMARDs on occurrence of CV events. We adjusted for baseline (ie, 1 year before index prescription) demographics, use of therapies for RA (eg, MTX, corticosteroid), CV-related medications and smoking deterrents, comorbidities (eg, dyslipidemia, hypertension, diabetes), history of CV events, and medical resource use. Subgroup and sensitivity analyses also were conducted.

Results: The study identified 109,462 patients with 105,920 total patient-years (PYs) of follow-up, including 48,621 PYs of exposure to anti-TNF therapies (31,466 as monotherapy), 35,480 PYs of exposure to MTX (18,325 as monotherapy) and 52,994 PYs of exposure to other nonbiologic DMARDs (9,441 as monotherapy). A total of 1743 patients (1.6%) had a CV event after their index prescription. In the multivariate regression model, each additional 6 months of anti-TNF therapy significantly reduced the risk for any study CV event (hazard ratio [HR]=0.87, 95% confidence interval [CI]=0.80–0.96, P=.005) and for MI (HR=0.80, CI=0.67–0.95, P=.013), compared with patients without anti-TNF biologics. The effects of cumulative use of MTX and other nonbiologic DMARDs were not statistically significant. In the subgroup analyses, each additional 6 months of anti-TNF therapy use was significantly associated with a reduction in CV events in patients aged ≥50 years (HR=0.86, CI=0.77–0.96, P=.007) and in those without prior MTX use (HR=0.85, CI=0.73–0.98, P=.022). When assessed individually, significant event risk reduction was also observed with MI, unstable angina, and CHF for patients with longer exposure to anti-TNF therapies compared with nonuse of anti-TNF therapies. In the full sample, the model predicted that cumulative use of anti-TNF therapy for 1, 2, or 3 years would reduce CV event risks by 24%, 42%, and 56%, respectively, compared to nonuse of anti-TNF therapies. 

Conclusion: Use of anti-TNF therapies vs. nonuse was associated with significantly lower risks for CV events (ie, inpatient diagnoses for MI, stroke, unstable angina, or HF) in patients with RA, older patients with RA, and patients without prior exposure to MTX, adjusting for use of MTX and other nonbiologic DMARDs.


Disclosure:

M. Nurmohamed,

Abbott Laboratories,

2,

Abbott Laboratories,

5,

Abbott Laboratories,

8;

Y. Bao,

Abbott Laboratories,

3,

Abbott Laboratories,

1;

J. Signorovitch,

Analysis Group,

3;

P. M. Mulani,

Abbott Laboratories,

3,

Abbott Laboratories,

1;

D. Furst,

Abbott Laboratories,

5,

Abbott Laboratories,

8,

Abbott Laboratories,

9.

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