medwireNews: Individuals with treatment-naïve early rheumatoid arthritis (RA) show evidence of cardiovascular disease (CVD) that improves following initiation of DMARD therapy, UK research shows.
The improvements occurred regardless of whether patients were being treated with a biologic or conventional DMARD, and imply that the benefits of therapy extend “beyond suppression of systemic inflammation, likely suggesting cardiometabolic changes and targeted effects on key immune mediators of CVD,” write Maya Buch (University of Manchester) and co-authors in the Annals of the Rheumatic Diseases.
The researchers found that the 81 individuals with early RA and no known history of CVD had abnormal vascular stiffness, reduced left ventricular mass, and evidence of diffuse myocardial fibrosis when compared with 30 matched controls without RA or risk factors for CVD.
Specifically, baseline mean aortic distensibility – a measure of vascular stiffness – was significantly lower among the patients with RA than among the controls, at 3.0×10−3 per mmHg versus 4.4×10−3 per mmHg, and remained so after adjustment for age, sex, blood pressure, and smoking.
Buch et al explain that they chose aortic distensibility as their primary endpoint because it “has been shown to predict major CV events independently of traditional clinical risk scoring models in patients without known [CVD].”
They believe “[t]he presence of abnormal vascular stiffness […] at the earliest stage of diagnosis of RA highlights the increased risk in this population.”
Left ventricular mass was also significantly lower in the RA versus control groups, at a mean of 78.2 g versus 92.9 g, whereas myocardial extracellular volume – a marker of myocardial fibrosis – was significantly higher, at 27.1% versus 24.9%.
Among the patients with RA, mean aortic distensibility improved by a significant 20% to 3.6×10−3 per mmHg following a year of randomly assigned treatment with either etanercept plus methotrexate or methotrexate monotherapy.
Left ventricular mass also improved significantly following DMARD treatment, to 81.4 g, and there was a nonsignificant improvement in myocardial extracellular volume, to 26.4%.
The investigators report that the observed improvements were sustained for up to 2 years and did not differ significantly between the two treatment arms or between responders and non-responders, as defined by a DAS28-ESR score below 2.6 points.
They comment that their findings could “have wider implications on RA management strategies including DMARD tapering.”
Buch and team conclude: “While this study was not designed to address this, by demonstrating improvement in CV markers, and until further data are available, this should be considered if contemplating drug tapering.”
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