Sevoflurane-induced cardioprotection in coronary artery bypass graft surgery: Randomised trial with clinical and ex-vivo endpoints.

Background: Myocardial ischaemia reperfusion injury following cardiac surgery with cardiopulmonary bypass (CPB) increases postoperative mortality. Setting techniques to protect the heart during this critical period therefore represents a considerable challenge.

Method: A randomised controlled study in Caen University Hospital Centre, investigated whether the clinical cardio protective effects of administration sevoflurane before cardiopulmonary bypass during coronary artery bypass graft surgery (CABG) could translate into protected atrial trabeculae contractility against hypoxia-reoxygenation in vitro. Patients undergoing elective on-pump CABG surgery were allocated to receive either sevoflurane (n=24) or no halogenated volatile anaesthetic (n=21).

Main Outcome Measures: the relationship between sevoflurane exposure before CPB and the incidence of major adverse cardiac events, with primary endpoint: the postoperative troponin I peak level, and secondary endpoints: the inotropic support, and the duration of stay in intensive unit and in-hospital stay were chosen as study endpoints. The right atrial was collected at the beginning of bypass surgery for the in vitro experimentation. Isometrically contracting isolated human right atrial trabeculae obtained from the two groups were exposed to 30-min hypoxia followed by 60-min reoxygenation.

Results: The patients receiving sevoflurane prior to aortic clamping significantly exhibited less cardiac Troponin I (1.39 [0.34-2.97] vs. 2.80 [2.54-3.64] ng·mL in Control; P=0.03) and required a reduced inotropic drug support (P<0.001). Isolated trabeculae from patients receiving sevoflurane enhanced the recovery of force after reoxygenation compared to the Control group (79±5% vs. 53±8% of baseline in Control; P<0.001).

Conclusions: Administration of sevoflurane before CPB induced cardioprotection in patients undergoing CABG and preconditioned human myocardium against hypoxia-reoxygenation in vitro.