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TNF inhibitors linked to lower risk for heart attack vs sDMARDs
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Patients with rheumatoid arthritis who received a tumor necrosis factor inhibitor had a reduced risk for heart attack compared with patients who received a synthetic disease-modifying antirheumatic drug, according to a recently published study.
“This might be attributed to a direct action of [tumor necrosis factor inhibitors] TNFi therapy on the atherosclerotic process or better overall disease control or both,” Audrey S. L. Low, MRCP, PhD, in the Arthritis Research UK Centre for Epidemiology at the University of Manchester, and colleagues wrote.
For the study, Low and colleagues included patients with rheumatoid arthritis (RA) who either received a TNFi — etanercept, infliximab or adalimumab — or a synthetic disease-modifying antirheumatic drug (sDMARD) between 2001 and 2009 as part of the British Society for Rheumatology Biologics Register for RA. Patients were linked to the Myocardial Ischaemia (MI) National Audit Project and were followed through questionnaires and a national death register linkage. Overall, there were 252 verified MIs. These included 58 in 3,058 patients who received sDMARDs and 194 in 11,200 patients who received a TNFi.
Researchers assessed the risk of first MI and compared findings between cohorts using Cox regression and adjusted propensity score deciles. They assessed 6-month mortality post-MI with logistic regression. In addition, researchers used descriptive statistics to compare MI phenotype and severity.
Researchers found patients who received a TNFi were less likely to have had MI (hazard ratio = 0.61). However, there were no significant differences between groups in MI severity or mortality.
“[This] warrants further exploration in collaborative analyses across other biologic registers,” the researchers wrote. – by Will Offit
Disclosure: One researcher reports to have received honoraria from Pfizer and AbbVie.
Perspective
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Calvin R. Brown Jr., MD
Clinicians often face the issue of using a TNFi in patients with cardiac disease. While much of this concern was related to heart failure, there was potential “spillover” concern about other cardiac complications, including MI. At the same time, patients who are candidates for TNFi have underlying diagnoses that make them at greater risk for MI with rheumatoid arthritis being a leading diagnosis. Therefore, the relationship between exposure to TNFi therapy and incidence and severity of MI in patients with rheumatoid arthritis (RA) is a relevant issue to examine. As we learned from the recent PRECISION study of cardiovascular events related to celecoxib therapy, it can take a long time to accrue enough events to detect any differences when studied in a prospective fashion.
By utilizing the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis, the authors have been able to prospectively collect data from a relatively large sample, albeit with the multiple confounders inherent in observational studies. Reassuringly, the authors found treatment with TNFi therapy added to conventional DMARD therapy for RA was associated with a reduced risk of MI during the medium term compared with conventional DMARD therapy alone. Differences in severity of MI were not detected. Of course, this study did not determine whether this reduction was due to a direct action of the TNFi on coronary arteries or better overall RA disease control.
For now, we can be confident counselling our patients who are considering or are already on TNFi therapy combined with DMARDs, that addition of the TNFi will not increase, but rather may decrease their MI risk.
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