Abstract 14059: High Serum Erythropoietin Levels and the Development of Heart Failure in the General Population
Aims: In patients with heart failure (HF), serum erythropoietin (EPO) levels are elevated and associated with disease severity and outcome. Clinical trials with erythropoiesis-stimulating agents in HF and chronic kidney disease showed more adverse events. Whether endogenous EPO levels are prospectively associated with the development of HF or cardiovascular events in the general population is unknown.
Methods and results: Serum EPO levels were measured at baseline in 6,686 subjects enrolled in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study. Mean age (±SD) was 53±12 years, 49.8% were male, and median (IQR) EPO level was 7.7 (5.9-10.2) IU/L. During a median follow-up of 8.3 (7.7-8.8) years, 209 (3.1%) subjects were newly diagnosed with HF, 97 (1.5%) died of a cardiovascular cause and 386 (6.0%) subjects had a non-fatal cardiovascular event (277 cardiac events and 93 strokes). Each doubling of EPO level was multivariably associated with new onset HF (HR: 1.41, 95% CI: 1.14-1.76, P=0.002). EPO levels showed interaction with urinary albumin excretion (P=0.002) and were only associated with HF in subjects with microalbuminuria (HR: 1.53, 95% CI: 1.21-1.92, P<0.001, Figure 1). Also, EPO levels were only independently associated with HF of ischemic origin (HR: 1.58, 95% CI: 1.14-2.20, P=0.006), not with HF of other etiologies. There was an independent association of EPO levels with stroke in women (HR: 1.82, 95% CI: 1.24-2.65, P=0.002), but not in men. No association was observed for EPO levels with other cardiovascular events or cardiovascular mortality.
Conclusion: High serum EPO levels are independently associated with an increased risk of new onset HF in subjects with microalbuminuria. The interaction between EPO and microalbuminuria might be indicative for a role of the vascular endothelium in the mechanism linking EPO to HF. However, more research is needed to understand this association.
Author Disclosures: N. Grote Beverborg: None. H.H. van der Wal: None. I.T. Klip: Speakers Bureau; Modest; Vifor Pharma. A.A. Voors: Research Grant; Significant; Vifor Pharma. Consultant/Advisory Board; Modest; Vifor Pharma. R.A. de Boer: None. W.H. van Gilst: None. D.J. van Veldhuisen: Consultant/Advisory Board; Modest; Vifor Pharma, Amgen Inc.. R.T. Gansevoort: None. H.L. Hillege: None. P. van der Harst: None. S.J. Bakker: None. P. van der Meer: Research Grant; Significant; Vifor Pharma. Consultant/Advisory Board; Modest; Vifor Pharma.
- © 2015 by American Heart Association, Inc.