BACKGROUND: Experimental studies indicate that isoflurane, a commonly used volatile anesthetic, mimics the cardioprotective effects of ischemic preconditioning, probably through ATP-sensitive K+ (KATP) channel activation. The aim of this study was to evaluate the impact of isoflurane during coronary bypass surgery (CABG) on troponin I release. MATERIAL AND METHODS: Forty consecutive patients with chronic stable angina and multivessel disease undergoing isolated CABG were randomized to a control (16 men and 4 women, aged 51 to 73 years, mean 62) orisoflurane (15 men and 5 women, aged 51 to 77 years, mean 65) group beforeaortic cross-clamping and cardioplegia. Serum levels of troponin I and creatine kinase (CK)-MB, as markers of ischemic injury, were obtained at 24 hours after CABG. Regional wall motion score and left ventricular ejection fraction (LVEF) at transthoracic echocardiography were assessed 5 days postoperatively. Comparisons between groups were performed in the entire population and, subsequently, in those patients with preoperative LVEF < 50%. RESULTS: There were no significant differences between isoflurane-treated patients and controls in cross-clamp time (49 +/- 14 vs 51 +/- 13 min, p = ns), peak values of troponin I (0.9 +/- 0.7 vs 1.4 +/- 1.3 ng/ml, p = ns) and CK-MB (62 +/- 27 vs 64 +/- 27 U/l, p = ns), or postoperative echocardiographic score (26 +/- 7 vs 22 +/- 5, p = ns) and LVEF (53 +/- 10 vs 55 +/- 7%, p = ns). When the comparisons were restricted to those patients with preoperative LVEF < 50%, at 24 hours the isoflurane-treated patients exhibited a smaller release of troponin I and of CK-MB than controls (1.1 +/- 0.7 vs 2.3 +/- 1.3 ng/ml, p = 0.03, and 39 +/- 10 vs 57 +/- 22 U/l, p = 0.04, respectively). CONCLUSIONS:Isoflurane reduces myocardial injury in patients with impaired left ventricular function undergoing CABG; thus, it can be safely used as an additional cardioprotective tool during routine CABG in high-risk patients with poor left ventricular function.
RCT Entities:
BACKGROUND: Experimental studies indicate that isoflurane, a commonly used volatile anesthetic, mimics the cardioprotective effects of ischemic preconditioning, probably through ATP-sensitive K+ (KATP) channel activation. The aim of this study was to evaluate the impact of isoflurane during coronary bypass surgery (CABG) on troponin I release. MATERIAL AND METHODS: Forty consecutive patients with chronic stable angina and multivessel disease undergoing isolated CABG were randomized to a control (16 men and 4 women, aged 51 to 73 years, mean 62) or isoflurane (15 men and 5 women, aged 51 to 77 years, mean 65) group before aortic cross-clamping and cardioplegia. Serum levels of troponin I and creatine kinase (CK)-MB, as markers of ischemic injury, were obtained at 24 hours after CABG. Regional wall motion score and left ventricular ejection fraction (LVEF) at transthoracic echocardiography were assessed 5 days postoperatively. Comparisons between groups were performed in the entire population and, subsequently, in those patients with preoperative LVEF < 50%. RESULTS: There were no significant differences between isoflurane-treated patients and controls in cross-clamp time (49 +/- 14 vs 51 +/- 13 min, p = ns), peak values of troponin I (0.9 +/- 0.7 vs 1.4 +/- 1.3 ng/ml, p = ns) and CK-MB (62 +/- 27 vs 64 +/- 27 U/l, p = ns), or postoperative echocardiographic score (26 +/- 7 vs 22 +/- 5, p = ns) and LVEF (53 +/- 10 vs 55 +/- 7%, p = ns). When the comparisons were restricted to those patients with preoperative LVEF < 50%, at 24 hours the isoflurane-treated patients exhibited a smaller release of troponin I and of CK-MB than controls (1.1 +/- 0.7 vs 2.3 +/- 1.3 ng/ml, p = 0.03, and 39 +/- 10 vs 57 +/- 22 U/l, p = 0.04, respectively). CONCLUSIONS:Isoflurane reduces myocardial injury in patients with impaired left ventricular function undergoing CABG; thus, it can be safely used as an additional cardioprotective tool during routine CABG in high-risk patients with poor left ventricular function.