Aubry M-C, Maradit-Kremers H, Reinalda MS, Crowson CS, Edwards WD, Gabriel SE. Differences in atherosclerotic coronary heart disease between subjects with and without rheumatoid arthritis. J Rheumatol first release. March 15, 2007.

Posted 3/21/2007

It has been well documented that people with rheumatoid arthritis (RA) have a reduced life expectancy compared with the general population. It also has been established that the excess mortality associated with RA can largely be attributed to cardiovascular disease (CVD). The underlying links between the two diseases, however, are not completely understood.

What Problem Was Studied?
Atherosclerosis (also called “hardening of the arteries”) occurs when plaques form within the arteries that feed the heart, closing the opening. Once the arteries close beyond a certain point, the condition is called coronary artery disease and the risk of heart attack, stroke, or sudden death are greatly increased. Atherosclerosis is generally recognized as an inflammatory immune disorder. Similarly, RA is an immune-mediated inflammatory disorder that can result in death due to CVD.

Researchers at the Mayo Clinic in Rochester, Minn., including past Arthritis Foundation grant recipient Sherine E. Gabriel, MD, MSc, have conducted a study that has given them insight as to what happens within the coronary arteries of people with these diseases. Results of their research were published in the Journal of Rheumatology, First Release March 15, 2007.

What Was Done in the Study?
Scientists studied the heart and arteries of 41 people with RA who had died and 82 age- and sex-matched people without RA who died within the same timeframe. The patients and controls were also matched as to the presence or absence of CVD. The autopsied coronary arteries were all examined under the microscope to look for similarities and differences among those with RA and those without.

An overall grade of stenosis (amount of obstruction due to plaque formation) was given for each artery, and the extent of atherosclerosis was defined by the total number of vessels with severe stenosis. Next, the cellular composition of the plaques was determined. Lastly, plaques were defined as vulnerable or stable. Vulnerable plaques are those with a greater number of inflammatory cells, are prone to rupture, and lead to acute coronary events, such as heart attack or stroke.

What Were the Study Results?
In the subset of subjects with CVD, significant differences were found in the arteries of people with RA compared to those without RA. Only 32% of RA patients with CVD had multiple-vessel disease, whereas 69% of CVD patients without RA had multiple-vessel disease. RA patients had an overall lower grade of stenosis compared with the non-RA subjects. RA patients with CVD had significantly more vulnerable plaques than CVD patients without RA (48% versus 22%).

All combined, the data collected by this research team showed increased inflammation in the walls of coronary arteries and an increased number of vulnerable plaques in RA patients with CVD compared to CVD patients without RA. Despite the inflammation and vulnerable plaques, RA patients with CVD had arteries with less stenosis (that is, were more open) than the controls with CVD but no RA.

What Does This Mean for People With RA?
The findings of this study suggest that inflammation plays an important role in the development of CVD in people with RA. Furthermore, the study authors indicate that because RA patients had less severe stenosis, a different biological mechanism must explain the excess risk of cardiovascular disease in this population. Additional studies will be needed to determine exactly what that mechanism is.

Considering the results of this study, lead investigator, Marie-Christine Aubry, MD, believes that people with RA and the physicians who care for them ought to be aware of their potentially increased risks for CVD and work together to minimize those risks.