MANCHESTER, UK—TNF blockers provided no greater protection against myocardial infarction (MI) than traditional disease-modifying antirheumatic drugs (DMARDs), but data from the British Society for Rheumatology biologics register showing lower MI risk in TNF-inhibitor responders support the idea that inflammation is a major contributor to the increased cardiac risk associated with RA. The study is reported in Arthritis & Rheumatism.1

"The suppression of joint disease with anti-TNFα therapy in RA patients may be associated with an early reduced risk of MI"—William G. Dixon, MD, MRCP.
"The suppression of joint disease with anti-TNFα therapy in RA patients may be associated with an early reduced risk of MI," writes lead author William G. Dixon, MD, MRCP, with the University of Manchester, in England.

Study compared MI rates with TNF inhibitors versus DMARDs

 The researchers compared rates of heart attack in 8670 RA patients who were treated with TNF-blockers and 2170 RA patients who were treated with traditional DMARDs. Overall, there were 63 heart attacks among patients taking TNF-blockers during 13,233 person-years of follow-up and 17 heart attacks among patients taking traditional DMARDs during 2893 person-years of follow-up through July 2006. This was equivalent to a rate of 4.8 events per 1000 person-years in the anti-TNFα cohort and 5.9 events per 1000 person-years in the DMARDs cohort.

The anti-TNFα regimens were not more effective than traditional DMARDs at preventing heart attacks (incidence rate ratio 1.44 [95% CI, 0.56-3.67]). However, a subgroup analysis of anti-TNFα responders versus nonresponders at 6 months found 3.5 heart attacks per 1000 person-years in responders versus 9.4 heart attacks per 1000 person-years in nonresponders (adjusted incidence rate ratio 0.36).

"This is consistent with the hypothesis that suppression of inflammation may reduce cardiovascular risk," the researchers write.

Lack of DAS28 data on DMARD group is a limitation

"Independent of what medication the patient is taking, if the patient's RA isn't under control, they are at greater risk of MI [and other cardiovascular] events," Kaleb Michaud, PhD, assistant professor of medicine at the University of Nebraska Medical Center, in Lincoln, told CIAOMed. "Unfortunately the authors did not have clinical measures for the non-TNF group so they were unable to confirm this hypothesis." This is because the study authors did not measure DAS28 at 6 months in the DMARD cohort.

Reference

1. Dixon WG, Watson KD, Lunt M, et al. Reduction in the incidence of myocardial infarction in patients with rheumatoid arthritis who respond to anti-tumor necrosis factor α therapy. Arthritis Rheum. 2007;56:2905-2912.