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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
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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.
Ovid Technologies (Wolters Kluwer Health)
Title: Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin After Brief Induced Coronary Artery Balloon Occlusion in Humans
Description:
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.
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