OBJECTIVE: To examine the role of sevoflurane in myocardial protection in patients undergoing coronary artery bypass graft (CABG) surgery. DESIGN: Prospective, randomized, controlled, double-blinded study. SETTING:Veterans Administration Medical Center (VAMC), Buffalo, New York. SUBJECTS:Twenty-one patients undergoing CABG were included in the study. Eleven patients were randomized to receive sevoflurane, and 10 patients served as controls. INTERVENTION: Total intravenous anesthesia was provided for both study and control groups by infusion of propofol, fentanyl, and midazolam. Sevoflurane 2% was added to the cardioplegia solution in the experimental group. MEASUREMENTS AND MAIN RESULTS:Neutrophil beta-integrins (CD11b/CD18), tumor necrosis factor alpha (TNF-alpha), and interleukin (IL)-6 were measured as indicators of the inflammatory response to myocardial ischemia-reperfusion injury. Blood samples were obtained from the aorta and coronary sinus before (T1) and immediately after cardiopulmonary bypass (CPB) (T2) and, in addition, from a peripheral artery 6 hours (T3) after CPB. Myocardial function was determined in all patients at each time point. Left ventricular stroke work index (LVSWI) was calculated as an estimation of left ventricular function. Left ventricular regional wall motion abnormality (RWMA) was assessed by transesophageal echocardiography at T1 and T2 time points. TNF-alpha was detectable only in the control group in arterial samples at T3. IL-6 levels (pg/mL) were found to be lower in the sevoflurane group compared with controls at T2 arterial circulation (38.2 +/- 21.1 v 60.6 +/- 19.1, p < 0.05) as well as in the coronary circulation (38.4 +/- 19.9 v 118.2 +/- 23.5, p < 0.01) at T2. CD11b/CD18 increased 79% after CPB in the control group while only increasing 36% in the sevoflurane group (p < 0.05). The post-CPB LVSWI was back to its baseline values in the sevoflurane group, whereas it was still significantly depressed in the control group. Eight of 10 patients in the control group showed a transient new-onset RWMA in either the septal or anteroseptal regions. Only 2 of 11 patients in the sevoflurane group showed transient RWMA of the LV. CONCLUSIONS:Sevoflurane decreases the inflammatory response after CPB, as measured by the release of IL-6, CD11b/CD18, and TNF-alpha. Myocardial function after CPB, as assessed by RWMA and LVSWI, was also improved with sevoflurane. The role of sevoflurane in myocardial protection and the inflammatory response to myocardial reperfusion should be considered.
RCT Entities:
OBJECTIVE: To examine the role of sevoflurane in myocardial protection in patients undergoing coronary artery bypass graft (CABG) surgery. DESIGN: Prospective, randomized, controlled, double-blinded study. SETTING: Veterans Administration Medical Center (VAMC), Buffalo, New York. SUBJECTS: Twenty-one patients undergoing CABG were included in the study. Eleven patients were randomized to receive sevoflurane, and 10 patients served as controls. INTERVENTION: Total intravenous anesthesia was provided for both study and control groups by infusion of propofol, fentanyl, and midazolam. Sevoflurane 2% was added to the cardioplegia solution in the experimental group. MEASUREMENTS AND MAIN RESULTS: Neutrophil beta-integrins (CD11b/CD18), tumor necrosis factor alpha (TNF-alpha), and interleukin (IL)-6 were measured as indicators of the inflammatory response to myocardial ischemia-reperfusion injury. Blood samples were obtained from the aorta and coronary sinus before (T1) and immediately after cardiopulmonary bypass (CPB) (T2) and, in addition, from a peripheral artery 6 hours (T3) after CPB. Myocardial function was determined in all patients at each time point. Left ventricular stroke work index (LVSWI) was calculated as an estimation of left ventricular function. Left ventricular regional wall motion abnormality (RWMA) was assessed by transesophageal echocardiography at T1 and T2 time points. TNF-alpha was detectable only in the control group in arterial samples at T3. IL-6 levels (pg/mL) were found to be lower in the sevoflurane group compared with controls at T2 arterial circulation (38.2 +/- 21.1 v 60.6 +/- 19.1, p < 0.05) as well as in the coronary circulation (38.4 +/- 19.9 v 118.2 +/- 23.5, p < 0.01) at T2. CD11b/CD18 increased 79% after CPB in the control group while only increasing 36% in the sevoflurane group (p < 0.05). The post-CPB LVSWI was back to its baseline values in the sevoflurane group, whereas it was still significantly depressed in the control group. Eight of 10 patients in the control group showed a transient new-onset RWMA in either the septal or anteroseptal regions. Only 2 of 11 patients in the sevoflurane group showed transient RWMA of the LV. CONCLUSIONS:Sevoflurane decreases the inflammatory response after CPB, as measured by the release of IL-6, CD11b/CD18, and TNF-alpha. Myocardial function after CPB, as assessed by RWMA and LVSWI, was also improved with sevoflurane. The role of sevoflurane in myocardial protection and the inflammatory response to myocardial reperfusion should be considered.