Chronic Inflammation May Explain Heart Disease in Rheumatoid Arthritis

Chronic Inflammation May Explain Heart Disease in Rheumatoid Arthritis

Patients with rheumatoid arthritis have chronic inflammation in the heart, which may explain the common occurrence of heart disease in this patient group. The good news is it may be possible to control the inflammation by increasing the intensity of arthritis treatment, which may act to prevent heart disease.

Those findings were presented at the 2016 ACR/ARHP Annual Meeting in Washington, D.C., Nov. 11-16. Researchers at Columbia University in New York City used the same method to analyze heart inflammation in rheumatoid arthritis patients in two studies.

Although the method, a type of positron emission tomography (PET) imaging, has been used to assess heart inflammation in a condition known as sarcoidosis, it never has been used to assess heart inflammation in rheumatoid arthritis.

The first study recruited 118 rheumatoid arthritis patients without known heart disease. In addition to assessing inflammation, the research team used three-dimensional echocardiography to evaluate the mass and volume of the left ventricle. They also analyzed how well the heart was working.

The patient group had an average age of 55 years, a mean body mass index (BMI) of 28.5, and 81% were women. Although they had been ill for a median of seven years, the majority had low disease activity, or were in remission during the study.

Researchers found that patients had 12% higher levels of an inflammation measure compared to 13 individuals in the control group. They also found that a higher BMI and more severe disease activity was linked to a higher degree of inflammation. When adjusting the analyses for BMI and treatment, patients with moderate or severe disease activity had 30% higher levels of inflammation than those with low disease activity.

Interestingly, the team found that patients treated with a biological drug other than a TNF (tumor necrosis factor) blocker had 35% lower levels of inflammation compared to patients who were not on biological treatment, or who were treated with a TNF blocker.

Also, the team could not find any links between the levels of inflammation and structural changes in the heart. But researchers argued that it is possible that inflammation precedes changes in heart structure or function.

“Further longitudinal studies are needed to assess the impact of baseline myocardial inflammation on adverse myocardial changes over time,” Joan M. Bathon, MD, Director of Rheumatology at Columbia, said in a press release.

Bathon also argued that the correlation between disease activity and inflammation pointed to the possibility that arthritis treatment could bring the inflammation under control.

So, in a second study, the team attempted to see how an increase in treatment with disease-modifying antirheumatic drugs (DMARDs) affected heart inflammation. The study recruited 12 patients who had not responded well to methotrexate treatment. After the initial heart scan, the patients’ treatment was increased, and they were analyzed again after six months.

Of the eight patients who completed the study, 25% were on a three-drug treatment, and 75% received a TNF blocker as an add-on to methotrexate. The study showed that the increased treatment lowered the levels of inflammation to the same levels as controls.

“Although this was a pilot study, we were excited to observe an improvement in myocardial inflammation with treatment of the patients’ RA,” said Bathon, adding that larger and longer studies are needed to confirm the findings.

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