LIVERPOOL, UK – Analysis of data from the British Society for Rheumatology Biologics Registry Study-Rheumatoid Arthritis (BSRBR-RA) suggests that, compared with traditional non-biologic disease-modifying anti-rheumatic drugs (nbDMARD), anti-tumor necrosis factor (anti-TNF) drugs reduce the risk of heart attack in rheumatoid arthritis (RA) patients, but by a mechanism unrelated to the anti-inflammatory effects of these drugs. The results of the study showed that patients treated with anti-TNF drugs had a 40 percent lower risk of myocardial infarction than those treated with nbDMARD. However, the researchers say this difference is not the result of anti-TNF drugs reducing the inflammatory response, but should be attributed in part to clinical efficacy related to the drugs themselves or more so. Patients with RA are known to be at elevated risk for cardiovascular disease, with cardiovascular morbidity and mortality about 50% higher than in the general population, and a corresponding increased risk of myocardial infarction in particular. Inflammation is thought to play a key role in the development of atherosclerosis and RA, and thus, suppression of inflammatory responses with anti-TNF agents has the potential to reduce the excess risk of cardiovascular disease in RA patients. The data analysis utilized both BSRBR-RA data and data from the UK National Myocardial Infarction Underlying Database (MINAP), which was established in 1999 from all patients admitted to hospital for heart attack in England and Wales and collects data on approximately 90,000 suspected myocardial infarction (MI) patients per year. By 2012, the database contained more than 1 million records. The researchers analyzed data from 14,258 patients with active RA, 11,200 of whom were treated with anti-TNF drugs and 3,058 with nbDMARD therapy. The researchers first compared the incidence of MI in the two groups and then determined whether the biologic agents affected the severity of MI. All RA patients who started treatment with adalimumab, etanercept, or infliximab and were recruited into BSRBR-RA from 2001 to 2008 were included, and those with a prior history of cardiovascular disease were excluded. To determine the prevalence of MI, data from BSRBR-RA and MINAP were matched using patient name, date of birth, NHS number, zip code and gender. Cardiovascular events in both databases that occurred within the same 30-day time window were considered the same event. MI events among them were identified using the criteria of the American College of Cardiology and the European Society of Cardiology, combined with the relevant criteria of the World Health Organization International Classification of Diseases, 10th Revision. A total of 252 MIs were identified, of which 194 occurred in the anti-TNF drug treatment group with a median time to occur of 5.3 years of follow-up. 58 occurred in the nbDMARD treatment group with a median time to occur of 3.5 years of follow-up. The corresponding annual mean crude incidence rates were 3.5/1000 and 5.6/1000, respectively. To compare the severity of MI in the two groups, the researchers analyzed the absolute levels of three cardiac enzymes in those MI patients with MINAP-related data (143 patients) and found that peak troponin I, peak troponin T, and peak creatine kinase were higher in the anti-TNF drug-treated MI patients than in the nbDMARD-treated group. were higher than those of MI patients in the nbDMARD treatment group. However, the sample size was too small to make this difference statistically significant. There were no significant differences in the type of MI (ST-segment elevation versus non-ST-segment elevation), cardiac arrest, or days in hospital, which reflect the severity of myocardial infarction. This led the researchers to conclude that anti-TNF drugs did not affect the severity of MI and post-MI mortality. The limitation of the study is that it failed to avoid the confounding effect of concomitant steroidal or non-steroidal anti-inflammatory drugs on the risk of MI.