Cardiac troponin I in neonates undergoing the arterial switch operation

Cardiac troponin I (TnI) is a sensitive and specific marker of myocardial injury, but little is known about its release after complex congenital heart surgery. We investigated whether TnI correlates with early clinical outcome in neonates undergoing the arterial switch operation (ASO) for transposition of the great arteries (TGA).

Troponin I was measured serially up to 48 hours postoperatively in 31 neonates undergoing the ASO alone (simple TGA) and 9 neonates undergoing the ASO combined with other procedures (complex TGA) (eg, closure of a ventricular septal defect) and correlated with intraoperative and postoperative clinical parameters.

There was no mortality. Troponin I peaked at either 4 or 12 hours postoperatively in all patients (median for simple TGA = 3.4 ng/mL, interquartile range 2.4 to 4.6; median for complex TGA = 4.7 ng/mL, interquartile range 3.2 to 6.8, p = 0.20). Peak TnI correlated with the durations of inotropic support (r = 0.54, p < 0.001), ventilation (r = 0.51, p < 0.01), and intensive care unit stay (r = 0.50, p < 0.01). The duration of cardiopulmonary bypass, aortic cross-clamping, and circulatory arrest did not correlate with the peak or total TnI release. The duration of aortic cross-clamping correlated poorly with the duration of inotropic support (r = 0.40, p < 0.05). The complex TGA group had longer aortic cross-clamp times, required more postoperative inotropic support, and had significantly higher total TnI release compared with the simple TGA group.

There are weak but statistically significant correlations between peak TnI and clinical outcome. Complexity of the defect and ischemic times may be as useful to predict outcome in this group of patients.