High-sensitivity cardiac troponin T is more helpful in detecting peri-operative myocardial injury and apoptosis during coronary artery bypass graft surgery

Abstract

Aim: To determine whether there is a correlation between cardiac markers and peri-operative myocardial injury (PMI) and apoptosis in coronary artery bypass graft (CABG) surgery and to compare the efficacy of cardiac markers to detect PMI.

Methods: The study population consisted of 37 patients (24 male, 13 female, mean age 63.4 ± 8.9 years) undergoing elective CABG. Arterial and coronary sinus blood samples were collected just before aortic cross-clamping (pre-ACC) and after aortic declamping (post-ACC). Creatine kinase-MB isoenzyme (CK-MB) activity, and high-sensitivity cardiac troponin T (hs-cTnT), creatine kinase-MB isoenzyme mass (CK-MB mass) and cardiac troponin I (cTnI) concentrations were measured in blood samples. Myocardial injury and apoptosis were examined in atrial biopsies.

Results: CABG caused PMI and apoptosis in all cases. Concentrations and net releases of cardiac markers significantly increased after aortic declamping (p < 0.001 for CK-MB and CK-MB mass, p < 0.01 for cTnI, p < 0.05 for hs-cTnT). A positive correlation was found between apoptotic index (r = 0.611, p < 0.001 for cTnI; r = 0.806, p < 0.001 for hs-cTnT), myocardial injury score (r = 0.544, p < 0.001 for cTnI; r = 0.719, p < 0.001 for hs-cTnT) and cTnI and hs-cTnT values in the post-ACC period. A positive correlation was found between apoptotic index (r = 0.507, p < 0.001), myocardial injury score (r = 0.416, p = 0.010) and net release of hs-cTnT. Furthermore, a positive correlation was found between aortic cross-clamp (ACC) time (r = 0.448, p = 0.007), cardiopulmonary bypass (CPB) time (r = 0.342, p = 0.047) and net release of hs-cTnT.

Conclusion: Although both cTnI and hs-cTnT may be specific and efficacious markers of myocardial apoptosis and injury occurring during CABG with CPB, hs-cTnT may be a more useful marker than cTnI to detect peri-operative myocardial apoptosis and injury.

Fig. 1.

Histopathological section of atrial tissue showing acute ischaemic changes with interstitial oedema (thin arrow). In addition, myofibrils show thinning and wavy patterns consistent with reperfusion injury (thick arrow) (Grade 1, H&E × 100).

Fig. 2.

High-power representation of the histopathological section of atrial tissue showing neutrophilic-tomixed inflammatory cell infiltration and transmigration (arrow). Neutrophil activation plays a prominent role in reperfusion injury (Grade 2, H&E × 200).

Fig. 3.

Histopathological section of atrial tissue showing neutrophilic-to-mixed inflammatory cell infiltration and transmigration (thin arrow) and necrotic myocytes (thick arrow). Neutrophil activation plays a prominent role in reperfusion injury (Grade 2, H&E × 200).

Fig. 4.

TUNEL-positive cardiomyocytes in an atrial tissue sample obtained during reperfusion after aortic declamping. The positive TUNEL reaction is visible as dark staining in the nucleus (arrow) (TUNEL × 40)..