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Increased plasma cathepsin S and trombospondin-1 in patients with acute ST-segment elevation myocardial infarction

BACKGROUND: The role of cathepsins in the pathological progression of atherosclerotic lesions in ischemic heart disease have been defined in detail more than numerous times. This investigation examined the platelet-specific biomarker trombospondin-1 (TSP-1) and platelet function ex vivo, and compare...

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Autores principales: Befekadu, Rahel, Christiansen, Kjeld, Larsson, Anders, Grenegård, Magnus
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Via Medica 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8084374/
https://www.ncbi.nlm.nih.gov/pubmed/29611169
http://dx.doi.org/10.5603/CJ.a2018.0030
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author Befekadu, Rahel
Christiansen, Kjeld
Larsson, Anders
Grenegård, Magnus
author_facet Befekadu, Rahel
Christiansen, Kjeld
Larsson, Anders
Grenegård, Magnus
author_sort Befekadu, Rahel
collection PubMed
description BACKGROUND: The role of cathepsins in the pathological progression of atherosclerotic lesions in ischemic heart disease have been defined in detail more than numerous times. This investigation examined the platelet-specific biomarker trombospondin-1 (TSP-1) and platelet function ex vivo, and compared this with cathepsin S (Cat-S; a biomarker unrelated to platelet activation but also associated this with increased mortality risk) in patients with ST-segment elevation myocardial infarction (STEMI). METHODS: The STEMI patients were divided into two groups depending on the degree of coronary vessel occlusion: those with closed (n = 90) and open culprit vessel (n = 40). Cat-S and TSP-1 were analyzed before, 1–3 days after and 3 months after percutanous coronary intervention (PCI). RESULTS: During acute STEMI, plasma TSP-1 was significantly elevated in patients with closed culprit lesions, but rapidly declined after PCI. In fact, TSP-1 after PCI was significantly lower inpatient samples compared to healthy individuals. In comparison, plasma Cat-S was significantly elevated both before and after PCI. In patients with closed culprit lesions, Cat-S was significantly higher compared to patients with open culprit lesions 3 months after PCI. Although troponin-I were higher (p < 0.01) in patients with closed culprit lesion, there was no correlation with Cat-S and TSP-1. CONCLUSIONS: Cat-S but not TSP-1 may be a useful risk biomarker in relation to the severity of STEMI. However, the causality of Cat-S as a predictor for long-term mortality in STEMI remains to be ascertained in future studies.
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spelling pubmed-80843742021-05-10 Increased plasma cathepsin S and trombospondin-1 in patients with acute ST-segment elevation myocardial infarction Befekadu, Rahel Christiansen, Kjeld Larsson, Anders Grenegård, Magnus Cardiol J Basic Science and Experimental Cardiology BACKGROUND: The role of cathepsins in the pathological progression of atherosclerotic lesions in ischemic heart disease have been defined in detail more than numerous times. This investigation examined the platelet-specific biomarker trombospondin-1 (TSP-1) and platelet function ex vivo, and compared this with cathepsin S (Cat-S; a biomarker unrelated to platelet activation but also associated this with increased mortality risk) in patients with ST-segment elevation myocardial infarction (STEMI). METHODS: The STEMI patients were divided into two groups depending on the degree of coronary vessel occlusion: those with closed (n = 90) and open culprit vessel (n = 40). Cat-S and TSP-1 were analyzed before, 1–3 days after and 3 months after percutanous coronary intervention (PCI). RESULTS: During acute STEMI, plasma TSP-1 was significantly elevated in patients with closed culprit lesions, but rapidly declined after PCI. In fact, TSP-1 after PCI was significantly lower inpatient samples compared to healthy individuals. In comparison, plasma Cat-S was significantly elevated both before and after PCI. In patients with closed culprit lesions, Cat-S was significantly higher compared to patients with open culprit lesions 3 months after PCI. Although troponin-I were higher (p < 0.01) in patients with closed culprit lesion, there was no correlation with Cat-S and TSP-1. CONCLUSIONS: Cat-S but not TSP-1 may be a useful risk biomarker in relation to the severity of STEMI. However, the causality of Cat-S as a predictor for long-term mortality in STEMI remains to be ascertained in future studies. Via Medica 2019-08-22 /pmc/articles/PMC8084374/ /pubmed/29611169 http://dx.doi.org/10.5603/CJ.a2018.0030 Text en Copyright © 2019 Via Medica https://creativecommons.org/licenses/by-nc-nd/4.0/This article is available in open access under Creative Common Attribution-Non-Commercial-No Derivatives 4.0 International (CC BY-NC-ND 4.0) license, allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.
spellingShingle Basic Science and Experimental Cardiology
Befekadu, Rahel
Christiansen, Kjeld
Larsson, Anders
Grenegård, Magnus
Increased plasma cathepsin S and trombospondin-1 in patients with acute ST-segment elevation myocardial infarction
title Increased plasma cathepsin S and trombospondin-1 in patients with acute ST-segment elevation myocardial infarction
title_full Increased plasma cathepsin S and trombospondin-1 in patients with acute ST-segment elevation myocardial infarction
title_fullStr Increased plasma cathepsin S and trombospondin-1 in patients with acute ST-segment elevation myocardial infarction
title_full_unstemmed Increased plasma cathepsin S and trombospondin-1 in patients with acute ST-segment elevation myocardial infarction
title_short Increased plasma cathepsin S and trombospondin-1 in patients with acute ST-segment elevation myocardial infarction
title_sort increased plasma cathepsin s and trombospondin-1 in patients with acute st-segment elevation myocardial infarction
topic Basic Science and Experimental Cardiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8084374/
https://www.ncbi.nlm.nih.gov/pubmed/29611169
http://dx.doi.org/10.5603/CJ.a2018.0030
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