SNOWMASS, COLO. — Coronary artery disease in patients with rheumatoid arthritis is characterized by less extensive atherosclerosis but more inflammation and unstable atherosclerotic plaques than is coronary artery disease in arthritis-free matched controls, according to a first-of-its-kind autopsy study.
“We see less garden-variety CAD, with less multiple-vessel disease and a lower overall grade of stenosis,” Dr. Sherine E. Gabriel said at a symposium sponsored by the American College of Rheumatology.
Rheumatoid arthritis (RA) patients are known to have an increased risk of ischemic heart disease, compared with the general population. This elevated risk is present early in the course of RA. By the time patients meet ACR criteria for a diagnosis of RA, they already have a several-fold greater prevalence of prior hospitalization for acute myocardial infarction and electrocardiogram evidence of silent MI than do matched controls, noted Dr. Gabriel, the William J. and Charles H. Mayo Professor of Medicine and Epidemiology at the Mayo Clinic, Rochester, Minn.
The study by Dr. Gabriel and colleagues in the Rochester Epidemiology Project included 41 RA patients who died at a mean age of 79 years, 25 with known cardiovascular disease, who were matched by age, gender, and cardiovascular disease history to 82 non-RA controls.
Among subjects with cardiovascular disease, only 32% of RA patients were found at autopsy to have multivessel disease, vs. 61% of controls. Stenoses of 51% or greater were present in the left main arteries of only 7% of RA patients, vs. 54% of non-RA controls; there were similar trends in the left anterior descending and right coronary arteries. Coronary atherosclerosis was less extensive in the RA group, with only 32% having a score greater than 2 on a 4-point scale, vs. 61% of controls.
However, unstable plaques were found in the left anterior descending arteries of 48% of RA patients with cardiovascular disease, but in only 22% of controls. In addition, medial inflammation of the left circumflex artery was detected in 30% of RA subjects, compared with 9% of controls. Inflammation was also significantly more common in the adventitia of the left anterior descending artery of the RA patients than it was in controls (J. Rheumatol. 2007;34:937–42).
Similar trends (more evidence of inflammation but less extensive and severe atherosclerosis in the RA group) were noted in the subgroup of 18 RA subjects and 34 controls with a history of heart failure, Dr. Gabriel added.
She also presented highlights of a Rochester Epidemiology Project study showing the increased risk of ischemic heart disease in patients with RA precedes a diagnosis of the rheumatologic disease. The retrospective study involved 603 patients diagnosed with RA by the relatively strict ACR criteria at a mean age of 58 years, and 603 matched non-RA controls. A comprehensive analysis of all in- and outpatient medical records from age 18 years on showed that the RA group already had a threefold greater history of acute MI by the time their rheumatologic disease was diagnosed. Coronary disease in the RA group tended to present atypically, with less angina pectoris.
During a mean of 15 years follow-up post RA diagnosis, the rate of sudden cardiac death was 35 cases per 10,000 person-years in the RA group and 18 per 10,000 in controls. The rate of silent MI was also greater in the RA group, but cumulative incidence of angina remained less than in controls (Arthritis Rheum. 2005; 52:402–11).
Seven other population-based studies published in the last 5 years have shown a roughly twofold increased risk of ischemic heart disease in RA, Dr. Gabriel noted.
In the RA patients, atherosclerosis was less extensive but there was more inflammation. DR. GABRIEL