(RxWiki News) People with rheumatoid arthritis suffer from inflammation of the joints. That inflammation can spread to other organs, causing additional health problems. Atherosclerosis (hardened arteries) may be one of these problems.
Plaque in the carotid arteries builds up early in rheumatoid arthritis patients. Inflammation in these patients may play a role in the progression of subclinical atherosclerosis (atherosclerosis that has yet to show symptoms).
"Get screened for atherosclerosis if you have rheumatoid arthritis."
Past studies have shown that rheumatoid arthritis patients have a high risk for atherosclerosis - a disease in which fat, cholesterol, and other substances build up on the walls of the arteries, blocking regular blood flow.
Atherosclerosis can cause a variety of health complications like heart attack and stroke.
Jon T. Giles, M.D., M.P.H., of Columbia University and colleagues wanted to find out if there were predictors for the progression of atherosclerosis in rheumatoid arthritis patients.
According to Frank W. Meissner, M.D., Clinical Assistant Professor of Medicine at the Paul L Foster School of Medicine at Texas Tech University Health Sciences Center in El Paso, Texas, "Epidemiological work has demonstrated for many years that rheumatoid arthritis is a significant risk factor for the development of symptomatic coronary artery disease and, as illustrated by the classical paper of Maradit-Kremers, et. al. (Mayo Clinic) Arthritis Rheum. 2005 Feb;52(2):402-11, the incidence of self report of angina (chest pain when the heart lacks oxygenated blood) symptoms is less in rheumatoid arthritis patients compared to non-arthritis patients, as well as this group has a higher rate of unrecognized [heart attack] and higher rate of sudden cardiac deaths."
For their study, Dr. Giles and colleagues measured the thickness of the common carotid artery, an artery that supplies blood to the head and neck, and the internal carotid arteries, arteries in the head and neck that supply blood to the brain, in 158 rheumatoid arthritis patients.
All of the participants in the study had their carotid arteries measured with ultrasonography at the start of the study and 3.2 years later. The thickness of these arteries is a measure of atherosclerosis.
The researchers found that the thickness of the common carotid artery increased in 82 percent of participants while the thickness of the internal carotid artery increased in 70 percent of participants.
Patients in the earlier stages of rheumatoid arthritis had much greater change in the thickness of their common carotid artery, compared to those who had rheumatoid arthritis for a longer period of time.
The researchers also found that drugs called tumor necrosis factor (TNF) inhibitors slowed down the growth of carotid arteries. Patients who took TNF inhibitors had a 37 percent lower rate of progression in the thickness of the common carotid artery, compared to those who did not take the drugs.
The authors conclude that the study's findings "provide evidence that inflammation is a contributor to the progression of subclinical atherosclerosis in [rheumatoid arthritis]."
"In my own clinical experience, this association between [heart disease] and rheumatoid arthritis is under-appreciated by both the general practitioner as well as many cardiovascular disease specialists," says Dr. Meissner, who was not involved in the study. "This may reflect the general bias to discount the probability of symptomatic CAD occurring in the patient due to gender, as many more women than men suffer from rheumatoid arthritis."
The study's authors add that TNF inhibitors had positive effects on the progression of disease, while glucocorticoids had a negative effect.
According to Dr. Meissner, "The paper by Giles, et. al. is consistent with an available and consistent body of literature suggesting an intimate link between cholesterol plaque progression and instability and the overall degree of inflammatory processes acting upon all patients, but especially in patient's with rheumatoid arthritis."
The study is published in Arthritis & Rheumatism.
