SAN FRANCISCO — Patients with rheumatoid arthritis have a “markedly” lower mean left ventricular mass than do age-matched controls, a finding that provides what may be a significant clue to elevated cardiovascular mortality in this population, according to a group of Maryland researchers.
The specific mechanisms underlying cardiovascular risk are only now being fully explored in this population, in part because RA patients often fail to present with the classic early signs and symptoms of cardiac disease, commented Dr. Jon Giles, who is a rheumatologist at the Johns Hopkins Division of Rheumatology in Baltimore, in a presentation given at the recent annual meeting of the American College of Rheumatology.
For example, Dr. Giles cited heart failure rates that are “nearly doubled” in RA patients.
Yet, “little is known about the myocardial changes that precede clinical heart failure in these patients,” he said.
Dr. Giles and his associates turned to cardiac MRI, a highly sensitive tool for assessing left ventricular structure and function, to hunt for preclinical risk factors for heart failure.
Rheumatoid arthritis patients with moderate disease (average 7 years' duration) who enrolled in the ESCAPE RA trial (n = 75) were compared with 775 participants in the Multi-Ethnic Study of Atherosclerosis who did not have RA. None of the members of either group had a history of cardiovascular events or procedures.
The rheumatoid arthritis cohort was younger than was the control group (mean age 59, compared with 63), and was also less likely to have a diagnosis of diabetes (4% versus 14%) or hypertension (32% versus 49%).
However, the patients' mean unadjusted left ventricular mass was 18% lower (120 g/m
The difference was particularly pronounced for male patients with RA, whose mean adjusted left ventricular mass was found to be fully 19% lower than that of men who did not have a rheumatoid arthritis diagnosis.
Female rheumatoid arthritis patients had a 9% lower left ventricular mass than did women without the inflammatory disease.
In both the RA and control groups, mean left ventricular mass decreased with age.
However, it was lower in rheumatoid arthritis patients than in controls in every age group, including the youngest patients in the study.
“In fact, the mean left ventricular mass was lower in 45-year-old RA patients than mean left ventricular mass in 80-year-old control patients, regardless of gender,” Dr. Giles commented during his podium presentation.
Left ventricular stroke volume was marginally lower in RA patients than in controls, significantly so in men.
“Small but significant” reductions in adjusted mean ejection fraction were seen as well, Dr. Giles said.
No differences were seen in RA patients and controls with regard to adjusted mean end diastolic volume.
The Johns Hopkins team also explored potentially significant associations between cardiovascular risk markers and RA disease characteristics such as disease severity, activity, treatment, and systemic inflammation.
They found only two factors that were independently associated with left ventricular mass, stroke volume, and end diastolic volume in rheumatoid arthritis patients.
One factor was increased anti-cyclic citrullinated peptide antibodies.
The other was the use of biological disease-modifying drugs (predominantly tumor necrosis factor-α inhibitors).
No characteristics were associated with ejection fraction.
The study findings raise intriguing questions about whether rheumatoid arthritis and its treatment heighten patients' cardiovascular risk through different mechanisms than in the general, non-RA population, said Dr. Giles.
For example, markedly lower left ventricular mass may reflect the “aftereffects” of subclinical myocarditis.
On the other hand, lower left ventricular mass measurements “may support the concept that RA is a disorder of accelerated aging,” he said.
Dr. Giles and his associates reported having no financial conflicts of interest with regard to this study.
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