Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin after Brief Induced Coronary Artery Balloon Occlusion in Humans

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Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin after Brief Induced Coronary Artery Balloon Occlusion in Humans. / Árnadóttir, Ásthildur; Pedersen, Sune; Bo Hasselbalch, Rasmus; Goetze, Jens P.; Friis-Hansen, Lennart J.; Bloch-Münster, Anna Marie; Skov Jensen, Jan; Bundgaard, Henning; Iversen, Kasper.

I: Circulation, Bind 143, Nr. 11, 2021, s. 1095-1104.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Árnadóttir, Á, Pedersen, S, Bo Hasselbalch, R, Goetze, JP, Friis-Hansen, LJ, Bloch-Münster, AM, Skov Jensen, J, Bundgaard, H & Iversen, K 2021, 'Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin after Brief Induced Coronary Artery Balloon Occlusion in Humans', Circulation, bind 143, nr. 11, s. 1095-1104. https://doi.org/10.1161/CIRCULATIONAHA.120.046574

APA

Árnadóttir, Á., Pedersen, S., Bo Hasselbalch, R., Goetze, J. P., Friis-Hansen, L. J., Bloch-Münster, A. M., Skov Jensen, J., Bundgaard, H., & Iversen, K. (2021). Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin after Brief Induced Coronary Artery Balloon Occlusion in Humans. Circulation, 143(11), 1095-1104. https://doi.org/10.1161/CIRCULATIONAHA.120.046574

Vancouver

Árnadóttir Á, Pedersen S, Bo Hasselbalch R, Goetze JP, Friis-Hansen LJ, Bloch-Münster AM o.a. Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin after Brief Induced Coronary Artery Balloon Occlusion in Humans. Circulation. 2021;143(11):1095-1104. https://doi.org/10.1161/CIRCULATIONAHA.120.046574

Author

Árnadóttir, Ásthildur ; Pedersen, Sune ; Bo Hasselbalch, Rasmus ; Goetze, Jens P. ; Friis-Hansen, Lennart J. ; Bloch-Münster, Anna Marie ; Skov Jensen, Jan ; Bundgaard, Henning ; Iversen, Kasper. / Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin after Brief Induced Coronary Artery Balloon Occlusion in Humans. I: Circulation. 2021 ; Bind 143, Nr. 11. s. 1095-1104.

Bibtex

@article{12ee51f09d964f7c9f3de5a6790d2307,
title = "Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin after Brief Induced Coronary Artery Balloon Occlusion in Humans",
abstract = "Background: Cardiac troponins (cTns) are the cornerstone of diagnosing acute myocardial infarction. There is limited knowledge on the duration of ischemia necessary to induce a measurable release of cTns or the very-early-release kinetics of cTns after an ischemic event. Copeptin may have a supplementary role in ruling out myocardial infarction early. We investigated the release of cTns and copeptin in the first hours after experimental balloon-induced ischemia in humans. Methods: Thirty-four patients (median age, 60 years [interquartile range, 51-64]; 15 men, 43%) with angiographically normal coronary arteries were randomly assigned into 4 groups with different durations of induced myocardial ischemia (0, 30, 60, 90 s). Ischemia was induced by inflating a balloon in the left anterior descending artery between the first and second diagonal branch. Blood was collected before balloon inflation (baseline) every 15 minutes for the first 3 hours, and every 30 minutes for the next 3 hours. The cTns were analyzed by 3 high-sensitivity (hs) cTn assays: hs-cTnT (Roche), hs-cTnI (Siemens), and hs-cTnI (Abbott). Copeptin was analyzed by a sandwich immunoluminometric assay. Results: None of the patients had any complications. Increased cTn concentrations were detected by all 3 assays, and the magnitude of the increase was associated with the duration of ischemia. Increased hs-cTnI (Siemens) concentrations were first detectable 15 minutes after 90-s ischemia (median 43.7% increase) and increased more steeply and had a higher peak than the other assays. Copeptin levels did not significantly change. Using the cTnT, hs-cTnI (Siemens), and hs-cTnI (Abbott) concentrations at 0 and 180 minutes, 1 (11%), 0, and 0 patients from the 60-s ischemia group and 5 (63%), 2 (25%), and 1 (11%) from the 90-s ischemia group, respectively, fulfilled criteria for a biochemical myocardial infarction. Conclusions: This study is the first to report the early-release kinetics of cTn concentrations after different durations of experimental coronary balloon occlusion in humans. All assays detected a cTn increase after only 30 s of ischemia. hs-cTnI (Siemens) rose faster and reached a higher peak. Copeptin levels did not change significantly. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03203057.",
keywords = "copeptins, myocardial ischemia, troponin I, troponin T",
author = "{\'A}sthildur {\'A}rnad{\'o}ttir and Sune Pedersen and {Bo Hasselbalch}, Rasmus and Goetze, {Jens P.} and Friis-Hansen, {Lennart J.} and Bloch-M{\"u}nster, {Anna Marie} and {Skov Jensen}, Jan and Henning Bundgaard and Kasper Iversen",
note = "Publisher Copyright: {\textcopyright} 2021 Lippincott Williams and Wilkins. All rights reserved.",
year = "2021",
doi = "10.1161/CIRCULATIONAHA.120.046574",
language = "English",
volume = "143",
pages = "1095--1104",
journal = "Circulation. Supplement",
issn = "0009-7322",
publisher = "Lippincott Williams & Wilkins",
number = "11",

}

RIS

TY - JOUR

T1 - Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin after Brief Induced Coronary Artery Balloon Occlusion in Humans

AU - Árnadóttir, Ásthildur

AU - Pedersen, Sune

AU - Bo Hasselbalch, Rasmus

AU - Goetze, Jens P.

AU - Friis-Hansen, Lennart J.

AU - Bloch-Münster, Anna Marie

AU - Skov Jensen, Jan

AU - Bundgaard, Henning

AU - Iversen, Kasper

N1 - Publisher Copyright: © 2021 Lippincott Williams and Wilkins. All rights reserved.

PY - 2021

Y1 - 2021

N2 - Background: Cardiac troponins (cTns) are the cornerstone of diagnosing acute myocardial infarction. There is limited knowledge on the duration of ischemia necessary to induce a measurable release of cTns or the very-early-release kinetics of cTns after an ischemic event. Copeptin may have a supplementary role in ruling out myocardial infarction early. We investigated the release of cTns and copeptin in the first hours after experimental balloon-induced ischemia in humans. Methods: Thirty-four patients (median age, 60 years [interquartile range, 51-64]; 15 men, 43%) with angiographically normal coronary arteries were randomly assigned into 4 groups with different durations of induced myocardial ischemia (0, 30, 60, 90 s). Ischemia was induced by inflating a balloon in the left anterior descending artery between the first and second diagonal branch. Blood was collected before balloon inflation (baseline) every 15 minutes for the first 3 hours, and every 30 minutes for the next 3 hours. The cTns were analyzed by 3 high-sensitivity (hs) cTn assays: hs-cTnT (Roche), hs-cTnI (Siemens), and hs-cTnI (Abbott). Copeptin was analyzed by a sandwich immunoluminometric assay. Results: None of the patients had any complications. Increased cTn concentrations were detected by all 3 assays, and the magnitude of the increase was associated with the duration of ischemia. Increased hs-cTnI (Siemens) concentrations were first detectable 15 minutes after 90-s ischemia (median 43.7% increase) and increased more steeply and had a higher peak than the other assays. Copeptin levels did not significantly change. Using the cTnT, hs-cTnI (Siemens), and hs-cTnI (Abbott) concentrations at 0 and 180 minutes, 1 (11%), 0, and 0 patients from the 60-s ischemia group and 5 (63%), 2 (25%), and 1 (11%) from the 90-s ischemia group, respectively, fulfilled criteria for a biochemical myocardial infarction. Conclusions: This study is the first to report the early-release kinetics of cTn concentrations after different durations of experimental coronary balloon occlusion in humans. All assays detected a cTn increase after only 30 s of ischemia. hs-cTnI (Siemens) rose faster and reached a higher peak. Copeptin levels did not change significantly. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03203057.

AB - Background: Cardiac troponins (cTns) are the cornerstone of diagnosing acute myocardial infarction. There is limited knowledge on the duration of ischemia necessary to induce a measurable release of cTns or the very-early-release kinetics of cTns after an ischemic event. Copeptin may have a supplementary role in ruling out myocardial infarction early. We investigated the release of cTns and copeptin in the first hours after experimental balloon-induced ischemia in humans. Methods: Thirty-four patients (median age, 60 years [interquartile range, 51-64]; 15 men, 43%) with angiographically normal coronary arteries were randomly assigned into 4 groups with different durations of induced myocardial ischemia (0, 30, 60, 90 s). Ischemia was induced by inflating a balloon in the left anterior descending artery between the first and second diagonal branch. Blood was collected before balloon inflation (baseline) every 15 minutes for the first 3 hours, and every 30 minutes for the next 3 hours. The cTns were analyzed by 3 high-sensitivity (hs) cTn assays: hs-cTnT (Roche), hs-cTnI (Siemens), and hs-cTnI (Abbott). Copeptin was analyzed by a sandwich immunoluminometric assay. Results: None of the patients had any complications. Increased cTn concentrations were detected by all 3 assays, and the magnitude of the increase was associated with the duration of ischemia. Increased hs-cTnI (Siemens) concentrations were first detectable 15 minutes after 90-s ischemia (median 43.7% increase) and increased more steeply and had a higher peak than the other assays. Copeptin levels did not significantly change. Using the cTnT, hs-cTnI (Siemens), and hs-cTnI (Abbott) concentrations at 0 and 180 minutes, 1 (11%), 0, and 0 patients from the 60-s ischemia group and 5 (63%), 2 (25%), and 1 (11%) from the 90-s ischemia group, respectively, fulfilled criteria for a biochemical myocardial infarction. Conclusions: This study is the first to report the early-release kinetics of cTn concentrations after different durations of experimental coronary balloon occlusion in humans. All assays detected a cTn increase after only 30 s of ischemia. hs-cTnI (Siemens) rose faster and reached a higher peak. Copeptin levels did not change significantly. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03203057.

KW - copeptins

KW - myocardial ischemia

KW - troponin I

KW - troponin T

U2 - 10.1161/CIRCULATIONAHA.120.046574

DO - 10.1161/CIRCULATIONAHA.120.046574

M3 - Journal article

C2 - 33297742

AN - SCOPUS:85102965220

VL - 143

SP - 1095

EP - 1104

JO - Circulation. Supplement

JF - Circulation. Supplement

SN - 0009-7322

IS - 11

ER -

ID: 281227896