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J Am Coll Cardiol. 2018 Apr 10;71(14):1540-1549. doi: 10.1016/j.jacc.2018.01.070.

Elevated Cardiac Troponin T in Patients With Skeletal Myopathies.

Author information

1
Division of Cardiology, Department of Internal Medicine, Medical University of Graz, Graz, Austria; Division of General Radiology, Department of Radiology, Medical University of Graz, Graz, Austria. Electronic address: johannes.schmid@medunigraz.at.
2
Department of Pathology, Medical University of Graz, Graz, Austria; Omics Center Graz, BioTechMed-Graz, Graz, Austria.
3
Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria.
4
Department of Laboratory Medicine, Konventhospital Barmherzige Brueder Linz, Linz, Austria.
5
Department of Pathology, Medical University of Graz, Graz, Austria.
6
Department of Orthopedics, Medical University of Graz, Graz, Austria.
7
Clinic for Diagnostic and Interventional Radiology, University Hospital Ulm, Ulm, Germany.
8
Department of Internal Medicine III-Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.
9
Division of General Radiology, Department of Radiology, Medical University of Graz, Graz, Austria.
10
Institute for Medical Informatics, Statistics and Documentation, Medical University of Graz, Graz, Austria.
11
Department of Neurology, Medical University of Graz, Graz, Austria.
12
Division of Cardiology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
13
Division of Cardiology, Department of Internal Medicine, Medical University of Graz, Graz, Austria. Electronic address: herzforschung@gmail.com.

Abstract

BACKGROUND:

Cardiac troponins are often elevated in patients with skeletal muscle disease who have no evidence of cardiac disease.

OBJECTIVES:

The goal of this study was to characterize cardiac troponin concentrations in patients with myopathies and derive insights regarding the source of elevated troponin T measurements.

METHODS:

Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) concentrations were determined by using high sensitivity assays in 74 patients with hereditary and acquired skeletal myopathies. Patients underwent comprehensive cardiac evaluation, including 12-lead electrocardiogram, 24-h electrocardiogram, cardiac magnetic resonance imaging, and coronary artery computed tomography. cTnT and cTnI protein expression was determined in skeletal muscle samples of 9 patients and in control tissues derived from autopsy using antibodies that are used in commercial assays. Relevant Western blot bands were subjected to liquid chromatography tandem mass spectrometry for protein identification.

RESULTS:

Levels of cTnT (median: 24 ng/l; interquartile range: 11 to 54 ng/l) were elevated (>14 ng/l) in 68.9% of patients; cTnI was elevated (>26 ng/l) in 4.1% of patients. Serum cTnT levels significantly correlated with creatine kinase and myoglobin (r = 0.679 and 0.786, respectively; both p < 0.001). Based on cTnT serial testing, 30.1% would have fulfilled current rule-in criteria for myocardial infarction. Noncoronary cardiac disease was present in 23%. Using cTnT antibodies, positive bands were found in both diseased and healthy skeletal muscle at molecular weights approximately 5 kDa below cTnT. Liquid chromatography tandem mass spectrometry identified the presence of skeletal troponin T isoforms in these bands.

CONCLUSIONS:

Measured cTnT concentrations were chronically elevated in the majority of patients with skeletal myopathies, whereas cTnI elevation was rare. Our data indicate that cross-reaction of the cTnT immunoassay with skeletal muscle troponin isoforms was the likely cause.

KEYWORDS:

cardiac troponin; myopathy; skeletal muscle

PMID:
29622161
DOI:
10.1016/j.jacc.2018.01.070
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