Skeletal Muscle Disorders: A Noncardiac Source of Cardiac Troponin T.
muscle, skeletal
myocardial infarction
myopathies, structural, congenital
troponin
Journal
Circulation
ISSN: 1524-4539
Titre abrégé: Circulation
Pays: United States
ID NLM: 0147763
Informations de publication
Date de publication:
14 06 2022
14 06 2022
Historique:
pubmed:
8
4
2022
medline:
16
6
2022
entrez:
7
4
2022
Statut:
ppublish
Résumé
Cardiac troponin (cTn) T and cTnI are considered cardiac specific and equivalent in the diagnosis of acute myocardial infarction. Previous studies suggested rare skeletal myopathies as a noncardiac source of cTnT. We aimed to confirm the reliability/cardiac specificity of cTnT in patients with various skeletal muscle disorders (SMDs). We prospectively enrolled patients presenting with muscular complaints (≥2 weeks) for elective evaluation in 4 hospitals in 2 countries. After a cardiac workup, patients were adjudicated into 3 predefined cardiac disease categories. Concentrations of cTnT/I and resulting cTnT/I mismatches were assessed with high-sensitivity (hs-) cTnT (hs-cTnT-Elecsys) and 3 hs-cTnI assays (hs-cTnI-Architect, hs-cTnI-Access, hs-cTnI-Vista) and compared with those of control subjects without SMD presenting with adjudicated noncardiac chest pain to the emergency department (n=3508; mean age, 55 years; 37% female). In patients with available skeletal muscle biopsies, Among 211 patients (mean age, 57 years; 42% female), 108 (51%) were adjudicated to having no cardiac disease, 44 (21%) to having mild disease, and 59 (28%) to having severe cardiac disease. hs-cTnT/I concentrations significantly increased from patients with no to those with mild and severe cardiac disease for all assays (all In patients with active chronic SMD, elevations in cTnT concentrations are common and not attributable to cardiac disease in the majority. This was not observed for cTnI and may be explained in part by re-expression of cTnT in skeletal muscle. URL: https://www. gov; Unique identifier: NCT03660969.
Sections du résumé
BACKGROUND
Cardiac troponin (cTn) T and cTnI are considered cardiac specific and equivalent in the diagnosis of acute myocardial infarction. Previous studies suggested rare skeletal myopathies as a noncardiac source of cTnT. We aimed to confirm the reliability/cardiac specificity of cTnT in patients with various skeletal muscle disorders (SMDs).
METHODS
We prospectively enrolled patients presenting with muscular complaints (≥2 weeks) for elective evaluation in 4 hospitals in 2 countries. After a cardiac workup, patients were adjudicated into 3 predefined cardiac disease categories. Concentrations of cTnT/I and resulting cTnT/I mismatches were assessed with high-sensitivity (hs-) cTnT (hs-cTnT-Elecsys) and 3 hs-cTnI assays (hs-cTnI-Architect, hs-cTnI-Access, hs-cTnI-Vista) and compared with those of control subjects without SMD presenting with adjudicated noncardiac chest pain to the emergency department (n=3508; mean age, 55 years; 37% female). In patients with available skeletal muscle biopsies,
RESULTS
Among 211 patients (mean age, 57 years; 42% female), 108 (51%) were adjudicated to having no cardiac disease, 44 (21%) to having mild disease, and 59 (28%) to having severe cardiac disease. hs-cTnT/I concentrations significantly increased from patients with no to those with mild and severe cardiac disease for all assays (all
CONCLUSIONS
In patients with active chronic SMD, elevations in cTnT concentrations are common and not attributable to cardiac disease in the majority. This was not observed for cTnI and may be explained in part by re-expression of cTnT in skeletal muscle.
REGISTRATION
URL: https://www.
CLINICALTRIALS
gov; Unique identifier: NCT03660969.
Identifiants
pubmed: 35389756
doi: 10.1161/CIRCULATIONAHA.121.058489
pmc: PMC10069758
doi:
Substances chimiques
Biomarkers
0
RNA, Messenger
0
Troponin I
0
Troponin T
0
Banques de données
ClinicalTrials.gov
['NCT03660969']
Types de publication
Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1764-1779Investigateurs
Tibor Zehntner
(T)
Raoul Giger
(R)
Thomas Stoll
(T)
Hadrien Schöpfer
(H)
Fabian Jordan
(F)
Michael Carigiet
(M)
Nicola Haeni
(N)
Vincent Gysin
(V)
Michele Sara Gafner
(MS)
Desiree Wussler
(D)
Luca Koechlin
(L)
Michael Freese
(M)
Christian Ruiz
(C)
Olivia Strauch
(O)
Tobias Zimmermann
(T)
Ivo Strebel
(I)
Ulrich A Walker
(UA)
Thomas Vogt
(T)
Martina Hartmann
(M)
Timo Kahles
(T)
Paul Hasler
(P)
Funda Seidel
(F)
Xenia Zavtsyea
(X)
Katharina Rentsch
(K)
Sandra Mitrovic
(S)
Arnold von Eckardstein
(A)
Johannes Mair
(J)
Michael Schreinlechner
(M)
Wijstke Wallimann
(W)
Manuel Dietrich
(M)
Tania Carrillo Roah
(TC)
Markus Knoll
(M)
Alexander Fuchs
(A)
Ellen Bruske
(E)
Matthias Munz
(M)
Stefan Kunzelmann
(S)
Gesa Albert
(G)
Tobias Becher
(T)
Peter Kastner
(P)
Samuel Katsuyuki Shinjo
(SK)
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Type : CommentIn
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