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A Possible Mechanism behind Faster Clearance and Higher Peak Concentrations of Cardiac Troponin I Compared with Troponin T in Acute Myocardial Infarction

Artikel i vetenskaplig tidskrift
Författare Karin Starnberg
Vincent Fridén
Aida Muslimovic
Sven-Erik Ricksten
Susanne Nyström
Niklas Forsgard
B. Lindahl
Kristina Vukusic
Joakim Sandstedt
Göran Dellgren
Ola Hammarsten
Publicerad i Clinical Chemistry
Volym 66
Nummer/häfte 2
Sidor 333-341
ISSN 0009-9147
Publiceringsår 2020
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för anestesiologi och intensivvård
Institutionen för biomedicin, avdelningen för laboratoriemedicin
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 333-341
Språk en
Länkar dx.doi.org/10.1093/clinchem/hvz003
https://academic.oup.com/clinchem/a...
Ämnesord creatine-kinase, rapid rule, plasma, kinetics, release, serum, elimination, Medical Laboratory Technology
Ämneskategorier Kardiologi

Sammanfattning

BACKGROUND: Although cardiac troponin I (cTnI) and troponin T (cTnT) form a complex in the human myocardium and bind to thin filaments in the sarcomere, cTnI often reaches higher concentrations and returns to normal concentrations faster than cTnT in patients with acute myocardial infarction (MI). METHODS: We compared the overall clearance of cTnT and cTnI in rats and in patients with heart failure and examined the release of cTnT and cTnI from damaged human cardiac tissue in vitro. RESULTS: Ground rat heart tissue was injected into the quadriceps muscle in rats to simulate myocardial damage with a defined onset. cTnT and cTnI peaked at the same time after injection. cTnI returned to baseline concentrations after 54 h, compared with 168 h for cTnT. There was no difference in the rate of clearance of solubilized cTnT or cTnI after intravenous or intramuscular injection. Renal clearance of cTnT and cTnI was similar in 7 heart failure patients. cTnI was degraded and released faster and reached higher concentrations than cTnT when human cardiac tissue was incubated in 37 degrees C plasma. CONCLUSION: Once cTnI and cTnT are released to the circulation, there seems to be no difference in clearance. However, cTnI is degraded and released faster than cTnT from necrotic cardiac tissue. Faster degradation and release may be the main reason why cTnI reaches higher peak concentrations and returns to normal concentrations faster in patients with MI.

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