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Pathology-related troponin I release and clinical outcome after pediatric open heart surgery
Paul Modi1, Hajime Imura, Gianni D Angelini
1Bristol Heart Institute, University of Bristol, Bristol, UK.
Insights
Troponin I (TnI) release after pediatric heart surgery varies by defect type and incision length. Higher TnI levels correlate with longer recovery, indicating myocardial damage from surgery.
Area of Science:
- Pediatric Cardiology
- Cardiac Surgery
- Biomarkers
Background:
- Perioperative myocardial injury is influenced by ischemia duration, pathology, and preoperative status.
- Troponin I (TnI) is a sensitive marker for myocardial injury.
Purpose of the Study:
- To assess pathology-specific differences in TnI release after pediatric open-heart surgery.
- To correlate TnI release with clinical outcomes.
Main Methods:
- Serial postoperative TnI measurements in 133 children undergoing atrial septal defect (ASD), ventricular septal defect (VSD), or tetralogy of Fallot (TOF) repair.
- Classification of right ventricular outflow tract (RVOT) incision length in TOF patients (minimum vs. extended).
Main Results:
- TnI levels were defect-specific; no correlation with outcome for ASDs.
- Peak TnI correlated with inotropic duration, ventilation, and ICU stay for VSD and TOF.
- Younger age (<1 year) in VSD and extended RVOT incision in TOF were linked to higher TnI release and worse outcomes.
Conclusions:
- Postoperative TnI release is pathology-dependent.
- TnI reflects myocardial damage from ischemia-reperfusion and direct trauma.
Background:
Perioperative myocardial injury is determined by the ischemic duration, pathology, and preoperative myocardial status. Our aim was to evaluate pathology-related differences in troponin I (TnI) release, a sensitive and specific marker of myocardial injury, and its relation to clinical outcome after pediatric open heart surgery.
Methods:
Troponin I was measured serially postoperatively in 133 children undergoing repair of atrial (ASD, n = 41) and ventricular septal defects (VSD, n = 46), and tetralogy of Fallot (TOF, n = 46). The length of the right ventricular outflow tract (RVOT) incision in the latter was classified as either minimum(n = 33) or extended(n = 13).
Results:
Postoperative TnI levels were lesion specific and did not correlate with clinical outcome for ASDs. Peak TnI correlated with inotropic duration for VSD (r = 0.69, p < 0.0001) and TOF (r = 0.51, p = 0.0004). Significant correlations were also observed for the durations of ventilation (r = 0.64 and 0.36, respectively) and ICU stay (r = 0.60 and 0.55). Younger age (<1 year old) in children with VSDs and an extended incision into the RVOT in TOF were associated with greater TnI release and worse clinical outcome.
Conclusions:
Postoperative TnI release is pathology related and reflects myocardial damage from both ischemia-reperfusion injury and direct myocardial trauma.
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