Sevoflurane in acute myocardial infarction: A pilot randomized study

Abstract

Experimental evidence suggests that the inhalational anesthetic sevoflurane has a cardioprotective effect. Our objective was to determine if sedation with sevoflurane will reduce infarct size in patients with acute myocardial infarction (MI) who are treated with primary percutaneous coronary intervention (PCI). We randomized 50 patients presenting with a first acute ST-elevation MI treated by primary PCI within 6 hours from symptom onset to sedation with sevoflurane inhalation or standard sedation (control). Coronary flow at the end of PCI was assessed by corrected Thrombolysis In Myocardial Infarction frame count. Myocardial reperfusion was assessed by ST-segment resolution 60 minutes post-PCI. Infarct size was assessed by release of creatinine kinase (CK) and troponin T. There was no difference in the primary end point: troponin T or CK release adjusted to the area at risk, between groups. However, among patients with anterior MI, there was a trend toward lower CK (P = .05) and nonsignificant decrease in troponin (P = .11) levels in the sevoflurane group. Corrected Thrombolysis In Myocardial Infarction frame count was 12.3 ± 1.5 in the sevoflurane group and 15.6 ± 9.1 in the control group (P = .16). There was more ST resolution in patients treated by sevoflurane 80.7% ± 25.8% versus 56.6% ± 35.7% (P = .01). Sevoflurane had no significant adverse effect during administration. Sevoflurane administration during primary PCI did not reduce infarct size. There was a trend toward a reduction in infarct size among patients with anterior MI. Sevoflurane administration was associated with improvement in ST-segment resolution.