Volatile Agents for Cardiac Protection in Noncardiac Surgery: A Randomized Controlled Study
ABSTRACT Volatile anesthetics reduce the risk of myocardial infarction and mortality in coronary artery surgery. Recently, the American College of Cardiology/American Heart Association Guidelines suggested the use of volatile anesthetic agents for the maintenance of general anesthesia during noncardiac surgery in patients at risk for perioperative myocardial ischemia, but no randomized experience to document the cardioprotective effects of these agents exists in this setting. Therefore, the authors performed a prospective, randomized, controlled trial to compare the effects of sevoflurane versus total intravenous anesthesia, in terms of postoperative cardiac troponin I release in patients undergoing noncardiac surgery.
A randomized, controlled trial.
A teaching hospital.
Eighty-eight consecutive patients undergoing noncardiac surgery.
Patients were allocated randomly to receive either volatile anesthetic (44 patients) as the main anesthetic agent or total intravenous anesthesia (TIVA) (44 patients).
Postoperative cardiac troponin I release was measured as a marker of myocardial necrosis. Patients with detectable postoperative troponin I in the sevoflurane group (12/44, 27.3%) were similar to those in the propofol group (9/44, 20.5%; p = 0.6). There was no significant reduction of postoperative median peak cTnI release (0.16 ± 0.71 ng/mL in the sevoflurane group compared with the TIVA group, 0.03 ± 0.08 ng/mL; p = 0.4). Three patients died at the 1-year follow-up for noncardiac causes (2 in the TIVA group).
In the authors' experience, patients undergoing noncardiac surgery did not benefit from anesthesia based on halogenated anesthetics. Further studies are necessary to evaluate the cardioprotective effects of volatile agents in noncardiac surgery.
- SourceAvailable from: Johan M Lorenzen[Show abstract] [Hide abstract]
ABSTRACT: The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. We hypothesized that endogenous estrogens play a role as mediators of desflurane-induced preconditioning against myocardial infarction. In this study, we tested the hypothesis that desflurane effects local estrogen synthesis by modulating enzyme aromatase expression and activity in the mouse heart. Aromatase metabolizes testosterone to 17b-estradiol (E2) and thereby significantly contributes to local estrogen synthesis. We tested aromatase effects in acute myocardial infarction model in male mice. The animals were randomized and subjected to four groups which were pre-treated with the selective aromatase inhibitor anastrozole (A group) and DES alone (DES group) or in combination (A+DES group) for 15 minutes prior to surgical intervention whereas the control group received 0.9% NaCl (CON group). All animals were subjected to 45 minutes ischemia following 180 minutes reperfusion. Anastrozole blocked DES induced preconditioning and increased infarct size compared to DES alone (37.94615.5% vs. 17.163.62%) without affecting area at risk and systemic hemodynamic parameters following ischemia/reperfusion. Protein localization studies revealed that aromatase was abundant in the murine cardiovascular system with the highest expression levels in endothelial and smooth muscle cells. Desflurane application at pharmacological concentrations efficiently upregulated aromatase expression in vivo and in vitro. We conclude that desflurane efficiently regulates aromatase expression and activity which might lead to increased local estrogen synthesis and thus preserve cellular integrity and reduce cardiac damage in an acute myocardial infarction model.PLoS ONE 08/2010; 7(8). DOI:10.1371/journal.pone.0042032 · 3.53 Impact Factor
- Journal of cardiothoracic and vascular anesthesia 09/2011; 25(6):899-901. DOI:10.1053/j.jvca.2011.08.004 · 1.48 Impact Factor
- Anaesthesia 02/2012; 67(2):106-9. DOI:10.1111/j.1365-2044.2011.07027.x · 3.85 Impact Factor