“Two of the main differences between our study and most previously published studies showing a decrease in risk are that the patients in our study had shorter disease duration, and that we defined the events as myocardial infarction or unstable angina, the two diagnoses that constitute acute coronary events,” says Dr. Ljung. “The accumulated burden of disease is lower early in the course, which might be one explanation of the difference.

“The most important message for our patients and for rheumatologists, I think, is that we should continue to measure and control known risk factors in order to minimize the cardiovascular risk, whether the patients are treated with anti-TNFs or not,” Dr. Ljung says.

Jon Giles, MD, an assistant professor of medicine in the division of rheumatology at Columbia University’s College of Physicians and Surgeons, was lead author of a study (when he was at Johns Hopkins University) that found TNF inhibitors reduced the amount of carotid artery thickening, a sign of plaque build-up. He agrees that all of these studies are looking at different groups of patients and different cardiovascular outcomes.

“We didn’t look at events in our study. We looked at progression of carotid atherosclerosis. So they could be different patients with RA,” Dr. Giles says.

But he also cautions against drawing too many conclusions from this study because he says TNF inhibitors are often given to patients with more extreme levels of inflammation, so the baseline of the two groups could have been different.

“It’s the problem of an observational study,” Dr. Giles says. “People taking anti-TNF medications may be at higher overall cardiovascular risk. People taking other medications may be at lower cardiovascular risk; thus, equivalent results could mean (the two groups) didn’t start at the same point but ended at the same point. There very well could be a benefit you aren’t picking up because you didn’t realize their risk of cardiovascular events was not equal at the beginning.”

Dr. Giles says the important thing for any RA patient to know is that maximal control of RA disease activity, regardless of what agent is used, is likely to improve cardiovascular outcomes in conjunction with control of traditional risk factors, such as high blood pressure, cholesterol, smoking, diabetes, and obesity.