WASHINGTON – Chronic cardiac inflammation is present in rheumatoid arthritis patients and appears to resolve when they achieve a good clinical response to medical therapy.
The findings of two cardiac imaging studies offer a tantalizing clue to the link between RA and heart failure, said Isabelle Amigues, MD, who reported the findings at the annual meeting of the American College of Rheumatology.
“We know that the inflammation of RA is not just restricted to joints,” said Dr. Amigues, a rheumatology fellow at Columbia University, New York. “We see it throughout the body, so of course it makes sense that we would see it in the heart as well. And now we see that we may be able to manage this with good disease management.
The study that found improvement of myocarditis with RA therapy was very small – just 8 patients and 12 controls – but the results were surprising and encouraging, Dr. Amigues said.
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The initial study examined chronic myocarditis in 119 patients with active RA; most (76%) were positive for anti-cyclic citrullinated peptides. They had a mean disease duration of 7 years. The mean Disease Activity Score was 3.8; 28% had low disease activity. About a third of the patients were taking a tumor necrosis factor inhibitor.
These patients were age- and gender-matched with 13 controls who did not have RA. All underwent cardiac FDG-PET scans as a marker of inflammation, as well as 3-D echocardiography to assess left ventricular mass and volume, and both systolic and diastolic function.
The maximum standard uptake value (SUVmax) in the scans was 12% higher in study patients than in the controls. This finding was associated with a higher body mass index and moderate to severe disease activity. After adjustment for BMI and RA treatment, the mean SUVmax was 30% higher for the patients with moderate to severe disease activity than in those who had low disease activity. Patients taking non-TNF biologics had 35% less cardiac inflammation than did those taking a TNF inhibitor or those not taking a biologic.
There were no significant associations with age, gender, race, diabetes, C-reactive protein or IL-6, coronary flow reserve, or coronary calcium. Inflammation was not related to any measure of cardiac structure or function on echocardiography.
“This finding makes sense, because we know that RA causes systemic inflammation, so it’s not surprising to see inflammation at the level of the heart,” Dr. Amigues said in an interview. “We do need longitudinal studies though to determine if structural or functional changes occur later on in the disease process.”
While the initial study didn’t look at cardiac changes in the disease process, Dr. Amigues’ subsequent study did find these associated with successful RA treatment. This follow-up study comprised eight patients who underwent PET scans and 3-D echocardiography at baseline and 6 months after initiation of a step-up treatment regimen. These were compared to 12 age- and gender-matched controls without RA, who had one baseline scan.
Most patients (87%) were women; their mean age was 62 years, and mean disease duration, 5 months. Most of the patients received TNF inhibitors with methotrexate as their step-up therapy; the rest were given triple therapy.
At the baseline scan, mean SUVmax was significantly higher in the patients than in controls (7.2 vs. 3.4 units). After 6 months of treatment, the mean DAS28 score among patients had decreased more than 1 point (4.57-3.51). Their mean SUVmax had also decreased to the level seen in controls. This was a significant improvement, Dr. Amigues said.
Again, there were no structural or functional differences between the two groups at baseline or follow-up, suggesting that cardiac inflammation is not inducing structural change – at least early in the RA disease process, Dr. Amigues said.
She reported having no relevant financial disclosures.
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