(RxWiki News) Rheumatoid arthritis patients have a higher risk of heart-related problems, including hardened arteries. In order to protect the heart health of these patients, researchers must find what causes these heightened risks.
In a recent study, people with rheumatoid arthritis developed hardened arteries (atherosclerosis) mainly due to the normal risks of heart disease, such as age and smoking.
Long-term use of steroids was the only factor related to rheumatoid arthritis that increased the risk of hardened arteries.
"Quit smoking to protect your heart."
Petros P. Sfikakis, M.D., of Athens University Medical School, and colleagues wanted to find out what leads to the formation of new carotid plaques (the substance that hardens arteries) in patients with rheumatoid arthritis.
The hardening of the arteries is also called atherosclerosis. This condition develops when fat, cholesterol, and other substances build up in the walls of the artery, forming a hard substance called plaque. Eventually, these plaques can grow so thick that they clog the arteries, leading to problems in many parts of the body.
From their study, the researchers found that the main difference between rheumatoid arthritis patients who developed new plaque and those who did not was age - a traditional risk factor for hardened arteries.
The researchers looked at a variety of factors related to rheumatoid arthritis that might increase the risk of hardened arteries. The arthritis-related factor that seemed to lead to the formation of new plaques was the long-term use of steroid drugs.
Smoking habits also played a role in the development of new plaques in people with rheumatoid arthritis.
"Smoking - which has a higher prevalence in Greece than in other European Union countries - and age were the main factors 'defining' the new carotid plaque formation in the present population as expected in [non-rheumatoid arthritis] populations," the authors write.
In other words, these normal risk factors for hardened arteries were the main reasons that the arthritis patients in this study developed new plaques.
"This clearly shows the need to optimally control classical [cardiovascular disease] risk factors in [rheumatoid arthritis] patients," the authors write.
"The association between accelerated progression of [coronary artery disease] and rheumatoid arthritis is well known and well described," says Frank Meissner, M.D., an invasive cardiologist and clinical assistant professor of medicine at the Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center.
"The current study while interesting has numerous methodological issues that make generalization of the results impossible," says Dr. Meissner, who was not involved in the study.
Previous research has found links between hardened arteries and inflammation. As rheumatoid arthritis is an inflammatory disease, it could be possible that the inflammation of arthritis somehow contributes to the hardening of the arteries.
This study's results, however, show no link between inflammation and traditional risk factors for heart-related problems.
"Striped of the statistics, the study concludes that in patients with rheumatoid arthritis, aging and the life limiting habit of tobacco smoking increases your risks of developing imaging detectable plaque. Hardly an exciting or revolutionary result," says Dr. Meissner.
"Furthermore, since all patients had [rheumatoid arthritis], there is no way to estimate the effects of [rheumatoid arthritis] alone on the development of plaque," he explains.
For their research, Dr. Sfikakis and colleagues looked for the formation of new plaques in 64 rheumatoid arthritis patients for an average of three and a half years. Of these patients, 35 were compared to otherwise healthy individuals.
The researchers found that rheumatoid arthritis patients had a similar number of new plaque formations as their "healthy" counterparts. However, more rheumatoid arthritis patients had plaques at the beginning of the study, compared to the healthy individuals.
The authors note that their study may have had difficulties pinpointing differences in risk for two reasons: the small size and the focus on new plaque formations rather than pre-existing plaques.
They conclude that the formation of new plaques depended mainly on traditional cardiovascular risk factors. While the use of steroids contributed to the formation of new plaques, it did not play as large of a role as age and smoking.
Dr. Meissner believes that the main result of interest is that steroid use is associated with "disease severity and activity, and thus stands in as surrogate marker for the effects of [rheumatoid arthritis] on risks for development of and clinical expression of atherosclerotic disease."
"So from my standpoint," says Dr. Meissner, "the principle result of the study of interest is that more severe [rheumatoid arthritis] (as evidenced by the chronic use of steroid therapy) makes it more likely that plaque would develop in the carotid arteries over the period of observation.
"This result is consistent with what is known about the coronary artery system. However, as to the practical, operational, or even theoretical understanding of coronary artery disease, the study has limited usefulness. However, it is consistent with the available body of knowledge related to atherosclerotic disease development and progression."
Dr. Sfikakis and colleagues believe that their findings suggest that rheumatoid arthritis treatments should be designed to both reduce inflammation and address the traditional risks of heart disease.
"Optimal [rheumatoid arthritis] management should aim to achieve not only sustained disease remission, but also successful tradition [cardiovascular disease] risk reduction and this may have implications in terms of drug regimen selection," they write.
This longitudinal study is published in the journal Arthritis Research & Therapy.
