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Troponin I, Troponin T, or Creatine Kinase-MB to Detect Perioperative Myocardial Damage After Coronary Artery Bypass Surgery: Conclusion

Troponin I, Troponin T, or Creatine Kinase-MB to Detect Perioperative Myocardial Damage After Coronary Artery Bypass Surgery: ConclusionEarly postoperative ventricular dysfunction, as observed with echocardiography, is more likely to occur because of reversible myocardial stunning during aortic occlusion and reperfusion injury. Creatine kinase (CK) and CKMB are often used with no clear threshold. In this study, it would have been inappropriate to use CK or CKMB, a cytosolic marker, to study the diagnostic accuracy of other cytosolic markers since their release is dependent on the same pathologic mechanisms. Since cTnl and cTnT have a cytosolic phase, we had to choose an independent means of assessing myocardial damage. Link The more sensitive ECG markers like ST segment depression or elevation and T-wave evolution have a low specificity in this setting. Therefore, to study a marker of myocardial lesion independent of the CK, we deliberately selected a restrictive ECG criterion, ie, the occurrence of new postoperative Q waves. In this group of patients, cTnl, cTnT, and CKMB increase to value similar to those reported on medical myocardial infarction and contrast with the low values observed in the other patients.
Limitations of This Study
Although justified, the choice of stringent ECG criteria constitutes the main limitation of this study. It has adversely affected the positive predictive accuracy of the enzyme markers. As shown by radionuclide techniques with single photon emission CT imaging, many episodes of myocardial necrosis do not result in Q-wave evolution, ie, “non-Q wave infarction.” These episodes could be responsible for an increase in cTnl and other biological indicators of myocardial necrosis and account for their low positive predictive value in this study. The ECG criteria have also restricted the power of the study and explain why the differences observed between cTnl and cTnT did not reach statistical significance.
The incidence of new or worsening Q wave appears relatively high and, given the limited number of patients, is probably explained by chance.
We did not quantify some intercurrent factors such as shed blood autotransfusion and its influence. In patients with no ECG signs of myocardial ischemia, shed blood autotransfusion significantly increases CKMB and cTnT. However, since we compared biological markers in the same patients, the influence of intercurrent factor is probably minimal.
There was little difference between cTnl, cTnT, and CKMB to diagnose perioperative myocardial damage after CABG as assessed by new Q waves on the ECG. However, and in concordance with previous data demonstrating the superiority of cTnl in other pathologic conditions, there was a trend of cTnl being a better discriminator than CKMB or cTnT. In CABG patients with the potential for concomitant myocardial and skeletal muscle injury, the high cardiospecificity of cTnl could make it a more reliable tool to diagnose perioperative myocardial infarction and to compare different cardioplegia techniques. cTnl values remained veiy low in most patients. Further studies to investigate the prognostic value of cTnl values >5 |xg/L after CABG would be of interest.

Category: Myocardial Damage

Tags: coronary artery bypass surgery, creatine kinase, myocardial infarction, troponin I, troponin T