This article is part of the supplement: 3rd International Symposium on the Pathophysiology of Cardiopulmonary Bypass. Myocardial cell damage and myocardial protection
Myocardial cell damage related to arterial switch operation in neonates with transposition of the great arteries
1 Departments of Paediatric Cardiology
2 Thoracic and Cardiovascular Surgery, Aachen University of Technology, Aachen, Germany
3 Department of Immunology, Hôpital Brugman, Brussels, Belgium
Critical Care 2001, 5(Suppl B):P16-114 doi:10.1186/cc1009
The electronic version of this article is the complete one and can be found online at: http://ccforum.com/content/5/SB/P16
| Received: | 12 February 2001 |
| Published: | 6 March 2001 |
© 2001 BioMed Central Ltd
Introduction
It was of objective of this study to investigate clinical and laboratory risk factors for myocardial dysfunction (MD) in neonates after arterial switch operation for transposition of the great arteries.
Method
Sixty-three neonates (age 2-28 [8.1 ± 4.6] days), who were operated on under combined deep hypothermic (15°C) circulatory arrest and low-flow cardiopulmonary bypass (CPB), were studied. Inclusion criteria were transposition of the great arteries with or without ventricular septal defect (VSD) that was suitable for arterial switch operation (VSD-; n = 53), and if necessary additional VSD closure (VSD+; n = 10). Patients were differentiated clinically into two groups by presence or absence of MD within 24 h after surgery. MD was defined as myocardial ischaemia after coronary reperfusion and/or myocardial hypocontractility as assessed by echocardiography. MD was related to clinical outcome parameters and to perioperative release of cardiac troponin-T (cTnT) and production of interleukin-6 and interleukin-8.
Results
MD was observed in 11 patients (17.5%). Two patients died early after surgery from myocardial infarction, and two died late after surgery (6.3%). CPB and cross-clamping, but not deep hypothermic circulatory arrest times, were correlated with MD; MD was more frequent in the VSD+ than in the VSD- group because of longer support times. Coronary status and age at surgery were not related to MD. Patients with MD had more frequently impaired cardiac, respiratory and renal functions. cTnT, interleukin-6 and interleukin-8 were significantly elevated at the end of CPB, and 4 and 24 h after surgery, as compared with preoperative values in both groups. Postoperative cTnT, interleukin-6 and interleukin-8 concentrations were significantly higher in MD patients than in the others. Multivariable analysis of independent risk factors for MD revealed interleukin-6 4 h after surgery to be significant (P = 0.04; odds ratio 1.24 [95% confidence interval 1.01-1.52] per 10 pg/ml). The cutoff point for prediction of MD was set at 500 pg/ml (specificity 95.4%, sensitivity 72.7%).
Conclusion
Cardiac operations in neonates induce the production of the proinflammatory cytokines interelukin-6 and interleukin-8, as well as release of cTnT. These results suggest that proinflammatory cytokines are, at least in part, responsible for myocardial cell damage and MD occurring after arterial switch operations in this age group.