Article Text

FRI0169 Influence of anti-tnf therapy on the risk of myocardial infarction in subjects with rheumatoid arthritis: results from the bsrbr-ra
  1. A. Low1,
  2. M. Lunt1,
  3. L. Mercer1,
  4. E. Bruce1,
  5. B. C. C. Consortium1,
  6. W. Dixon1,
  7. K. Hyrich1,
  8. D. Symmons1 on behalf of the British Society for Rheumatology Biologics Registers (BSRBR)
  1. 1Arthritis Research UK Epidemiology Unit, UNIVERSITY OF MANCHESTER, Manchester, United Kingdom


Background Subjects with RA are at increased risk of premature cardiovascular disease (CVD) including myocardial infarction (MI), partly through shared inflammatory mechanisms. Anti-TNF therapy may influence this risk through control of inflammation and mediation of other CV risk factors.

Objectives The aim of the analysis was to study the association of anti-TNF therapy with the risk of MI in routine UK clinical practice.

Methods The BSRBR-RA is an ongoing national prospective observational cohort study. Subjects with RA starting anti-TNF (etanercept, infliximab, adalimumab) and a biologic-naïve comparator cohort of subjects exposed to nbDMARD were recruited 2001-2009. All were followed by clinician & patient questionnaires 6-monthly for 3 years, annual clinician questionnaires thereafter and linked to the national death register. All reported MIs from any source were validated against the 2007 AHA/ESC MI criteria. Additional criteria were acute thrombolysis/angioplasty for MI or MI as the underlying cause of death on death certificates. Subjects were censored at 20/4/2010, death, incident MI or date of last clinician follow-up, whichever came first. Subjects with prior CVD were excluded from analysis. Risk of MI was compared between nbDMARD and subjects ever exposed to anti-TNF therapy using Cox regression adjusted by propensity score deciles (PD; Table). The PD included age, gender, RA-related factors, CV risk factors & drugs. Risk of MI was explored further with different drug exposure models and also modelled over time. 30-day and 1-year all-cause mortality post-MI was compared between nbDMARD and anti-TNF subjects using multivariate logistic regression, adjusted for the same confounders.

Results 235 verified incident MIs were analysed; nbDMARD: 43 in 10337 person-years (pyrs), anti-TNF: 192 in 55636 pyrs (42 v 35 per 10,000 pyrs; Table). There was a trend for a reduced risk of MI in subjects ever exposed to anti-TNF compared to nbDMARD: PD-adjusted hazard ratio 0.65 (0.42-1.01). Risk estimates were similar when limited to periods receiving anti-TNF drug only and did not vary over time. 30-day and 1-year mortality post-MI was not associated with ever-exposure to anti-TNF: adjusted odds ratios (OR) 0.93 (0.29-2.95), OR 0.97 (0.33-2.79) respectively.

Conclusions Subjects with RA ever exposed to anti-TNF experienced a reduced risk of MI over the medium term, further supporting the role of TNF and inflammation in CVD.

Disclosure of Interest None Declared

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