TROPONIN-T RELEASE AFTER HEART-TRANSPLANTATION

Citation
R. Zimmermann et al., TROPONIN-T RELEASE AFTER HEART-TRANSPLANTATION, British Heart Journal, 69(5), 1993, pp. 395-398
Citations number
9
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00070769
Volume
69
Issue
5
Year of publication
1993
Pages
395 - 398
Database
ISI
SICI code
0007-0769(1993)69:5<395:TRAH>2.0.ZU;2-M
Abstract
Background-For the diagnosis of myocardial cell damage the measurement of the serum concentrations of myofibrillar antigens has several pote ntial advantages over the assessment of traditional serological marker s. These include the expression of myofibrillar antigens as cardiospec ific isoforms and their high intracellular concentrations. Recently a sensitive and specific enzyme immunoassay for cardiac troponin T has b een developed that shows little cross-reactivity with skeletal isoform s. Objective-To characterise myocardial cell damage after orthotopic h eart transplantation, concentrations of circulating troponin T were me asured prospectively in serial blood samples from 19 consecutive patie nts taken during the first three months after transplantation. Results -Mean (SD) serum concentrations of cardiac troponin T reached a maximu m of 3-6 (1.8) mug/l at 7-1 (4.2) days after transplantation and remai ned higher than 0.5 mug/l (twice the detection limit of the assay) in all patients for at least 43 days (mean (SD) 59 (20) days). There was considerable variation in cumulative troponin T release (area under th e concentration curve) between the patients (ranging from 27 to 150 mu g x days/1) that was not related to the total ischaemic time before tr ansplantation or to the patient's renal or hepatic function, preoperat ive cardiac diseases, major histocompatibility complex matching or the number of complications related to rejection. Conclusions-Because the half life of cardiac troponin T in serum is 2 h the current data show that antigen continued to be released from implanted hearts during th e first postoperative months in quantities similar to minor Q wave myo cardial infarction. Troponin T release after transplantation continued for much longer than after myocardial infarction or other cardiac sur gery. Processes other than perioperative ischaemic damage must be resp onsible for the considerable individual differences in the release of cardiac troponin T.