
Myosin Heavy-Chain Fragments and Cardiac Troponins in the Serum in RhabdomyolysisDiagnostic Specificity of New Biochemical Markers
Mervi Löfberg, MD;
Riitta Tähtelä, MSc;
Matti Härkönen, MD, PhD;
Hannu Somer, MD, PhD
Arch Neurol. 1995;52(12):1210-1214.
Abstract
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Background Myosin is the major structural protein in muscle. Antibodies to β-type heavy meromyosin react with cardiac and slow-twitch skeletal muscle. Cardiac TnT and TnI were developed as tissue-specific indicators.
Objectives To study myosin heavy-chain fragments as a delayed marker of previous rhabdomyolysis. To examine the cardiac specificity of cardiac troponin T (TnT) and cardiac troponin I (TnI) in patients with severe skeletal muscle damage.
Design and Methods Serum myosin heavy-chain fragments, TnT, and TnI were studied up to 12 days after diagnosis in relationship to the serum creatine kinase level in 20 patients with rhabdomyolysis. The mean peak serum creatine kinase activity was 91 300 U/L. Myosin heavy-chain fragments were measured by an immunoradiometric assay, TnT by a one-step immunoenzymometric assay, and TnI by an immunoenzymometric assay.
Results Values for serum myosin heavy-chain fragments were greater than the upper limit of normal in all patients. The peak value (70 times the upper normal limit, on average) was usually achieved 4 to 7 days after the diagnosis of rhabdomyolysis, and it was increased up to 12 days. The peak level of TnT was increased in 95% of the patients, and it correlated strongly with the peak activity of serum creatine kinase. The highest TnI value was above the detection limit of myocardial infarction in 30% of the patients. Half of these patients were the only patients with ischemic changes observed on an electrocardiogram performed on admission to the hospital.
Conclusions The measurement of myosin heavychain fragments was useful in the diagnosis of previous rhabdomyolysis up to 12 days. The role of TnT was negligible as an indicator of cardiac muscle damage in patients with severe rhabdomyolysis. Cardiac TnI is a more tissue-specific marker for myocardial damage even with concurrent rhabdomyolysis.
Author Affiliations
From the Departments of Neurology (Drs Löfberg and Somer) and Clinical Chemistry (Ms Tähtelä and Dr Härkönen), Helsinki University Central Hospital, Helsinki, Finland.
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