Plasma Volume Status and Its Association With In-Hospital and Postdischarge Outcomes in Decompensated Heart Failure.


Journal

Journal of cardiac failure
ISSN: 1532-8414
Titre abrégé: J Card Fail
Pays: United States
ID NLM: 9442138

Informations de publication

Date de publication:
03 2021
Historique:
received: 29 03 2020
revised: 27 07 2020
accepted: 23 09 2020
pubmed: 11 10 2020
medline: 18 9 2021
entrez: 10 10 2020
Statut: ppublish

Résumé

Prior analyses suggest an association between formula-based plasma volume (PV) estimates and outcomes in heart failure (HF). We assessed the association between estimated PV status by the Duarte-ePV and Kaplan Hakim (KH-ePVS) formulas, and in-hospital and postdischarge clinical outcomes, in the ASCEND-HF trial. The KH-ePVS and Duarte-ePV were calculated on admission. We assessed associations with in-hospital worsening HF, 30-day composite cardiovascular mortality or HF rehospitalization and 180-day all-cause mortality. There were 6373 (89.2%), and 6354 (89.0%) patients who had necessary characteristics to calculate KH-ePVS and Duarte-ePV, respectively. There was no association between PV by either formula with in-hospital worsening HF. KH-ePVS showed a weak correlation with N-terminal prohormone BNP, and with measures of decongestion such as body weight change and urine output (r < 0.3 for all). Duarte-ePV was trending toward an association with worse 30-day (adjusted odds ratio 1.07, 95% confidence interval [CI] 1.00-1.15, P = .058), but not 180-day outcomes (adjusted hazard ratio 1.03, 95% CI 0.97-1.09, P = .289). A continuous KH-ePVS of >0 (per 10-unit increase) was associated with improved 30-day outcomes (adjusted odds ratio 0.75, 95% CI 0.62-0.91, P = .004). The continuous KH-ePVS was not associated with 180-day outcomes (adjusted hazard ratio 1.05, 95% CI 0.98-1.12, P = .139). Baseline PV estimates had a weak association with in-hospital measures of decongestion. The Duarte-ePV trended toward an association with early clinical outcomes in decompensated HF, and may improve risk stratification in HF.

Sections du résumé

BACKGROUND
Prior analyses suggest an association between formula-based plasma volume (PV) estimates and outcomes in heart failure (HF). We assessed the association between estimated PV status by the Duarte-ePV and Kaplan Hakim (KH-ePVS) formulas, and in-hospital and postdischarge clinical outcomes, in the ASCEND-HF trial.
METHODS AND RESULTS
The KH-ePVS and Duarte-ePV were calculated on admission. We assessed associations with in-hospital worsening HF, 30-day composite cardiovascular mortality or HF rehospitalization and 180-day all-cause mortality. There were 6373 (89.2%), and 6354 (89.0%) patients who had necessary characteristics to calculate KH-ePVS and Duarte-ePV, respectively. There was no association between PV by either formula with in-hospital worsening HF. KH-ePVS showed a weak correlation with N-terminal prohormone BNP, and with measures of decongestion such as body weight change and urine output (r < 0.3 for all). Duarte-ePV was trending toward an association with worse 30-day (adjusted odds ratio 1.07, 95% confidence interval [CI] 1.00-1.15, P = .058), but not 180-day outcomes (adjusted hazard ratio 1.03, 95% CI 0.97-1.09, P = .289). A continuous KH-ePVS of >0 (per 10-unit increase) was associated with improved 30-day outcomes (adjusted odds ratio 0.75, 95% CI 0.62-0.91, P = .004). The continuous KH-ePVS was not associated with 180-day outcomes (adjusted hazard ratio 1.05, 95% CI 0.98-1.12, P = .139).
CONCLUSIONS
Baseline PV estimates had a weak association with in-hospital measures of decongestion. The Duarte-ePV trended toward an association with early clinical outcomes in decompensated HF, and may improve risk stratification in HF.

Identifiants

pubmed: 33038532
pii: S1071-9164(20)31468-8
doi: 10.1016/j.cardfail.2020.09.478
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

297-308

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Marat Fudim (M)

Duke Clinical Research Institute, Durham, North Carolina; Division of Cardiology, Duke University Medical Center, Durham, North Carolina.

Joseph B Lerman (JB)

Division of Cardiology, Duke University Medical Center, Durham, North Carolina.

Courtney Page (C)

Duke Clinical Research Institute, Durham, North Carolina.

Brooke Alhanti (B)

Duke Clinical Research Institute, Durham, North Carolina.

Robert M Califf (RM)

Duke Clinical Research Institute, Durham, North Carolina.

Justin A Ezekowitz (JA)

Canadian VIGOUR Centre, University of Alberta, Edmonton, Canada.

Nicolas Girerd (N)

Université de Lorraine, Centre d'Investigation Clinique Plurithématique 1433, INSERM U1116, CHRU de Nancy, FCRIN INI-CRCT, Nancy, France.

Justin L Grodin (JL)

Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.

Wayne L Miller (WL)

Division of Cardiology, Mayo Clinic, Rochester, Minnesota.

Ambarish Pandey (A)

Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.

Patrick Rossignol (P)

Université de Lorraine, Centre d'Investigation Clinique Plurithématique 1433, INSERM U1116, CHRU de Nancy, FCRIN INI-CRCT, Nancy, France.

Randall C Starling (RC)

Division of Cardiology, Cleveland Clinic, Cleveland, Ohio.

W H Wilson Tang (WHW)

Division of Cardiology, Cleveland Clinic, Cleveland, Ohio.

Faiez Zannad (F)

Université de Lorraine, Centre d'Investigation Clinique Plurithématique 1433, INSERM U1116, CHRU de Nancy, FCRIN INI-CRCT, Nancy, France.

Adrian F Hernandez (AF)

Duke Clinical Research Institute, Durham, North Carolina; Division of Cardiology, Duke University Medical Center, Durham, North Carolina.

Christopher M O'connor (CM)

Inova Heart and Vascular Institute, Falls Church, Virginia.

Robert J Mentz (RJ)

Duke Clinical Research Institute, Durham, North Carolina; Division of Cardiology, Duke University Medical Center, Durham, North Carolina. Electronic address: robert.mentz@duke.edu.

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