The presence of rheumatoid arthritis in individuals who died from a myocardial infarction was associated with greater inflammatory burden at different levels of myocardial tissue than in those without the disease in a small, retrospective, case-control autopsy study.
“These findings support the hypothesis that RA [rheumatoid arthritis] patients are prone to develop more vulnerable plaques due to more inflammation in the coronary arteries, but also develop increased intramyocardial inflammation indicative of a higher risk of myocardial tissue damage post MI. This might not only explain the higher incidence of cardiovascular events in this population, but also the higher fatality rate after myocardial infarction,” wrote Dr. Inge A.M. van den Oever of the Amsterdam Rheumatology and Immunology Center and colleagues (Int J Cardiol. 2016 Feb 3. doi: 10.1016/j.ijcard.2016.02.065).
The investigators took tissue samples from the infarcted left ventricle and microscopically determined infarct border area of five patients with RA and MI and five controls with MI but without RA. They found that RA patients had a greater burden of inflammatory cells in the adventitia of infarct-related epicardial coronary arteries, the intramyocardial vasculature, and the border area of the infarcted heart, compared with controls matched for age, sex, year of death, grade of stenosis, and infarct phase.
Specifically, the adventitial layer of the infarct-related epicardial coronary artery of RA patients had significantly more lymphocytes and mast cells. Intramyocardial arteries in infarct and infarct border areas of RA patients, compared with controls, showed significantly greater staining for advanced glycation end product N-epsilon-(carboxymethyl) lysine (CML), which is thought to reflect oxidative damage to cells, as well as noninfarcted tissues taken from the right ventricle.
The researchers included cases and controls from a postmortem tissue database of subjects who underwent autopsy within 24 hours after death at the VU University Medical Centre, Amsterdam, between January 1990 and December 2010.
The research was partly funded by a grant from the Dutch Society for Rheumatology. The authors had no conflicts of interest to declare.