Improved Prognostic Performance of Cardiac Power Output With Right Atrial Pressure: A Subanalysis of the ESCAPE Trial.


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:
05 2022
Historique:
received: 29 08 2021
revised: 24 10 2021
accepted: 02 11 2021
pubmed: 15 11 2021
medline: 18 5 2022
entrez: 14 11 2021
Statut: ppublish

Résumé

The initial derivation of cardiac power output (CPO) included the difference between mean arterial pressure (MAP) and right atrial pressure (RAP) in the numerator, before multiplying by cardiac output (CO). We hypothesized that the inclusion of RAP (CPO-RAP) would enhance the prognostic performance of this parameter in those with an elevated RAP. We obtained patient-level data from the ESCAPE trial via the Biolincc database. Participants with full final hemodynamics were included in the analysis. The CPO-RAP was calculated as [(MAP - RAP) × CO)]/451 Watts (W), and the CPO was calculated as (MAP × CO)/451. The primary outcome was freedom from left ventricular assist device, heart transplant, or death at 6 months. Included participants (n = 157) were a median of 58 years of age (interquartile range [IQR] 49-67 years), 27% were women, and 59% had ischemic cardiomyopathy. The median CPO was 0.70 W (IQR 0.50-0.90 W), and the median CPO-RAP was 0.62 W (IQR 0.47-0.79 W). In univariable logistic regressions, the CPO was not associated with the primary outcome (odds ratio 0.32, 95% confidence interval 0.08-1.29, P = .11), but the CPO-RAP was (odds ratio 0.10, 95% confidence interval 0.02-0.54, P < .01). In Kaplan-Meier analyses, there were no significant difference in outcomes with CPO (76% vs 64%, P = .08), but for CPO-RAP, there were significant differences in outcomes (81% vs 63%, P = .01). When further delineating CPO-RAP by RAP above or below the median, there was no significant difference in the outcome for participants with a RAP 8 or less (94% vs 79%, P = .07), but a significant difference in participants with a RAP of more than 8 mm Hg (66% vs 45%, P < .05). The inclusion of RAP resulted in a significant association with the primary outcome; CPO alone was not.

Sections du résumé

BACKGROUND
The initial derivation of cardiac power output (CPO) included the difference between mean arterial pressure (MAP) and right atrial pressure (RAP) in the numerator, before multiplying by cardiac output (CO). We hypothesized that the inclusion of RAP (CPO-RAP) would enhance the prognostic performance of this parameter in those with an elevated RAP.
METHODS AND RESULTS
We obtained patient-level data from the ESCAPE trial via the Biolincc database. Participants with full final hemodynamics were included in the analysis. The CPO-RAP was calculated as [(MAP - RAP) × CO)]/451 Watts (W), and the CPO was calculated as (MAP × CO)/451. The primary outcome was freedom from left ventricular assist device, heart transplant, or death at 6 months. Included participants (n = 157) were a median of 58 years of age (interquartile range [IQR] 49-67 years), 27% were women, and 59% had ischemic cardiomyopathy. The median CPO was 0.70 W (IQR 0.50-0.90 W), and the median CPO-RAP was 0.62 W (IQR 0.47-0.79 W). In univariable logistic regressions, the CPO was not associated with the primary outcome (odds ratio 0.32, 95% confidence interval 0.08-1.29, P = .11), but the CPO-RAP was (odds ratio 0.10, 95% confidence interval 0.02-0.54, P < .01). In Kaplan-Meier analyses, there were no significant difference in outcomes with CPO (76% vs 64%, P = .08), but for CPO-RAP, there were significant differences in outcomes (81% vs 63%, P = .01). When further delineating CPO-RAP by RAP above or below the median, there was no significant difference in the outcome for participants with a RAP 8 or less (94% vs 79%, P = .07), but a significant difference in participants with a RAP of more than 8 mm Hg (66% vs 45%, P < .05).
CONCLUSIONS
The inclusion of RAP resulted in a significant association with the primary outcome; CPO alone was not.

Identifiants

pubmed: 34774746
pii: S1071-9164(21)00440-1
doi: 10.1016/j.cardfail.2021.11.001
pmc: PMC9085968
mid: NIHMS1796341
pii:
doi:

Types de publication

Clinical Trial Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

866-869

Subventions

Organisme : NHLBI NIH HHS
ID : T32 HL007381
Pays : United States

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Références

ESC Heart Fail. 2021 Apr;8(2):1522-1530
pubmed: 33595923
Lancet. 1986 Dec 13;2(8520):1360-3
pubmed: 2878226
JAMA. 2005 Oct 5;294(13):1625-33
pubmed: 16204662
BMJ Open. 2016 Sep 26;6(9):e012769
pubmed: 27670522
J Am Coll Cardiol. 2004 Jul 21;44(2):340-8
pubmed: 15261929
Circ Heart Fail. 2020 Oct;13(10):e007393
pubmed: 32993372

Auteurs

Mark N Belkin (MN)

From the University of Chicago Medicine, Section of Cardiology, Chicago, Illinois.

Francis J Alenghat (FJ)

From the University of Chicago Medicine, Section of Cardiology, Chicago, Illinois.

Stephanie A Besser (SA)

From the University of Chicago Medicine, Section of Cardiology, Chicago, Illinois.

Sean P Pinney (SP)

From the University of Chicago Medicine, Section of Cardiology, Chicago, Illinois.

Jonathan Grinstein (J)

From the University of Chicago Medicine, Section of Cardiology, Chicago, Illinois. Electronic address: jgrinstein@medicine.bsd.uchicago.edu.

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