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Ann Thorac Surg 2006;82:1649
© 2006 The Society of Thoracic Surgeons
Department of Surgery, University Hospital, Klin Abteilung fur Herzchirurgie, Med Univklinikum Graz, LKH, Auenbruggerplatz 29, Graz, 8036 Austria
(Email: bruno.rigler{at}meduni-graz.at).
Isoenzyme cardiac troponin T (cTnT) is one component of a complex of three separate proteins that, together with tropomyosin, confers calcium sensitivity to the process of actin-myosin cross-bridge formation in the myocardial cell. Found exclusively in the myocardium, it is a potent inhibitor of these interactions and is a more sensitive and specific index of myocardial cell damage than creatine kinase-MB (CK-MB) fraction, CK-MB mass, and myoglobin level. Therefore, cTnT has emerged as a strong predictive variable of complications and clinical outcome after cardiac surgery.
Mildh and colleagues [1] report a series of 1001 consecutive pediatric patients operated on during a recent 5-year period. Even though this study was done retrospectively, specific findings were accurate and multivariate analysis emphasized cTnT as a strong independent predictor for death at day 30 after cardiac surgery. Variable cTnT levels exceeding 5.9 µg/L measured on the first postoperative day and intensive care unit (ICU) admission lactate levels exceeding 5.2 mmol/L predicted hospital mortality.
Several studies have described the kinetics of cTnT elevation in the plasma in adult patients. It has been shown that cardiac surgery per se induces an increase in the plasma level of cTnT, even in the absence of ischemic myocardial damage. This increase depends on the type of surgery and the subsequent degree of direct surgical trauma. In cases of significant myocardial infarction (MI), such as Q-wave MI, peak levels of cTnT occur 20 hours after the end of cardiac surgery and then decrease slowly. In the absence of documented myocardial infarction, cTnT peaks earlier and plasma levels remain lower.
What is the specific relation between cTnT/higher mortality and congenital diagnosis or complexity of the performed procedure? How should we tax variables like cardioplegic solution, bypass, cross-clamp time, or even cyanosis?
According to published reports, cTnT was not a useful marker of clinical outcome after repair of atrial septal defects, probably due to short ischemic duration and the relatively minor degree of myocardial injury. It might be that during surgical repair, a threshold level of myocardial damage (and cTnT release) has to occur before functional impairment is manifested with the requirement for higher degrees of inotropic support, longer durations of mechanical ventilation, and resultant prolongation of ICU stay.
Patients with ventricular septal defects exhibited higher postoperative cTnT release and longer durations of inotropic support, ventilation, and ICU stay. In tetralogy of Fallot patients, a negative correlation was found between preoperative arterial oxygen saturation and early clinical outcome. No correlation was found between saturation and cTnT release, suggesting that the severity of myocardial damage may be independent of the degree of preoperative hypoxia. It was also demonstrated that the length of the right ventriculotomy adversely affects clinical outcome of tetralogy of Fallot patients. This is not always proportional to the amount of myocardial resection as, in some cases, there might be extensive division or resection of muscle bands within the right ventricular cavity, but a "minimal" incision.
As a matter of fact, only further prospective studies will provide a more specific interpretation of changes in this marker protein.
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