BACKGROUND: Myocardial acidosis during cardiac surgery and postoperative troponin I are markers of myocardial damage that have been shown to predict adverse outcomes. We investigated the relationship between troponin I and myocardial tissue pH, patient outcomes, and cost. METHODS: Data were prospectively collected on 205 cardiac surgery patients. Troponin I was sampled upon arrival to the intensive care unit (ICU) and every 6 hours thereafter for 24 hours. The lowest pH encountered during aortic cross clamp (LpH) was related to postoperative troponin I on the multivariate level. Multivariate models were constructed to predict adverse events (AE) and cost. RESULTS: LpH was an independent inverse determinant of postoperative troponin I (P = .0067). Troponin I and its interaction with LpH were multivariate predictors of AE (P = .0012; .0001;odds ratio = 6.9, 10.2, respectively). Troponin I independently predicts surgical ICU (SICU) cost (P = .0256). CONCLUSION: Postoperative troponin I elevation reflects intraoperative myocardial acidosis and damage. The strong relationship between troponin I, AE, and cost indicates the damage incurred is clinically and economically relevant. Strategies to ameliorate intraoperative myocardial tissue acidosis will decrease troponin I release, subsequent AE, and associated costs.
BACKGROUND:Myocardial acidosis during cardiac surgery and postoperative troponin I are markers of myocardial damage that have been shown to predict adverse outcomes. We investigated the relationship between troponin I and myocardial tissue pH, patient outcomes, and cost. METHODS: Data were prospectively collected on 205 cardiac surgery patients. Troponin I was sampled upon arrival to the intensive care unit (ICU) and every 6 hours thereafter for 24 hours. The lowest pH encountered during aortic cross clamp (LpH) was related to postoperative troponin I on the multivariate level. Multivariate models were constructed to predict adverse events (AE) and cost. RESULTS:LpH was an independent inverse determinant of postoperative troponin I (P = .0067). Troponin I and its interaction with LpH were multivariate predictors of AE (P = .0012; .0001;odds ratio = 6.9, 10.2, respectively). Troponin I independently predicts surgical ICU (SICU) cost (P = .0256). CONCLUSION: Postoperative troponin I elevation reflects intraoperative myocardial acidosis and damage. The strong relationship between troponin I, AE, and cost indicates the damage incurred is clinically and economically relevant. Strategies to ameliorate intraoperative myocardial tissue acidosis will decrease troponin I release, subsequent AE, and associated costs.
Authors: Monesha Gupta-Malhotra; Jeffrey H Kern; Patrick A Flynn; Myles S Schiller; Jan M Quaegebeur; Deborah M Friedman Journal: Congenit Heart Dis Date: 2010 May-Jun Impact factor: 2.007