Biomarkers in acutely decompensated heart failure with preserved or reduced ejection fraction

Kalkidan Bishu, Anita Deswal, Horng Haur Chen, Martin M. Lewinter, Gregory D. Lewis, Marc J. Semigran, Barry A Borlaug, Steven McNulty, Adrian F. Hernandez, Eugene Braunwald, Margaret May Redfield

Research output: Contribution to journalArticle

61 Citations (Scopus)

Abstract

Background: Acute decompensated heart failure (ADHF) occurs with preserved (heart failure with preserved ejection fraction [HFpEF] ≥50%) or reduced (heart failure with reduced ejection fraction [HFrEF] <50%) ejection fraction. Natriuretic peptide (NP) levels are lower in HFpEF than HFrEF. We hypothesized that lower NP levels in HFpEF may be associated with other differences in biomarkers, specifically, renin-angiotensin-aldosterone system (RAAS) activation, oxidative stress, and a biomarker that reflects collagen synthesis. Methods: In this prespecified ancillary analysis of patients with ADHF enrolled in the Diuretic Optimization Strategies Evaluation study, clinical features and N-terminal pro-B-type NP, cystatin C, plasma renin activity, aldosterone, oxidative stress (uric acid), and procollagen type III N-terminal peptide were compared in HFpEF and HFrEF at enrollment and 60-day follow-up. Results: Compared with HFrEF (n = 219), HFpEF (n = 81) patients were older, heavier, more commonly female, less treated with RAAS antagonists, but with similar New York Heart Association class, jugular venous pressure, and edema severity. N-terminal pro-B-type NP was lower, and systolic blood pressure and cystatin C were higher in HFpEF. Despite higher systolic blood pressure and less RAAS antagonist use in HFpEF, plasma renin activity and aldosterone levels were similar in HFpEF and HFrEF as were uric acid and procollagen type III N-terminal peptide levels. Changes in biomarker levels from enrollment to 60 days were similar between HFrEF (n = 149) and HFpEF (n = 50). Conclusion: Lower NP levels in decompensated HFpEF occur in association with similar ADHF severity, more impaired vascular and renal function but similar elevation of biomarkers that reflect RAAS activation, oxidative stress, and collagen synthesis as in HFrEF.

Original languageEnglish (US)
JournalAmerican Heart Journal
Volume164
Issue number5
DOIs
StatePublished - Nov 2012

Fingerprint

Heart Failure
Biomarkers
Renin-Angiotensin System
Natriuretic Peptides
Mineralocorticoid Receptor Antagonists
Cystatin C
Oxidative Stress
Brain Natriuretic Peptide
Blood Pressure
Uric Acid
Aldosterone
Renin
Collagen
Venous Pressure
Diuretics
Blood Vessels
Edema
Neck

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Biomarkers in acutely decompensated heart failure with preserved or reduced ejection fraction. / Bishu, Kalkidan; Deswal, Anita; Chen, Horng Haur; Lewinter, Martin M.; Lewis, Gregory D.; Semigran, Marc J.; Borlaug, Barry A; McNulty, Steven; Hernandez, Adrian F.; Braunwald, Eugene; Redfield, Margaret May.

In: American Heart Journal, Vol. 164, No. 5, 11.2012.

Research output: Contribution to journalArticle

Bishu, Kalkidan ; Deswal, Anita ; Chen, Horng Haur ; Lewinter, Martin M. ; Lewis, Gregory D. ; Semigran, Marc J. ; Borlaug, Barry A ; McNulty, Steven ; Hernandez, Adrian F. ; Braunwald, Eugene ; Redfield, Margaret May. / Biomarkers in acutely decompensated heart failure with preserved or reduced ejection fraction. In: American Heart Journal. 2012 ; Vol. 164, No. 5.
@article{90c935dffe5f49a6b4576b3ccaa8f693,
title = "Biomarkers in acutely decompensated heart failure with preserved or reduced ejection fraction",
abstract = "Background: Acute decompensated heart failure (ADHF) occurs with preserved (heart failure with preserved ejection fraction [HFpEF] ≥50{\%}) or reduced (heart failure with reduced ejection fraction [HFrEF] <50{\%}) ejection fraction. Natriuretic peptide (NP) levels are lower in HFpEF than HFrEF. We hypothesized that lower NP levels in HFpEF may be associated with other differences in biomarkers, specifically, renin-angiotensin-aldosterone system (RAAS) activation, oxidative stress, and a biomarker that reflects collagen synthesis. Methods: In this prespecified ancillary analysis of patients with ADHF enrolled in the Diuretic Optimization Strategies Evaluation study, clinical features and N-terminal pro-B-type NP, cystatin C, plasma renin activity, aldosterone, oxidative stress (uric acid), and procollagen type III N-terminal peptide were compared in HFpEF and HFrEF at enrollment and 60-day follow-up. Results: Compared with HFrEF (n = 219), HFpEF (n = 81) patients were older, heavier, more commonly female, less treated with RAAS antagonists, but with similar New York Heart Association class, jugular venous pressure, and edema severity. N-terminal pro-B-type NP was lower, and systolic blood pressure and cystatin C were higher in HFpEF. Despite higher systolic blood pressure and less RAAS antagonist use in HFpEF, plasma renin activity and aldosterone levels were similar in HFpEF and HFrEF as were uric acid and procollagen type III N-terminal peptide levels. Changes in biomarker levels from enrollment to 60 days were similar between HFrEF (n = 149) and HFpEF (n = 50). Conclusion: Lower NP levels in decompensated HFpEF occur in association with similar ADHF severity, more impaired vascular and renal function but similar elevation of biomarkers that reflect RAAS activation, oxidative stress, and collagen synthesis as in HFrEF.",
author = "Kalkidan Bishu and Anita Deswal and Chen, {Horng Haur} and Lewinter, {Martin M.} and Lewis, {Gregory D.} and Semigran, {Marc J.} and Borlaug, {Barry A} and Steven McNulty and Hernandez, {Adrian F.} and Eugene Braunwald and Redfield, {Margaret May}",
year = "2012",
month = "11",
doi = "10.1016/j.ahj.2012.08.014",
language = "English (US)",
volume = "164",
journal = "American Heart Journal",
issn = "0002-8703",
publisher = "Mosby Inc.",
number = "5",

}

TY - JOUR

T1 - Biomarkers in acutely decompensated heart failure with preserved or reduced ejection fraction

AU - Bishu, Kalkidan

AU - Deswal, Anita

AU - Chen, Horng Haur

AU - Lewinter, Martin M.

AU - Lewis, Gregory D.

AU - Semigran, Marc J.

AU - Borlaug, Barry A

AU - McNulty, Steven

AU - Hernandez, Adrian F.

AU - Braunwald, Eugene

AU - Redfield, Margaret May

PY - 2012/11

Y1 - 2012/11

N2 - Background: Acute decompensated heart failure (ADHF) occurs with preserved (heart failure with preserved ejection fraction [HFpEF] ≥50%) or reduced (heart failure with reduced ejection fraction [HFrEF] <50%) ejection fraction. Natriuretic peptide (NP) levels are lower in HFpEF than HFrEF. We hypothesized that lower NP levels in HFpEF may be associated with other differences in biomarkers, specifically, renin-angiotensin-aldosterone system (RAAS) activation, oxidative stress, and a biomarker that reflects collagen synthesis. Methods: In this prespecified ancillary analysis of patients with ADHF enrolled in the Diuretic Optimization Strategies Evaluation study, clinical features and N-terminal pro-B-type NP, cystatin C, plasma renin activity, aldosterone, oxidative stress (uric acid), and procollagen type III N-terminal peptide were compared in HFpEF and HFrEF at enrollment and 60-day follow-up. Results: Compared with HFrEF (n = 219), HFpEF (n = 81) patients were older, heavier, more commonly female, less treated with RAAS antagonists, but with similar New York Heart Association class, jugular venous pressure, and edema severity. N-terminal pro-B-type NP was lower, and systolic blood pressure and cystatin C were higher in HFpEF. Despite higher systolic blood pressure and less RAAS antagonist use in HFpEF, plasma renin activity and aldosterone levels were similar in HFpEF and HFrEF as were uric acid and procollagen type III N-terminal peptide levels. Changes in biomarker levels from enrollment to 60 days were similar between HFrEF (n = 149) and HFpEF (n = 50). Conclusion: Lower NP levels in decompensated HFpEF occur in association with similar ADHF severity, more impaired vascular and renal function but similar elevation of biomarkers that reflect RAAS activation, oxidative stress, and collagen synthesis as in HFrEF.

AB - Background: Acute decompensated heart failure (ADHF) occurs with preserved (heart failure with preserved ejection fraction [HFpEF] ≥50%) or reduced (heart failure with reduced ejection fraction [HFrEF] <50%) ejection fraction. Natriuretic peptide (NP) levels are lower in HFpEF than HFrEF. We hypothesized that lower NP levels in HFpEF may be associated with other differences in biomarkers, specifically, renin-angiotensin-aldosterone system (RAAS) activation, oxidative stress, and a biomarker that reflects collagen synthesis. Methods: In this prespecified ancillary analysis of patients with ADHF enrolled in the Diuretic Optimization Strategies Evaluation study, clinical features and N-terminal pro-B-type NP, cystatin C, plasma renin activity, aldosterone, oxidative stress (uric acid), and procollagen type III N-terminal peptide were compared in HFpEF and HFrEF at enrollment and 60-day follow-up. Results: Compared with HFrEF (n = 219), HFpEF (n = 81) patients were older, heavier, more commonly female, less treated with RAAS antagonists, but with similar New York Heart Association class, jugular venous pressure, and edema severity. N-terminal pro-B-type NP was lower, and systolic blood pressure and cystatin C were higher in HFpEF. Despite higher systolic blood pressure and less RAAS antagonist use in HFpEF, plasma renin activity and aldosterone levels were similar in HFpEF and HFrEF as were uric acid and procollagen type III N-terminal peptide levels. Changes in biomarker levels from enrollment to 60 days were similar between HFrEF (n = 149) and HFpEF (n = 50). Conclusion: Lower NP levels in decompensated HFpEF occur in association with similar ADHF severity, more impaired vascular and renal function but similar elevation of biomarkers that reflect RAAS activation, oxidative stress, and collagen synthesis as in HFrEF.

UR - http://www.scopus.com/inward/record.url?scp=84868602444&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84868602444&partnerID=8YFLogxK

U2 - 10.1016/j.ahj.2012.08.014

DO - 10.1016/j.ahj.2012.08.014

M3 - Article

C2 - 23137508

AN - SCOPUS:84868602444

VL - 164

JO - American Heart Journal

JF - American Heart Journal

SN - 0002-8703

IS - 5

ER -