Anti-TNFalpha therapy did not reduce myocardial infarction incidence compared with traditional DMARDs in RA patients (IRR 1.44; 95% CI 0.56-3.67), but risk was lower in treatment responders.
Observational (n=10,840)
Yes
Does anti-TNFalpha therapy reduce the incidence of myocardial infarction in patients with rheumatoid arthritis compared to traditional DMARDs?
While overall anti-TNFalpha therapy did not reduce MI risk compared to traditional DMARDs, achieving a clinical response to anti-TNFalpha by 6 months was associated with a markedly reduced risk of MI, supporting the role of inflammation in cardiovascular events.
Effect estimate: IRR 1.44 (95% CI 0.56-3.67)
Absolute Event Rate: 4.8% vs 5.9%
OBJECTIVE: Rheumatoid arthritis (RA) is associated with an increased risk of coronary artery disease, possibly acting via shared mechanisms of inflammation. This study was undertaken to test the hypothesis that the powerful antiinflammatory effect of anti-tumor necrosis alpha (anti-TNFalpha) therapy might lead to a reduction in the incidence of myocardial infarction (MI) in patients with RA. METHODS: Using data from the British Society for Rheumatology Biologics Register, a national prospective observational study, we compared MI rates in 8,670 patients with RA treated with anti-TNFalpha and 2,170 patients with active RA treated with traditional disease-modifying antirheumatic drugs (DMARDs). RESULTS: Through July 2006, 63 MIs occurred in the anti-TNFalpha cohort during 13,233 person-years of followup and 17 MIs occurred in the DMARD cohort during 2,893 person-years of followup, equivalent to a rate of 4.8 events per 1,000 person-years and 5.9 events per 1,000 person-years, respectively. After adjustment for baseline risk factors, there was no reduction in the rate of MI in the anti-TNFalpha cohort compared with the DMARD cohort (incidence rate ratio 1.44 95% confidence interval 0.56-3.67). In an analysis of anti-TNFalpha-treated patients who responded to the treatment within 6 months versus those who did not, MI rates were found to be 3.5 events per 1,000 person-years in responders and 9.4 events per 1,000 person-years in nonresponders. The adjusted incidence rate ratio (95% confidence interval) for responders compared with nonresponders was 0.36 (0.19-0.69). CONCLUSION: These results indicate that RA patients treated with anti-TNFalpha do not have a lower incidence of MI compared with RA patients treated with traditional DMARDs. However, the risk of MI is markedly reduced in those who respond to anti-TNFalpha therapy by 6 months compared with nonresponders. This finding supports the notion that inflammation plays a pivotal role in MI.
Dixon et al. (Thu,) conducted a observational in Rheumatoid arthritis (n=10,840). Anti-TNFalpha therapy vs. Traditional disease-modifying antirheumatic drugs (DMARDs) was evaluated on Incidence of myocardial infarction (IRR 1.44, 95% CI 0.56-3.67). Anti-TNFalpha therapy did not reduce myocardial infarction incidence compared with traditional DMARDs in RA patients (IRR 1.44; 95% CI 0.56-3.67), but risk was lower in treatment responders.
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