2022
DOI: 10.1161/circulationaha.122.061976
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Response by du Fay de Lavallaz et al to Letter Regarding Article, “Skeletal Muscle Disorders: A Noncardiac Source of Cardiac Troponin T”

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Cited by 3 publications
(5 citation statements)
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“…Particularly, in ICI‐related myocarditis hs‐TnT was found to be persistently elevated for up to 60 days 18 . Moreover, there is evidence of ectopic TnT expression in the setting of both non‐inflammatory myopathies and myositis, likely related to an overexpression of the TNNT2 gene 19 . It will be hence important to investigate whether this ectopic de novo expression of TnT can also occur in response to certain therapies including ICIs or cancer metastases, or whether it relates to local expression in peripheral myositis.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Particularly, in ICI‐related myocarditis hs‐TnT was found to be persistently elevated for up to 60 days 18 . Moreover, there is evidence of ectopic TnT expression in the setting of both non‐inflammatory myopathies and myositis, likely related to an overexpression of the TNNT2 gene 19 . It will be hence important to investigate whether this ectopic de novo expression of TnT can also occur in response to certain therapies including ICIs or cancer metastases, or whether it relates to local expression in peripheral myositis.…”
Section: Discussionmentioning
confidence: 99%
“…18 Moreover, there is evidence of ectopic TnT expression in the setting of both non-inflammatory myopathies and myositis, likely related to an overexpression of the TNNT2 gene. 19 It will be hence important to investigate whether this ectopic de novo expression of TnT can also occur in response to certain therapies including ICIs or cancer metastases, or whether it relates to local expression in peripheral myositis. Of interest, hs-TnI has been associated with early signs of left ventricular dysfunction, as shown by reduced left ventricular longitudinal strain in patients under ICI therapy.…”
Section: Discussionmentioning
confidence: 99%
“…It is well established that neurofilament levels reflect neuroaxonal damage 31,32 . The published information on the origin of serum cTnT levels in ALS is more circumstantial, but evidence from neuromuscular diseases supports that striated muscle expresses cTnT under pathological conditions 8 .…”
Section: Resultsmentioning
confidence: 99%
“…Serum cardiac Troponin T (cTnT), widely in use as a serum marker of myocardial injury, has recently emerged as a promising candidate serum biomarker for ALS, correlating with disease severity and progression 6,7 . Accumulating evidence suggests that degenerating or regenerating skeletal muscle is an extracardiac source of serum cTnT, and can lead to serum cTnT elevations independent of myocardial damage [8][9][10] .…”
Section: Introductionmentioning
confidence: 99%
“…While data on cardiac troponin I are not available in current study, highsensitivity cTnT has been suggested to have stronger association with non-CV comorbidities in head-to-head comparisons even with high-sensitivity troponin I [20]. The ability of cTnT to reflect abnormalities at the level of diseased skeletal muscle [21] might also contribute to these adverse all-cause and non-CV outcomes, given that skeletal muscle dysfunction is prevalent in patients with dyspnea [22]. Robust evidence exists supporting role of cardiac troponins as prognostic markers of mortality and readmissions in both HFpEF and HFrEF patients [15,23].…”
mentioning
confidence: 92%