An observational study in Myopathy, Muscle Weakness and Muscle Damage, sponsored by University Hospital, Basel, Switzerland. Active, not recruiting at 5 sites in 2 countries. Open to participants aged 18 Years and older. Per ClinicalTrials.gov, last updated 2026-09-21.
Sponsored by University Hospital, Basel, Switzerland · Observational
Visits to the emergency department (ED) for chest pain are extremely common and require a safe, rapid and efficacious treatment algorithm to exclude a possible AMI. These diagnostic algorithms are partly based on an important laboratory value, which showed growing utility in the diagnostic and prognostic of many cardiovascular diseases in the last years : cardiac troponin.
However, some patients with muscle disease often present with unexplained elevated high-sensitive cardiac Troponin T (hs-cTnT) levels in the absence of cardiac disease. The investigators aim at the characterization of the behaviour of this biomarker and its alternative (high-sensitive cardiac Troponin I), which will have important clinical implications on patients management.
Introduction: The detection of cardiomyocyte injury as quantified by blood concentrations of cardiac troponin T (cTnT) or I (cTnI) is central in the diagnosis of acute myocardial infarction (AMI). While multiple cardiac disorders other than AMI may also lead to cardiomyocyte injury and therefore elevations in cTnT and cTnI, latest generations of cTnT and cTnI assays are considered to have near exclusive cardiac-specificity. Overall, both analytes (cTnT and cTnI) seem to have comparable diagnostic accuracy among patients presenting with suspected AMI to the emergency department (ED). However, their use in the diagnosis of AMI in patients with a skeletal muscle disease is questioned, as especially cTnT was found to be elevated in this setting. These increased cTnT levels have been successively attributed to a possible re-expression of cTnT isoforms in the diseased muscle, to a primary cardiac involvement associated with the muscle disease or to a cross-reaction of the hs-cTnT assay with TnT of muscle origin.
Aim: To characterize cTn levels in patients with a skeletal muscle disease to assess their utility in the field of cardiology (through their implication in AMI diagnosis and their diagnostic and prognostic accuracy regarding a possible cardiac involvement) and in the field of neurology (for the detection and risk-stratification of the muscle disorder itself).
Methodology: This study will be conducted at the University Hospital of Basel, at the Kantonsspital Aarau, both in Switzerland, and at the University Hospital of Innsbruck, Austria. A prospective cohort patient will be recruited through the neurology, rheumatology and cardiology clinics of these three hospitals. This prospective cohort of patients presenting with skeletal muscle disease will allow us to systematically screen patients for cTn increases, to investigate the prevalence and characteristics of a possible primary cardiac involvement (as documented by electrocardiogram, echocardiography, magnetic resonance imaging, cTnI, NT-proBNP (N-terminal pro-B-type Natriuretic Peptide) and any available further cardiac testing) and to explore the origins of the elevated cTn levels using muscle biopsies. Furthermore, this prospective cohort will document the role of these biomarkers in the diagnosis, prognosis and risk-stratification of the muscle disease. Patients will receive a 1- and 3-year follow-up visit with blood draw in order to measure cTn and other biomarkers and record the impact of the evolution and treatment of the muscle disease on these levels. Major adverse cardiac events including cardiovascular death, AMI, hospitalization for heart failure, and the development of clinical or subclinical heart failure as quantified by elevated blood concentrations of NT-proBNP will be recorded during follow-up.
Potential significance: Elevated cTnT levels do not only have consequences regarding the diagnosis of AMI but also raise many questions regarding their possible use as a diagnostic, prognostic and risk-stratification marker regarding the different muscle injuries and their possible primary cardiac involvement.
232 studies on the registry are indexed under Muscular Diseases; 54 are open to participants now.
This study's enrollment of 797 is above the median of 95 across 85 observational studies indexed under Muscular Diseases.
Browse Muscular Diseases studies →University Hospital, Basel, Switzerland is the lead sponsor of 990 studies on the registry; 189 are open to participants now.
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Consecutive participants which have been or currently are in treatment for a muscle disease at the University hospital of Basel, at the Canton Hospital of Aarau, University Hospital of Zürich or Bern or at the Medical University of Innsbruck, or who received a new diagnosis/suspicion of such a disease will be included.
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Exclusion Criteria:
Comparison of cTnT and cTnI levels as measured by different hs-cTn assays in patients with skeletal muscle disease.
Time frame: 1 year
Comparison of levels of cTnT and cTnI as measured by hs-assays in matched patients with and without skeletal muscle disease.
Time frame: 1 year
Regression model of diverse patients' characteristics on levels of hs-cTnI and hs-cTnT in the context of skeletal muscle disease versus no skeletal muscle disease.
Time frame: 1 year
Prognostic value of hs-cTn levels in patients with and without skeletal muscle disease.
Time frame: 3 years
Characterization of cTnT and cTnI on skeletal muscle biopsies from myopathic patients.
Time frame: 1 year
Characterization of the impact of cTnT and cTnI on the diagnosis and prognosis of muscle diseases
Prognosis defined as the incidence of Major Cardiovascular Events (MACE is defined as a composite of death, acute myocardial infarction, life-threatening arrhythmia (cardiac arrest, sustained ventricular tachycardia, atrioventricular (AV) -block III), cardiac arrest/reanimation, acute heart failure (requiring admission to a hospital or intra-hospital transfer to the intensive care unit), stroke/transient ischemic attack, pulmonary embolism)
Time frame: 3 years
Research on the development of a new cTnT-assay
Time frame: 3 years
Protein characterization
Time frame: 3 years
Cardiac troponin as predictors or screening tools for a cardiac involvement
Time frame: 3 years
Cardiac troponin as predictor of evolution and therapeutic response of the muscle disease or muscle regeneration.
Time frame: 3 years
Characterisation of cardiac troponin in diseases of various etiologies involving muscles
Time frame: 3 years
Impact of muscle symptoms on cardiac troponin
Time frame: 3 years
Cardiac troponin versus other markers (e.g. CK) of inflammation/necrosis of peripheral muscles.
Time frame: 3 years
Plan to share: Undecided
This study is active, not recruiting, as verified in Sep 2026. You cannot join it, but the record below documents what was studied.
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University Hospital, Basel, Switzerland →