title: Concentration time courses of troponin and myosin subunits after acute myocardial infarction.
abstract: BACKGROUND
  As a result of the limited sensitivity and specificity of creatine kinase and lactate dehydrogenase (LDH) as well as their isoenzymes, there is increasing interest in the use of cardiac contractile proteins for the diagnosis of acute myocardial infarction (AMI) and myocardial damage.
  
  
  METHODS
  This study compared the release of creatine kinase, creatine kinase MB, myoglobin, cardiac troponin I (cTnI), cardiac troponin T (cTnT), cardiac myosin light chain-1 (cMLC-1), and beta-type myosin heavy chains (bMHC) in serial blood samples from 13 patients (10 men, three women; median age 54 years, range 40-74 years) with first-time AMI (11 Q-wave, two non-Q-wave AMI; three anterior and 10 inferior wall AMI). All but one patient received intravenous thrombolytic treatment.
  
  
  RESULTS
  Myoglobin was the first marker to increase in blood after AMI and showed the earliest peak levels, whereas bMHC increased latest, showing the latest peak levels. cTnI and cTnT increased significantly earlier than cMLC-1 and bMHC. cTnI and cTnT increased and reached peak levels parallel to each other, but the latter tended to stay increased longer. cTnT time courses were biphasic in the majority of AMI patients, unlike cTnI time courses. cMLC-1 release was mostly biphasic. cMLC-1 allows diagnosis during the acute phase as well as several days after the onset of AMI. The time courses of bMHC were usually monophasic. Its delayed appearance makes it useful for the diagnosis of remote infarction. In contrast to cTnI and cTnT, cMLC-1 and bMHC time courses were not significantly influenced by early reperfusion.
  
  
  CONCLUSIONS
  Our results demonstrate the impact of the intracellular compartmentation of an intramyocardial protein (cytosolic, structurally bound, or structurally bound with soluble pool) on its concentration time course after AMI, particularly on the rapidity of its release.
authors.affiliation: Department of Medical Chemistry and Biochemistry, University of Innsbruck Medical School, Austria.
authors.forename: J
authors.initials: J
authors.lastname: Mair
authors.forename: B
authors.initials: B
authors.lastname: Thome-Kromer
authors.forename: I
authors.initials: I
authors.lastname: Wagner
authors.forename: P
authors.initials: P
authors.lastname: Lechleitner
authors.forename: F
authors.initials: F
authors.lastname: Dienstl
authors.forename: B
authors.initials: B
authors.lastname: Puschendorf
authors.forename: G
authors.initials: G
authors.lastname: Michel
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D003402:Creatine Kinase / Q000097:blood / Q000378:metabolism; D005260:Female; D006801:Humans; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis / Q000378:metabolism; D009211:Myoglobin / Q000097:blood / Q000378:metabolism; D009218:Myosins / Q000097:blood* / Q000378:metabolism; D013997:Time Factors; D014336:Troponin / Q000097:blood* / Q000378:metabolism
chemical_list: D015415:Biomarkers; D009211:Myoglobin; D014336:Troponin; D003402:Creatine Kinase; D009218:Myosins