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Study: MRI-detected myocardial inflammation and fibrosis are associated with RA
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Cardiac MRI findings indicated myocardial inflammation and fibrosis were associated with rheumatoid arthritis disease activity, according to published results.
Researchers studied 60 patients with rheumatoid arthritis (RA; mean age, 57 years; 14% were men) with no known heart disease or risk factors who underwent gadolinium-enhanced cardiac MRI. Patients were recruited between December 2012 and May 2015. Lett-ventricular (LV) structural and functional parameters and myocardial late gadolinium enhancement (LGE), an indicator of myocardial fibrosis and T2-weighted imaging were measured through the images.
“We modeled the assocations between RA characteristics and N terminal pro-brain natriuretic protein (NT-proBNP) levels with LGE and T2-weighted imaging,” the researchers wrote. “We also assessed whether LGE and/or T2-weighted imaging were associated with abnormal LV structure of dysfunction.”
LGE was found in 32% of patients and T-2 weighted imaging was found in 12% of patients, including five patients who also had LGE. There were higher odds of LGE related to each additional swollen joint (OR = 1.87), each additional log unit of C-reactive protein level (OR = 3.36) and each additional unit of NT-proBNP (OR = 20.61) after investigators adjusted for relevant confounders.
Patients with T2-weighted imaging had a 135% higher NT-proBNP compared with patients without T2-weighted imaging or LGE.
“Higher LV mass index and LV mass:end diastolic volume ratio were observed in those with T2-weighted imaging in those with T2-weighted imaging than in those with no myocardial abnormalities and in those with LGE without T2-weighted imaging; however, ejection fraction was not reduced in those with either LGE or T2-weighted imaging,” the researchers wrote.
“[Our] data suggest that cardiac MR findings indicating myocardial inflammation and fibrosis are correlated with RA activity, systemic inflammation and alterations in myocardial structure known to be associated with myocardial dysfunction and precede clinical [heart failure] HF,” the researchers concluded. “Additionally, NT-proBNP may prove to be a useful biomarker of these myocardial abnormalities, leading to the identification of high-risk RA patients and possibly a tool for HF prevention.” – Bruce Thiel
Disclosures: The researchers report no relevant financial disclosures.
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Kobayashi H, et al. Arthritis Care & Res. 2017;doi:10.1002/acr.23138
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