Cathepsin S Levels and Survival Among Patients With Non-ST-Segment Elevation Acute Coronary Syndromes.


Journal

Journal of the American College of Cardiology
ISSN: 1558-3597
Titre abrégé: J Am Coll Cardiol
Pays: United States
ID NLM: 8301365

Informations de publication

Date de publication:
06 09 2022
Historique:
received: 18 03 2022
revised: 09 05 2022
accepted: 31 05 2022
entrez: 1 9 2022
pubmed: 2 9 2022
medline: 9 9 2022
Statut: ppublish

Résumé

Patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACS) are at high residual risk for long-term cardiovascular (CV) mortality. Cathepsin S (CTSS) is a lysosomal cysteine protease with elastolytic and collagenolytic activity that has been involved in atherosclerotic plaque rupture. The purpose of this study was to determine the following: 1) the prognostic value of circulating CTSS measured at patient admission for long-term mortality in NSTE-ACS; and 2) its additive value over the GRACE (Global Registry of Acute Coronary Events) risk score. This was a single-center cohort study, consecutively recruiting patients with adjudicated NSTE-ACS (n = 1,112) from the emergency department of an academic hospital. CTSS was measured in serum using enzyme-linked immunosorbent assay. All-cause mortality at 8 years was the primary endpoint. CV death was the secondary endpoint. In total, 367 (33.0%) deaths were recorded. CTSS was associated with increased risk of all-cause mortality (HR for highest vs lowest quarter of CTSS: 1.89; 95% CI: 1.34-2.66; P < 0.001) and CV death (HR: 2.58; 95% CI: 1.15-5.77; P = 0.021) after adjusting for traditional CV risk factors, high-sensitivity C-reactive protein, left ventricular ejection fraction, high-sensitivity troponin-T, revascularization and index diagnosis (unstable angina/ non-ST-segment elevation myocardial infarction). When CTSS was added to the GRACE score, it conferred significant discrimination and reclassification value for all-cause mortality (Delta Harrell's C: 0.03; 95% CI: 0.012-0.047; P = 0.001; and net reclassification improvement = 0.202; P = 0.003) and CV death (AUC: 0.056; 95% CI: 0.017-0.095; P = 0.005; and net reclassification improvement = 0.390; P = 0.001) even after additionally considering high-sensitivity troponin-T and left ventricular ejection fraction. Circulating CTSS is a predictor of long-term mortality and improves risk stratification of patients with NSTE-ACS over the GRACE score.

Sections du résumé

BACKGROUND
Patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACS) are at high residual risk for long-term cardiovascular (CV) mortality. Cathepsin S (CTSS) is a lysosomal cysteine protease with elastolytic and collagenolytic activity that has been involved in atherosclerotic plaque rupture.
OBJECTIVES
The purpose of this study was to determine the following: 1) the prognostic value of circulating CTSS measured at patient admission for long-term mortality in NSTE-ACS; and 2) its additive value over the GRACE (Global Registry of Acute Coronary Events) risk score.
METHODS
This was a single-center cohort study, consecutively recruiting patients with adjudicated NSTE-ACS (n = 1,112) from the emergency department of an academic hospital. CTSS was measured in serum using enzyme-linked immunosorbent assay. All-cause mortality at 8 years was the primary endpoint. CV death was the secondary endpoint.
RESULTS
In total, 367 (33.0%) deaths were recorded. CTSS was associated with increased risk of all-cause mortality (HR for highest vs lowest quarter of CTSS: 1.89; 95% CI: 1.34-2.66; P < 0.001) and CV death (HR: 2.58; 95% CI: 1.15-5.77; P = 0.021) after adjusting for traditional CV risk factors, high-sensitivity C-reactive protein, left ventricular ejection fraction, high-sensitivity troponin-T, revascularization and index diagnosis (unstable angina/ non-ST-segment elevation myocardial infarction). When CTSS was added to the GRACE score, it conferred significant discrimination and reclassification value for all-cause mortality (Delta Harrell's C: 0.03; 95% CI: 0.012-0.047; P = 0.001; and net reclassification improvement = 0.202; P = 0.003) and CV death (AUC: 0.056; 95% CI: 0.017-0.095; P = 0.005; and net reclassification improvement = 0.390; P = 0.001) even after additionally considering high-sensitivity troponin-T and left ventricular ejection fraction.
CONCLUSIONS
Circulating CTSS is a predictor of long-term mortality and improves risk stratification of patients with NSTE-ACS over the GRACE score.

Identifiants

pubmed: 36049808
pii: S0735-1097(22)05469-9
doi: 10.1016/j.jacc.2022.05.055
pii:
doi:

Substances chimiques

Troponin T 0
Cathepsins EC 3.4.-
cathepsin S EC 3.4.22.27

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

998-1010

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures This research was funded by the German Research Foundation DFG (SFB834 project number 75732319) and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program (grant agreement No 759248) (to Dr Stellos). Dr Sopova was supported with a scholarship from the German Heart Foundation (Deutsche Herzstiftung). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Kimon Stamatelopoulos (K)

Department of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece; Biosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom. Electronic address: kstamatel@med.uoa.gr.

Matthias Mueller-Hennessen (M)

Department of Internal Medicine III, Cardiology, University Hospital Heidelberg, Heidelberg, Germany; German Centre for Cardiovascular Research (DZHK), partner site Heidelberg/Mannheim, Mannheim, Germany.

Georgios Georgiopoulos (G)

Department of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece; Biosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.

Pedro Lopez-Ayala (P)

Cardiovascular Research Institute Basel and University Hospital of Basel, Basel, Switzerland.

Marco Sachse (M)

Department of Cardiovascular Research, European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.

Nikolaos I Vlachogiannis (NI)

Biosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.

Kateryna Sopova (K)

Translational and Clinical Research Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom; Department of Cardiology, Newcastle Hospitals NHS Foundation Trust, Newcastle Upon Tyne, United Kingdom.

Dimitrios Delialis (D)

Department of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Francesca Bonini (F)

Department of Cardiovascular Research, European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.

Raphael Patras (R)

Department of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Giorgia Ciliberti (G)

Department of Cardiovascular Research, European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.

Mehrshad Vafaie (M)

Department of Internal Medicine III, Cardiology, University Hospital Heidelberg, Heidelberg, Germany.

Moritz Biener (M)

Department of Internal Medicine III, Cardiology, University Hospital Heidelberg, Heidelberg, Germany.

Jasper Boeddinghaus (J)

Cardiovascular Research Institute Basel and University Hospital of Basel, Basel, Switzerland.

Thomas Nestelberger (T)

Cardiovascular Research Institute Basel and University Hospital of Basel, Basel, Switzerland.

Luca Koechlin (L)

Cardiovascular Research Institute Basel and University Hospital of Basel, Basel, Switzerland.

Simon Tual-Chalot (S)

Biosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.

Ioannis Kanakakis (I)

Department of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Aikaterini Gatsiou (A)

Biosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.

Hugo Katus (H)

Department of Internal Medicine III, Cardiology, University Hospital Heidelberg, Heidelberg, Germany; German Centre for Cardiovascular Research (DZHK), partner site Heidelberg/Mannheim, Mannheim, Germany.

Ioakim Spyridopoulos (I)

Translational and Clinical Research Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom; Department of Cardiology, Newcastle Hospitals NHS Foundation Trust, Newcastle Upon Tyne, United Kingdom.

Christian Mueller (C)

Cardiovascular Research Institute Basel and University Hospital of Basel, Basel, Switzerland.

Evangelos Giannitsis (E)

Department of Internal Medicine III, Cardiology, University Hospital Heidelberg, Heidelberg, Germany; German Centre for Cardiovascular Research (DZHK), partner site Heidelberg/Mannheim, Mannheim, Germany.

Konstantinos Stellos (K)

Biosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom; German Centre for Cardiovascular Research (DZHK), partner site Heidelberg/Mannheim, Mannheim, Germany; Department of Cardiovascular Research, European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; Department of Cardiology, Newcastle Hospitals NHS Foundation Trust, Newcastle Upon Tyne, United Kingdom; Department of Cardiology, University Hospital Mannheim, Heidelberg University, Manheim, Germany. Electronic address: konstantinos.stellos@medma.uni-heidelberg.de.

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Classifications MeSH