Anesthetic-Induced Myocardial Preconditioning and Some Biochemical Markers for Cardiac and Coronary Failures after Aortocoronary Bypass Surgery

Objective: to provide a rationale for the efficiency of sevoflurane-induced cardiac preconditioning (CPC), by assessing the pattern of recovery of heart rate and by estimating troponin I levels and changes in NT-proBNP concentrations in patients undergoing aortocoronary bypass surgery (ACBS) under extracorporeal circulation (EC). Subjects and methods. Sixty patients aged 60.6±8 years (M±&) were examined after elective ACBS using EC and divided into two groups of 30 patients each: 1) inhalation induction and maintenance of anesthesia (IIMA) with sevoflurane and fentanyl, with CPC being simulated; 2) total intravenous anesthesia (TIA) with propofol and fentanyl. Inhalation induction of sevoflurane anesthesia was performed in the IIMA group. Ten minutes before aortic ligation, the dose of the anesthetic was increased up to 2 MAC for CPC. Inhaled anesthetics were not used in the TIA group. The authors assessed the pattern of cardiac performance recovery and estimated the level of NT-proBNP 24 and 48 hours after tracheal intubation and that of troponin I following 24 hours of the intubation. Results. Defibrillation was required in one patient from the TIA group who developed ventricular fibrillation. The baseline levels of NT-proBNP were comparable in both groups. Following 24 hours, its level was more than thrice higher in the TIA group than that in the IIMA one (p<0.05). By the end of 2 days, the concentration of NT-proBNP continued to rise (up to 480% of the baseline level) in the TIA group and returned to the preoperative values in the IIMA group (p=0.05). Twenty-four hours after tracheal intubation the level of troponin I was insignificantly higher in the TIA group than that in the IIMA group (p=0.1). Conclusion. Sevoflurane has cardioprotective properties in preventing and/or reducing the degree of heart failure after ACBS using EC. There is a need to continue the study in increased cohort to provide evidence that sevoflurane-induced CPC can lower cardiomyocyte damage due to ischemia/perfusion.