Rheumatoid arthritis (RA) is a lifelong and developing disease that is characterized by increasing inflammation of the joints throughout the body. It generally involves the patient’s immune system attacking the joints and causing them to be warm, swollen, and painful. Furthermore, it is known that the disease might also affect other body organs and tissues causing anemia and inflammation around the lungs and heart.
A recent study led by Dr. John M. Davis III looked at the influence of RA on this last particular vital organ. The study included 160 RA patients and 1,391 healthy individuals from the Rochester Epidemiology Project, who were followed for 4-5 years. Patients were evaluated by a registered diagnostic cardiac sonographer that used electrocardiography to assess the structural and hemodynamic parameters of the heart.
The study presented during this year’s European League Against Rheumatism Annual European Congress of Rheumatology showed there are differences in the hearts of RA patients compared to healthy controls. This might be a hint of the effect of these specific autoimmune processes in the heart. RA patients have accelerated diastolic heart dysfunction, a form of heart failure mainly affecting elderly, diabetic and hypertensive patients.
The data presented by the researchers might help doctors address particular needs of RA patients regarding heart health status in the future, either with directed therapies or early diagnosis of clinically meaningful heart failure.
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A new study led by researchers at The Walter and Eliza Hall Institute of Medical Research and the University of Melbourne in Australia recently revealed a link between rheumatoid arthritis (RA) and heart valve disease, based on a key inflammatory protein. The study was recently published in the journal Proceedings of the National Academy of Sciences (PNAS) and is entitled “Spontaneous retrotransposon insertion into TNF 3′UTR causes heart valve disease and chronic polyarthritis”. This is the first study involving an animal model that demonstrated polyarthritis and heart disease can result from TNF deregulation, suggesting that drugs able to block and remove TNF, and consequently reduce inflammation, could be investigated as a therapy for heart valve diseases.