MACH, Lukáš, Tomas KONECNY, Kateřina HELÁNOVÁ, Allan S. JAFFE, Eric J. SORENSON, Virend K. SOMERS and Guy S. REEDER. Elevation of cardiac troponin T in patients with amyotrophic lateral sclerosis. Acta Neurologica Belgica. Heidelberg: Springer Heidelberg, 2016, vol. 116, No 4, p. 557-564. ISSN 0300-9009. Available from: https://dx.doi.org/10.1007/s13760-015-0596-8.
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Basic information
Original name Elevation of cardiac troponin T in patients with amyotrophic lateral sclerosis
Authors MACH, Lukáš (203 Czech Republic, belonging to the institution), Tomas KONECNY (203 Czech Republic), Kateřina HELÁNOVÁ (203 Czech Republic, guarantor), Allan S. JAFFE (840 United States of America), Eric J. SORENSON (840 United States of America), Virend K. SOMERS (840 United States of America) and Guy S. REEDER (840 United States of America).
Edition Acta Neurologica Belgica, Heidelberg, Springer Heidelberg, 2016, 0300-9009.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30201 Cardiac and Cardiovascular systems
Country of publisher Germany
Confidentiality degree is not subject to a state or trade secret
WWW URL
Impact factor Impact factor: 1.722
RIV identification code RIV/00216224:14110/16:00089280
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.1007/s13760-015-0596-8
UT WoS 000387681300019
Keywords in English Acute coronary syndrome; Neuromuscular disease; Amyotrophic lateral sclerosis; Troponin T
Tags EL OK
Tags International impact, Reviewed
Changed by Changed by: Mgr. Michal Petr, učo 65024. Changed: 12/5/2017 12:32.
Abstract
Limited evidence suggests that specificity of cardiac troponin T (cTnT), a highly sensitive biomarker of myocardial injury, is reduced in patients with skeletal myopathies. Whether amyotrophic lateral sclerosis (ALS) the most common motor neuron disease could be also associated with abnormal plasma or serum cTnT levels remains unclear. Our objective was to assess cTnT levels in patients with ALS without known cTnT elevating conditions. Among ALS patients seen at our institution until 2012 we identified those who had their cTnT measured. Patients who suffered from conditions known to elevate cTnT were excluded. A case–control analysis comparing cTnT levels of these ALS patients to matched non-ALS controls fulfilling the same inclusion criteria was performed. We included 40 ALS patients of whom 27 (68 %) patients had a positive cTnT. In the control group (n = 40), 2 (5 %) tested as cTnT positive. Among the ALS patients who underwent cTnT evaluation on more occasions (n = 7; median followup = 1.08 years), 2 (29 %) patients tested positive during the initial measurement while 6 (86 %) of them had positive cTnT at the subsequent evaluations. ALS patients with increased cTnT had been diagnosed with ALS significantly earlier than those without the elevation. Our findings raise the possibility that ALS may cause cTnT elevations. Further studies are needed to confirm these findings, clarify the pathophysiological mechanism, and establish the significance of cTnT elevations in patients with ALS.
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