Invited Commentary

Abstract

Myocardial infarction (MI) occurring in the context of cardiac surgery is a complication difficult to define and to diagnose. The edge between innocuous ischemia induced by cardioplegic arrest and clinically relevant myocardial cell damage is often vague. Most surgeons will indulge with elevated postoperative cardiac troponin I (cTnI) or CK-MB release finding it difficult to associate this finding with a relevant clinical outcome. In many postoperative intensive care units, these biomarkers are not even measured. The study by Lim and colleagues [1Lim C.C.S. Cuculi F. van Gaal W.J. et al.Early diagnosis of perioperative myocardial infarction after coronary bypass grafting: a study using biomarkers and cardiac magnetic resonance imaging.Ann Thorac Surg. 2011; 92: 2046-2053Abstract Full Text Full Text PDF PubMed Scopus (42) Google Scholar] provides useful information: they demonstrate that even limited cTnI postoperative release is associated with myocardial cell necrosis detected by cardiac magnetic resonance late gadolinium enhancement (CMR-LGE). They confirm cTnI as being, so far, the best predictor of significant myocardial damage after cardiac operations. Previous studies have demonstrated a clear and independent association between cTnI postoperative release and clinical outcome. Knowing this, surgery should be aimed to limit cTnI release at the smaller amount possible: most often operations are performed on patients with severely compromised heart function and further deterioration of the ventricular function can be associated with poor short-term and long-term outcome. Unfortunately, the article by Lim and colleagues does not help us to understand the cause of perioperative myocardial damage: is it caused by poor myocardial protection, early graft closure, incomplete revascularization, surgical manipulation, or iatrogenic coronary damage? This information would be essential to adopt adequate management. The authors suggest that early angiography or surgical inspection should be considered when cTnI is elevated early postoperatively given that cTnI >7.5 ng/mL 1 hour after the end of the operation has a 95% specificity to detect new MI with CMR-LGE. Is it enough information to bring a patient back to the operating room or to the catheter-laboratory? Probably not. An excellent clinical judgment is required to portray laboratory findings. An early postoperative cTnI peak measured 2–3 hours after the operation followed by a rapid decrease is probably the effect of imperfect myocardial protection: in this situation, a chest re-opening or angiography would only be harmful. On the other hand, a progressive cTnI increase with an elevated peak value observed 36–48 hours after the operation, associated or not with ECG abnormalities and hemodynamic instability, is probably caused by an ongoing ischemic trigger (graft closure, incomplete revascularization, or coronary damage): in this case, an aggressive management would probably lead to the recognition of the ischemic trigger and to an adequate treatment. Another interesting finding of the study is that patients with postoperative LGE had an increased systemic inflammatory reaction measured by interleukin 6 (IL-6) and TNFa. Future studies will be needed to clarify the reason of this finding: is it myocardial ischemia causing enhanced inflammatory reaction or is it excessive systemic inflammatory response leading to myocardial cell damage? Early Diagnosis of Perioperative Myocardial Infarction After Coronary Bypass Grafting: A Study Using Biomarkers and Cardiac Magnetic Resonance ImagingThe Annals of Thoracic SurgeryVol. 92Issue 6PreviewMyocardial injury related to coronary artery bypass grafting (CABG) is poorly characterized, and understanding the characteristic release of biomarkers associated with revascularization injury might provide novel therapeutic opportunities. This study characterized early changes in biomarkers after revascularization injury during on-pump CABG. Full-Text PDF