Title

P6223 Restless legs syndrome is an independent risk factor for heart failure with preserved ejection fraction

Aurora Affiliations

Center for Integrative Research on Cardiovascular Aging

Aurora Research Institute

Aurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke's Medical Centers

Abstract

Background: Restless legs syndrome (RLS), a poorly recognised sleep disorder, has been recently associated with atrial fibrillation and ventricular hypertrophy but its association with heart failure with preserved ejection fraction (HFpEF) is not known.

Methods: RLS patients fulfilling International Restless Legs Syndrome Study Group criteria were identified from a large community-based sleep center and those without history of heart failure (HF) and with preserved left ventricular ejection fraction (LVEF) (≥50%) were propensity-matched (age, sex, hypertension, hyperlipidemia, diabetes, prior myocardial infarction (MI), atrial fibrillation) to non-RLS patients. Development of new onset HFpEF in the two groups, and predictors of HFpEF were determined using Cox Proportional hazard model.

Results: A total of 432 patients with RLS who had a baseline echocardiogram with preserved LVEF between 2012–2015 were identified and 1:1 propensity-matched to non-RLS patients with preserved LVEF (mean age 56±13.7 years, 62% female). Over a mean follow-up of 18±8 months, new onset heart failure developed in 63 (14.6%) patients with RLS compared to 37 (8.6%) in non-RLS group (OR 1.9, 95% CI 1.2–2.9; p=0.004). Only 5% of patients with new onset HF had reduced LVEF (mean 33.7%±10.8%), while 95% had LVEF ≥50% (mean 62.8% ± 0.7% p<0.001). RLS (OR 2.16, 95% CI 1.36–3.42; p=0.001), prior MI (OR 3.89, 95% CI 1.38–10.95; p=0.01), hypertension (OR 3.66, 95% CI 1.25–10.76; p=0.02), diabetes mellitus (OR 2.75, 95% CI 1.64–4.59; p<0.01), and age (OR 1.05, 95% CI 1.02–1.07; p<0.001) were independent predictors of HFpEF.

Conclusion: Independent of prior MI, hypertension, diabetes and age, the presence of RLS was associated with the development of HFpEF, suggesting this to be an unrecognized risk factor for HF. Further investigation confirming this association, mechanisms and whether control of RLS reduces the development of HFpEF are warranted.

Document Type

Poster

DOI

10.1093/eurheartj/ehx493.P6223

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