Authors
Jasper Tromp
Mohsin A.F. Khan
IJsbrand T. Klip
Sven Meyer
Rudolf A. de Boer
Tiny Jaarsma, Australian Catholic University
Hans L. Hillege
Dirk J. van Veldhuisen
Peter van der Meer
Adriaan A. Voors
Publication Date
1-1-2017
Publication Details
Tromp, J., Khan, M. A, Klip, I. T, Meyer, S., de Boer, R. A, Jaarsma, T., Hillege, H. L, van Veldhuisen, D. J, van der Meer, P. & Voors, AA. (2017). Biomarker profiles in heart failure patients with preserved and reduced ejection fraction. Journal of the American Heart Association,6(4), J. A. Vita. 1-25. United States: Wiley-Blackwell Publishing, Inc.. Retrieved from https://doi.org/10.1161/JAHA.116.003989
Abstract
Background--Biomarkers may help us to unravel differences in the underlying pathophysiology between heart failure (HF) patients with a reduced ejection fraction (HFrEF) and a preserved ejection fraction (HFpEF). Therefore, we compared biomarker profiles to characterize pathophysiological differences between patients with HFrEF and HFpEF. Methods and Results--We retrospectively analyzed 33 biomarkers from different pathophysiological domains (inflammation, oxidative stress, remodeling, cardiac stretch, angiogenesis, arteriosclerosis, and renal function) in 460 HF patients (21% HFpEF, left ventricular ejection fraction ≥45%) measured at discharge after hospitalization for acute HF. The association between these markers and the occurrence of all-cause mortality and/or HF-related rehospitalizations at 18 months was compared between patients with HFrEF and HFpEF. Patients were 70.6±11.4 years old and 37.4% were female. Patients with HFpEF were older, more often female, and had a higher systolic blood pressure. Levels of high-sensitive C-reactive protein were significantly higher in HFpEF, while levels of pro-atrial-type natriuretic peptide and N-terminal pro-brain natriuretic peptide were higher in HFrEF. Linear regression followed by network analyses revealed prominent inflammation and angiogenesis-associated interactions inHFpEF and mainly cardiac stretch-associated interactions in HFrEF. The angiogenesis-specific marker, neuropilin and the remodeling-specific marker, osteopontin were predictive for all-cause mortality and/or HF-related rehospitalizations at 18 months in HFpEF, but not in HFrEF (P for interaction < 0.05). Conclusions-In HFpEF, inflammation and angiogenesis-mediated interactions are predominantly observed, while stretchmediated interactions are found in HFrEF. The remodeling marker osteopontin and the angiogenesis marker neuropilin predicted outcome in HFpEF, but not in HFrEF.
School/Institute
Mary MacKillop Institute for Health Research
Document Type
Journal Article
Access Rights
ERA Access