Myocardial Inflammation Detected in Once Heart-Healthy RA Patients

Jan 18, 2017

Myocardial inflammation/fibrosis has been identified in a study of rheumatoid arthritis patients with no known history of heart disease.

Researchers writing in Arthritis Care & Research say that they have identified associations between myocardial inflammation/fibrosis and adult rheumatoid arthritis using cardiac magnetic resonance imaging.

Heart failure and myocardial dysfunction are more common among patients with rheumatoid arthritis as compared with non-rheumatoid arthritis patients, and associated with higher death rates from heart disease. This study demonstrated the value of using cardiac magnetic resonance (cMR) imaging to examine the myocardium of rheumatoid arthritis patients. Knowledge gained from this research may help with early identification of myocardial abnormalities and enhance the use of novel imaging techniques with rheumatoid arthritis patients.

“Our data suggest that cMR findings indicating myocardial inflammation and fibrosis are correlated with RA disease activity, systemic inflammation, and alterations in myocardial structure known to associate with myocardial dysfunction and precede clinical heart failure. Additionally, NT-proBNP may prove a useful biomarker of these myocardial abnormalities, leading to the identification of high-risk RA patients and possibly a tool for HF prevention,” wrote researchers led by Jon T. Giles, M.D., MPH, of Columbia University.

Historically, studies of myocardial histopathology have been difficult because they often involved invasive biopsies of endomyocardial tissue. Today, more non-invasive tools like cardiac magnetic resonance imaging are available to researchers. A benefit of cardiac magnetic resonance imaging is that it can locate structural and functional changes in the left ventricle that may lead to heart failure.

The Study

This study was conducted with 60 rheumatoid arthritis patients with no known heart disease or risk factors for heart disease. Patients underwent gadolinium-enhanced cardiac magnetic resonance imaging to assess left-ventricular structure and functional parameters, myocardial late gadolinium enhancement (a signal for myocardial fibrosis) and T2-weighted imaging (a signal for active inflammation or myocarditis). Using various statistical methods, associations between rheumatoid arthritis characteristics and N-terminal pro-brain natriuretic protein levels with myocardial late gadolinium enhancement and T2-weighted imaging were evaluated.

“To our knowledge, ours is among the largest studies of cMR abnormalities in RA, and the only study to explore the multivariable associations of RA characteristics, systemic inflammatory markers, CVD risk factors, and NTproBNP with cMR-assessed myocardial abnormalities. We observed that LGE was independently associated with RA disease activity and systemic inflammation. Secondly, higher NTproBNP was associated with a more than 20-fold higher odds of LGE, and median NT-proBNP was more than double in the group with T2WI compared with the group without any myocardial abnormality,” the researchers wrote.

Other imaging findings demonstrated that myocarditis was associated with myocardial hypertrophy and ventricular thinning. This relationship suggests some degree of cardiomyopathy.

There were a number of limitations to this study, including the small sample size. However, the authors noted, even small differences were statistically significant.

Recommended Next Steps

More imaging studies are needed better understand the associations between rheumatoid arthritis and heart disease. Future research in this area may improve the identification of biomarkers for heart disease in patients with rheumatoid arthritis, and reduce morbidity and mortality.

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References:

Hitomi Kobayshi, Yasuyuki Kobayashi, Isamu Yokoe, et. al. “Magnetic Resonance-Detected Myocardial Inflammation and Fibrosis in Rheumatoid Arthritis: Associations of Disease Characteristics and N-terminal pro Brain Natriuretic Peptide Levels.” Arthritis Care & Research. Published online November 3, 2016. DOI: 10.1002/acr.23138

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