scholarly journals Current state of cardiac troponin testing in Duchenne muscular dystrophy cardiomyopathy: review and recommendations from the Parent Project Muscular Dystrophy expert panel

Open Heart ◽  
2021 ◽  
Vol 8 (1) ◽  
pp. e001592
Author(s):  
Christopher F Spurney ◽  
Deborah Ascheim ◽  
Lawrence Charnas ◽  
Linda Cripe ◽  
Kan Hor ◽  
...  
Keyword(s):  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Cardiac Disease ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Expert Panel ◽  
High Sensitivity ◽  
Parent Project ◽  
Silver Spring ◽  
Prospective Longitudinal

Cardiac disease is now the leading cause of death in Duchenne muscular dystrophy (DMD). Clinical evaluations over time have demonstrated asymptomatic cardiac troponin elevations and acute elevations are associated with symptoms and cardiac dysfunction in DMD. Clinicians require a better understanding of the relationship of symptoms, troponin levels and progression of cardiac disease in DMD. As clinical trials begin to assess novel cardiac therapeutics in DMD, troponin levels in DMD are important for safety monitoring and outcome measures. The Parent Project Muscular Dystrophy convened an expert panel of cardiologists, scientists, and regulatory and industry specialists on 16 December 2019 in Silver Spring, Maryland and reviewed published and unpublished data from their institutions. The panel recommended retrospective troponin data analyses, prospective longitudinal troponin collection using high-sensitivity cardiac troponin I assays, inclusion of troponin in future clinical trial outcomes and future development of clinical guidelines for monitoring and treating troponin elevations in DMD.

scholarly journals Myocardial Injury and the Release of Troponins I and T in the Blood of Patients

2020 ◽  
Author(s):  
Ivan A Katrukha ◽  
Alexey G Katrukha
Keyword(s):  
Cardiac Disease ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Clinical Evidence ◽  
Troponin I ◽  
High Sensitivity ◽  
Clinical Settings ◽  
Diagnostic Systems ◽  
Troponin Release

Abstract Background Cardiac troponin I (cTnI) and cTnT are the established biomarkers of cardiomyocyte damage and the recommended biomarkers for the diagnosis of acute myocardial infarction (MI). High-sensitivity immunochemical diagnostic systems are able to measure the cTn concentrations in the blood of a majority of healthy people. At the same time, the concentration of cTn may be increased not only after MI but also because of other pathologies that might affect myocardium. This effect reduces the clinical specificity of cTn for MI and may complicate the diagnosis. Content This review summarizes the existing information regarding the causes and mechanisms that lead to the increase of cTn concentration in blood and the forms of cTn that are present in circulation after MI or other types of myocardial injury. Summary Different etiologies of disease associated with increases of cTn above the 99th percentile and various mechanisms of troponin release from myocardium could result in the appearance of different forms of cTn in blood and provide the first clinical evidence of injury. Additional research is needed for the careful characterization of cTn forms that are present in the blood in different clinical settings. That knowledge may lead to the development of immunochemical systems that would differentiate certain forms of troponins and possibly certain types of cardiac disease.

Abstract 2498: Minor Myocardial Damage and LV Dysfunction in Patients with Duchenne Muscular Dystrophy-The Preventive Efficacy of Carvedilol on Plasma Cardiac Troponin I-

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Takao Nishizawa ◽  
Fumihiko Yasuma ◽  
Motoko Sakai ◽  
Satoshi Kuru ◽  
Seigo Kimura ◽  
...  
Keyword(s):  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Systolic Dysfunction ◽  
Myocardial Damage ◽  
Cardiac Troponin I ◽  
Progression Rate ◽  
Lv Dysfunction ◽  
Minor Myocardial Damage

Background: Cardiac dysfunction is one of the major prognostic factors in patients with Duchenne muscular dystrophy (DMD). Minor myocardial damage assessed by plasma cardiac troponin I (cTnI) is often observed in patients with DMD. However, it is unclear that how the minor myocardial damage occurs to which patient with DMD and how it relates to LV dysfunction. Therefore, we assessed the hypothesis that minor myocardial damage is associated with LV dysfunction, the evaluation of plasma cTnI helps the prediction of LV functional deterioration, and carvedilol prevents elevation of plasma cTnI in patients with DMD. Methods: Plasma cTnI were repeatedly (every 3 months) measured for 2 years and LV function was assessed by echocardiography in 58 patients with DMD. Carvedilol (2.5–5 mg/day) was orally administered for a year to the patients who have shown plasma cTnI elevation (positive cTnI, cut off 0.06ng/mL). Results: There were 3 differential groups regarding the progression rate of LV systolic dysfunction, i.e. rapid (19% of total, LVEF < 50% in their 10 th ), slow (50% of total, LVEF > 50% in their 20 –30 th ), and unchanged group (31% of total, LVEF < 50% in their 20 –30 th ). The episode of positive cTnI was observed in 27 (46%) of total patients with DMD. LVEF was lower in patients with positive cTnI than that with negative cTnI (42 ± 2 vs. 52 ± 2%, p < 0.05). Positive cTnI was observed in all patients in rapid group, 84% of patients in slow group, and only 6% of patients in unchanged group. Fourteen differential dystrophin gene mutations were recognized in 48 patients but they were not associated with those 3 differential groups or patients with positive cTnI. Administration of carvedilol in 13 patients (LVEF 40 ± 3) decreased the cTnI detection rate (from 44 ± 5% to 26 ± 10%, p < 0.05), while it was unchanged in 14 patients (LVEF 41 ± 3) without carvedilol treatment (from 44 ± 7% to 39 ± 6%) during same observation period. Conclusions: The elevation of plasma cTnI was associated with LV systolic dysfunction in patients with DMD. The prediction of LV dysfunction in patients with DMD may be feasible with combinations of age, LVEF, and plasma cTnI elevation. Carvedilol could be a new therapeutic strategy to prevent minor myocardial damage in patients with DMD.

scholarly journals Safety and disease monitoring biomarkers in Duchenne muscular dystrophy: results from a Phase II trial

2021 ◽  
Author(s):  
Kathryn R Wagner ◽  
Michaela Guglieri ◽  
Shashi K Ramaiah ◽  
Lawrence Charnas ◽  
Shannon Marraffino ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Liver Injury ◽  
Phase Ii ◽  
Cardiac Troponin ◽  
Muscle Injury ◽  
Troponin I ◽  
Phase Ii Trial ◽  
Muscle Health

Aim: Evaluate the utility of glutamate dehydrogenase (GLDH) and cardiac troponin I as safety biomarkers, and creatine kinase and muscle injury panel as muscle health biomarkers in Duchenne muscular dystrophy. Patients & methods: Data were collected during a Phase II trial of domagrozumab. Results: GLDH was a more specific biomarker for liver injury than alanine aminotransferase. Cardiac troponin I elevations were variable and not sustained, limiting its applicability as a biomarker. Muscle injury panel biomarkers were no more informative than creatine kinase as a muscle health biomarker. Conclusion: Results support the use of GLDH as a specific biomarker for liver injury in patients with Duchenne muscular dystrophy. Clinical trial registration: ClinicalTrials.gov , NCT02310763 .

Analytical assessment of ortho clinical diagnostics high-sensitivity cardiac troponin I assay

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Peter A. Kavsak ◽  
Tara Edge ◽  
Chantele Roy ◽  
Paul Malinowski ◽  
Karen Bamford ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Limit Of Detection ◽  
Clinical Performance ◽  
Characteristic Curve ◽  
Area Under The Curve ◽  
High Sensitivity ◽  
Cardiac Troponin I ◽  
Clinical Diagnostics ◽  
Ortho Clinical Diagnostics

AbstractObjectivesTo analytically evaluate Ortho Clinical Diagnostics VITROS high-sensitivity cardiac troponin I (hs-cTnI) assay in specific matrices with comparison to other hs-cTn assays.MethodsThe limit of detection (LoD), imprecision, interference and stability testing for both serum and lithium heparin (Li-Hep) plasma for the VITROS hs-cTnI assay was determined. We performed Passing-Bablok regression analyses between sample types for the VITROS hs-cTnI assay and compared them to the Abbott ARCHITECT, Beckman Access and the Siemens ADVIA Centaur hs-cTnI assays. We also performed Receiver-operating characteristic curve analyses with the area under the curve (AUC) determined in an emergency department (ED)-study population (n=131) for myocardial infarction (MI).ResultsThe VITROS hs-cTnI LoD was 0.73 ng/L (serum) and 1.4 ng/L (Li-Hep). Stability up to five freeze-thaws was observed for the Ortho hs-cTnI assay, with the analyte stability at room temperature in serum superior to Li-Hep with gross hemolysis also affecting Li-Hep plasma hs-cTnI results. Comparison of Li-Hep to serum concentrations (n=202), yielded proportionally lower concentrations in plasma with the VITROS hs-cTnI assay (slope=0.85; 95% confidence interval [CI]:0.83–0.88). In serum, the VITROS hs-cTnI concentrations were proportionally lower compared to other hs-cTnI assays, with similar slopes observed between assays in samples frozen <−70 °C for 17 years (ED-study) or in 2020. In the ED-study, the VITROS hs-cTnI assay had an AUC of 0.974 (95%CI:0.929–0.994) for MI, similar to the AUCs of other hs-cTn assays.ConclusionsLack of standardization of hs-cTnI assays across manufacturers is evident. The VITROS hs-cTnI assay yields lower concentrations compared to other hs-cTnI assays. Important differences exist between Li-Hep plasma and serum, with evidence of stability and excellent clinical performance comparable to other hs-cTn assays.

scholarly journals Misclassification of Myocardial Injury by a High-Sensitivity Cardiac Troponin I Assay

2021 ◽  
Author(s):  
Peter A. Kavsak ◽  
Shawn Mondoux ◽  
Andrew Worster ◽  
Janet Martin ◽  
Vikas Tandon ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
High Sensitivity ◽  
Cardiac Troponin I
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