NEW YORK (Reuters Health)—Patients with active rheumatoid arthritis (RA) and no known heart disease may have subclinical myocardial inflammation, which improves with disease-modifying therapy, new research shows.
“We know that patients with RA have higher risk of cardiovascular events, including heart failure and we really don’t know why. Maybe myocardial inflammation is one of the mechanisms,” lead author Dr. Isabelle Amigues of Columbia University in New York noted in a phone interview with Reuters Health.
“Despite the many advances of rheumatology care, this study shows there is inflammation of the heart that we can actually see on the PET scan. This is important,” Dr. Amigues said, “because as a clinician with a patient who has high disease activity, I can tell them, this is not just about your joints, it’s also about your heart.”
Dr. Amigues presented the findings November 14 at the American College of Rheumatology annual meeting in New Orleans.
She and her colleagues investigated the prevalence of myocardial inflammation in 118 RA patients without prior CVD events and 13 well-matched controls without RA.
The RA patients had a mean age of 55 years, a mean BMI of 28.5 and their median disease duration was seven years. The patients had a mean disease activity score in 28 joints (DAS28) of 3.78, and 28% had Clinical Disease Activity Index (CDAI) less than 10, consistent with low disease activity or remission. Forty-five patients used biologics, primarily TNF inhibitors (TNFi).
Using cardiac FDG-PET-CT imaging that can detect inflammation in the myocardium, the researchers compared mean maximal standardized uptake value (SUVmax) for myocardial FDG uptake to disease activity scores.
Median SUVmax was 12% higher in the RA patients relative to control patients.
In RA patients, higher BMI and moderate-to-severe disease activity were positively associated with SUVmax. After adjusting for BMI and RA therapy, mean SUVmax was 30% higher in patients with moderate-to-severe disease activity compared with to those with low disease activity.
RA patients treated with a non-TNFi biologic had a 35% lower mean SUVmax compared to those either not on a biologic or on a TNFi. “It seems that disease activity is linked to higher inflammation,” Dr. Amigues told Reuters Health.
“This is the first report of a quantitative assessment of myocardial inflammation and the largest number of RA patients ever studied for myocardial inflammation,” Dr. Joan M. Bathon, director of rheumatology at Columbia, said in a news release.
She said the link between myocardial inflammation and articular inflammation is compelling, as it suggests that treating the joint inflammation might also lessen myocardial inflammation.
“Although we did not see an association of FDG uptake with abnormal heart structure or function in this cross-sectional analysis of RA patients with no clinical cardiovascular disease, it is possible that myocardial inflammation precedes any structural or functional changes. Further longitudinal studies are needed to assess the impact of baseline myocardial inflammation on adverse myocardial changes over time,” Dr. Bathon said.
In a related nested sub-study involving eight of the RA patients, the Columbia team found that treatment with disease-modifying antirheumatic drugs (DMARDs) appears to improve subclinical myocardial inflammation.
“In this longitudinal study, where we looked at myocardial inflammation before and six months after step-up therapy, we saw that patients responded to the therapy, and with a decrease of disease activity we saw decreased inflammation in the heart,” Dr. Amigues said. “Disease activity is linked to heart inflammation and treating RA does help with the heart inflammation.”
The study had no commercial funding and the authors have disclosed no relevant financial relationships.
SOURCE: http://bit.ly/2fFuLHu and http://bit.ly/2fx3Sb0
American College of Rheumatology Annual Meeting 2016.
