Left Ventricular End-Diastolic Pressure for the Prediction of Contrast-Induced Nephropathy and Clinical Outcomes in Patients With ST-Elevation Myocardial Infarction Who Underwent Primary Percutaneous Intervention (the ELEVATE Study).


Journal

The American journal of cardiology
ISSN: 1879-1913
Titre abrégé: Am J Cardiol
Pays: United States
ID NLM: 0207277

Informations de publication

Date de publication:
15 09 2023
Historique:
received: 06 03 2023
revised: 10 06 2023
accepted: 26 06 2023
medline: 28 8 2023
pubmed: 28 7 2023
entrez: 27 7 2023
Statut: ppublish

Résumé

Contrast-induced nephropathy (CIN) is an important complication of percutaneous coronary intervention (PCI). We investigated whether left ventricular end-diastolic pressure (LVEDP) in patients who underwent PCI might be additive to current risk stratification of CIN. Data from consecutive patients who underwent primary PCI for ST-elevation myocardial infarction between 2013 and 2018 at Western Health in Victoria, Australia were analyzed. CIN was defined as a 25% increase in serum creatinine from baseline or 44 µmol/L increase in absolute value within 48 hours of contrast administration. Compared with patients without CIN (n = 455, 93%), those who developed CIN (n = 35, 7%) were older (64 vs 58 years, p = 0.006), and had higher peak creatine kinase (2,862 [1,258 to 3,952] vs 1,341 U/L [641 to 2,613], p = 0.02). The CIN group had higher median LVEDP (30 [21-33] vs 25 mm Hg [20-30], p = 0.013) and higher median Mehran risk score (MRS) (5 [2-8] vs 2 [1-5], p <0.001). Patients with CIN had more in-hospital major adverse cardiovascular and cerebrovascular events (composite end point of death, new or recurrent myocardial infarction or stent thrombosis, target vessel revascularization or stroke) (23% vs 8.6%, p = 0.01), but similar 30-day major adverse cardiovascular and cerebrovascular events (20% vs 15%, p = 0.46). An LVEDP >30 mm Hg independently predicted CIN (odds ratio 3.4, 95% confidence interval 1.46 to 8.03, p = 0.005). The addition of LVEDP ≥30 mm Hg to MRS marginally improved risk prediction for CIN compared with MRS alone (area-under-curve, c-statistic = 0.71 vs c-statistic = 0.63, p = 0.08). In conclusion, elevated LVEDP ≥30 mm Hg during primary PCI was an independent predictor of CIN in patients treated for ST-elevation myocardial infarction. The addition of LVEDP to the MRS may improve risk prediction for CIN.

Identifiants

pubmed: 37499602
pii: S0002-9149(23)00519-2
doi: 10.1016/j.amjcard.2023.06.111
pii:
doi:

Substances chimiques

Contrast Media 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

219-225

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2023 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors have no conflicts of interest to declare.

Auteurs

Laura Hanson (L)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia; Department of Cardiology, Alfred Health, Melbourne, Victoria, Australia.

Sara Vogrin (S)

Department of Medicine, University of Melbourne, Melbourne, Australia.

Samer Noaman (S)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia; Department of Cardiology, Alfred Health, Melbourne, Victoria, Australia.

Cheng Yee Goh (CY)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia; Department of Cardiology, University of Ottawa Heart Institute Ottawa, Ontario, Canada.

Wayne Zheng (W)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia; Department of Cardiology, Alfred Health, Melbourne, Victoria, Australia.

Noah Wexler (N)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia.

Haider Jumaah (H)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia.

Omar Al-Mukhtar (O)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia.

Jason Bloom (J)

Department of Cardiology, Alfred Health, Melbourne, Victoria, Australia.

Kawa Haji (K)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia; Department of Cardiology, Alfred Health, Melbourne, Victoria, Australia.

Daniel Schneider (D)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia; Department of Gastroenterology, The Royal Melbourne Hospital, Melbourne, Victoria, Australia.

Ahmed Kadhmawi (A)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia.

Dion Stub (D)

Department of Cardiology, Alfred Health, Melbourne, Victoria, Australia; Department of Epidemiology and Preventive Medicine, Monash University, Victoria, Australia; The Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia.

Nicholas Cox (N)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia; Department of Medicine, University of Melbourne, Melbourne, Australia.

William Chan (W)

Department of Cardiology, Western Health, Melbourne, Victoria, Australia; Department of Cardiology, Alfred Health, Melbourne, Victoria, Australia; Department of Medicine, University of Melbourne, Melbourne, Australia; The Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia. Electronic address: william.chan@unimelb.edu.au.

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