Rheumatoid Arthritis Linked to Heart Disease Risk
Rheumatic and myocardial inflammation can be treated with disease modifying anti-rheumatic drugs.
A pair of new studies out of Columbia University assert that rheumatic and myocardial inflammation can go hand-in-hand, but can be treated with disease modifying anti-rheumatic drugs (DMARDs). The 2 works were announced and presented in conjunction at the 2016 American College of Rheumatology conference in Washington, DC.
The first of the 2, which Joan M. Bathon, MD, of Columbia describes as “the largest number of RA patients ever studied for myocardial inflammation”, examined 118 patients with rheumatoid arthritis (RA) with no previously reported record of cardiovascular disease (CVD).
These patients underwent 18-F-FDG-PET-CT scanning, as well as echocardiography to measure left ventricular mass and function. A gender-and-age-matched group of 13 patients without RA were administered the same tests to create a standard for normal vs. abnormal values.
Patients were also observed for body mass index (BMI), DAS28 disease score, and anti-CCP. The metric by which patients were compared was maximal standardized uptake value (SUVmax) for fluorodeoxyglucose (FDG).
They found that patients with RA, specifically those with moderate-to-severe disease scores and higher BMIs, had higher SUVmax than the healthy controls. Those undergoing treatment with biologic drugs that weren’t tumor necrotic factor inhibitors (TNFi) had SUVmax values 35% lower than those on a TNFi or on no treatment. Diabetes prevalence and demographic factors were not considered related to SUVmax.
The findings indicated an increased presence of myocardial inflammation in those with RA, but that it could countered with treatment with non-TNFi biologic DMARDs. The second study, much smaller, attempted to verify the extent to which this was true. In this search, 12 RA patients and 13 controls underwent the same scans to quantify the degree of inflammation.
The RA patients underwent scans at both baseline and 6 months, and findings showed that myocardial FDG uptake dropped concurrently with disease activity.
Despite the small sample of the second study, Dr Bathon believes that “It supports the concept that appropriate treatment of the joint manifestations of their disease may also suppress and/or prevent myocardial inflammation and, potentially, the development of heart failure.”