Background: Postoperative troponin I and lactate elevation are related to cardiac complications after myocardial revascularization. We sought to evaluate earlier predictive value for acute myocardial infarction (AMI) and myocardial damage of troponin I and lactate after myocardial revascularization.
Methods: In all, 183 consecutive isolated myocardial revascularizations were prospectively enrolled in the study. Troponin I and lactate were sampled preoperatively and intraoperatively from the coronary sinus, and at 12, 24, 48, and 72 hours. Hospital outcome was recorded. Receiver operating curves for coronary sinus troponin I and lactate were constructed to differentiate patients with or without AMI and myocardial damage.
Results: Acute myocardial infarction developed in 6 patients (3.2%), with higher troponin I and lactate at all time points (p < 0.05), longer intubation time (p = 0.003), intensive care unit stay (p = 0.001), hospital stay (p = 0.001), higher atrial fibrillation (p = 0.001), and worse ventricular function (p = 0.001). Myocardial damage developed in 6 patients (3.2%), showing higher troponin I at all time points (p < 0.001), higher intraoperative lactate (p = 0.04), longer intubation time (p = 0.005), and intensive care unit stay (p = 0.03). Receiver operating characteristic curves demonstrated coronary sinus troponin I greater than 0.94 microg/L (area under the curve [AUC] 0.820 +/- 0.075; sensitivity 90.0%, specificity 68.9%) as a better discriminator between patients with or without AMI than lactate level greater than 2.85 mmol/L (AUC 0.686 +/- 0.090; sensitivity 80.0%; specificity 72.9%); troponin I greater than 0.65 microg/L was a better discriminator between patients with or without myocardial damage (AUC 0.834 +/- 0.061; sensitivity 93.8%, specificity 71.5%), than lactate greater than 2.05 mmol/L (AUC 0.627 +/- 0.067; sensitivity 87.5%; specificity 70.7%).
Conclusions: Coronary sinus troponin I and lactate are predictive for cardiac complications after myocardial revascularization. Intraoperative biochemical assays should be routinely performed to establish preventative strategies to reduce further myocardial damage.