Cardiac troponin and β-type myosin heavy chain concentrations in patients with polymyositis or dermatomyositis

被引:66
作者
Erlacher, P
Lercher, A
Falkensammer, J
Nassonov, EL
Samsonov, MI
Shtutman, VZ
Puschendorf, B
Mair, J
机构
[1] Univ Innsbruck, Innere Med Klin, Klin Abt Kardiol, Dept Internal Med,Div Cardiol, A-6020 Innsbruck, Austria
[2] Univ Innsbruck, Dept Med Chem & Biochem, Div Clin Biochem, A-6020 Innsbruck, Austria
[3] Cardiovasc Res Ctr, Moscow, Russia
关键词
polymyositis; dermatomyositis; creatine kinase isoenzyme MB; cardiac troponin I; cardiac troponin T; myoglobin; myosin heavy chain;
D O I
10.1016/S0009-8981(01)00392-8
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Cardiac troponin T (cTnT), cardiac troponin I(cTnI), myosin heavy chains (MHC), myoglobin, creatine kinase (CK), and creatine kinase isoenzyme MB (CKMB), were measured in blood samples from 39 polymyositis (PM) or dermatomyositis (DM) patients without clinical evidence for cardiac involvement to evaluate their clinical usefulness in this patient population. MHC, myoglobin, and CKMB were frequently elevated and correlated with each other and with disease severity. Undetectable cTnI in all but one patient indicated that MHC was released from skeletal muscle, thereby providing the first laboratory evidence of frequent slow-twitch muscle fibre-necrosis in patients with PM or DM. CKMB was elevated in 51%, cTnT in 41%, and cTnI in only 2.5% of patients, cTnI did not correlate with other markers or with disease severity scores. The close correlations found between cTnT and skeletal muscle damage markers and the relationship between cTnT with disease severity without clinical evidence for myocardial damage suggest a release of cTnT from skeletal muscle. The relationship of cTnT with disease severity indicates a possible role of the marker for risk stratification. However, the prognostic values of cardiac troponins and other muscle damage markers in PM/DM patients remain to be compared in prospective outcome trials. (C) 2001 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:27 / 33
页数:7
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