Evolution of renal function and predictive value of serial renal assessments among patients with acute coronary syndrome: BIOMArCS study.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 01 2020
Historique:
received: 01 05 2019
revised: 11 07 2019
accepted: 15 07 2019
pubmed: 30 7 2019
medline: 24 11 2020
entrez: 30 7 2019
Statut: ppublish

Résumé

Impaired renal function predicts mortality in acute coronary syndrome (ACS), but its evolution immediately following index ACS and preceding next ACS has not been described in detail. We aimed to describe this evolution using serial measurements of creatinine, glomerular filtration rate [eGFR From 844 ACS patients included in the BIOMArCS study, we analysed patient-specific longitudinal marker trajectories from the case-cohort of 187 patients to determine the risk of the endpoint (cardiovascular death or hospitalization for recurrent non-fatal ACS) during 1-year follow-up. Study included only patients with eGFR Mean age was 63 years, 79% were men, 43% had STEMI, and 67% were in eGFR stages 2-3. During hospitalization for index ACS (median [IQR] duration: 5 (3-7) days), CysC levels indicated deterioration of renal function earlier than creatinine did (CysC peaked on day 3, versus day 6 for creatinine), and both stabilized after two weeks. Higher CysC levels, but not creatinine, predicted the endpoint independently of the GRACE score within the first year after index ACS (adjusted HR [95% CI] per 1SD increase: 1.68 [1.03-2.74]). Immediately following index ACS, plasma CysC levels deteriorate earlier than creatinine-based indices do, but neither marker stabilizes during hospitalization but on average two weeks after ACS. Serially measured CysC levels predict mortality or recurrence of ACS during 1-year follow-up independently of patients' GRACE risk score.

Sections du résumé

BACKGROUND
Impaired renal function predicts mortality in acute coronary syndrome (ACS), but its evolution immediately following index ACS and preceding next ACS has not been described in detail. We aimed to describe this evolution using serial measurements of creatinine, glomerular filtration rate [eGFR
METHODS
From 844 ACS patients included in the BIOMArCS study, we analysed patient-specific longitudinal marker trajectories from the case-cohort of 187 patients to determine the risk of the endpoint (cardiovascular death or hospitalization for recurrent non-fatal ACS) during 1-year follow-up. Study included only patients with eGFR
RESULTS
Mean age was 63 years, 79% were men, 43% had STEMI, and 67% were in eGFR stages 2-3. During hospitalization for index ACS (median [IQR] duration: 5 (3-7) days), CysC levels indicated deterioration of renal function earlier than creatinine did (CysC peaked on day 3, versus day 6 for creatinine), and both stabilized after two weeks. Higher CysC levels, but not creatinine, predicted the endpoint independently of the GRACE score within the first year after index ACS (adjusted HR [95% CI] per 1SD increase: 1.68 [1.03-2.74]).
CONCLUSION
Immediately following index ACS, plasma CysC levels deteriorate earlier than creatinine-based indices do, but neither marker stabilizes during hospitalization but on average two weeks after ACS. Serially measured CysC levels predict mortality or recurrence of ACS during 1-year follow-up independently of patients' GRACE risk score.

Identifiants

pubmed: 31353156
pii: S0167-5273(19)32246-6
doi: 10.1016/j.ijcard.2019.07.052
pii:
doi:

Substances chimiques

Biomarkers 0
CST3 protein, human 0
Cystatin C 0
Creatinine AYI8EX34EU

Types de publication

Journal Article Multicenter Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

12-19

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Milos Brankovic (M)

Department of Cardiology, Erasmus MC, Rotterdam, the Netherlands.

Isabella Kardys (I)

Department of Cardiology, Erasmus MC, Rotterdam, the Netherlands.

Victor van den Berg (V)

Department of Cardiology, Erasmus MC, Rotterdam, the Netherlands; Netherlands Heart Institute, Utrecht, the Netherlands.

Rohit Oemrawsingh (R)

Department of Cardiology, Erasmus MC, Rotterdam, the Netherlands; Netherlands Heart Institute, Utrecht, the Netherlands.

Folkert W Asselbergs (FW)

Laboratory of Clinical Chemistry and Hematology, UMC Utrecht, Utrecht, the Netherlands; Department of Cardiology, Division Heart & Lungs, University Medical Center Utrecht, University of Utrecht, the Netherlands; Durrer Center for Cardiovascular Research, Netherlands Heart Institute, Utrecht, the Netherlands.

Pim van der Harst (P)

University Medical Center Groningen, Groningen, the Netherlands.

Imo E Hoefer (IE)

Laboratory of Clinical Chemistry and Hematology, UMC Utrecht, Utrecht, the Netherlands.

Anho Liem (A)

Sint Franciscus Gasthuis, Rotterdam, the Netherlands.

Arthur Maas (A)

Gelre Hospital, Zutphen, the Netherlands.

Eelko Ronner (E)

Reinier de Graaf Hospital, Delft, the Netherlands.

Carl Schotborgh (C)

HagaZiekenhuis, Den Haag, the Netherlands.

S Hong Kie The (SHK)

Treant Zorggroep, location Bethesda, Hoogeveen, the Netherlands.

Ewout J Hoorn (EJ)

Department of Internal Medicine, Division of Nephrology and Transplantation, Erasmus MC, Rotterdam, the Netherlands.

Eric Boersma (E)

Department of Cardiology, Erasmus MC, Rotterdam, the Netherlands. Electronic address: h.boersma@erasmusmc.nl.

K Martijn Akkerhuis (KM)

Department of Cardiology, Erasmus MC, Rotterdam, the Netherlands.

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Classifications MeSH