Thoracic Epidural Anesthesia in Abdominal Aortic Surgery: Use and Advantages

We read with interest the prospective, randomized, controlled trial by Lindholm et al.¹  where they compare the troponin T release after elective major vascular surgery in two groups of patients: one group with fentanyl–sevoflurane anesthesia and the other with propofol–remifentanil anesthesia. These authors concluded that sevoflurane-based anesthesia did not reduce myocardial injury, evaluated by troponin T release, compared with total intravenous anesthesia, suggesting that volatile anesthesia is no more protective than total intravenous anesthesia in elective abdominal aortic surgery. In this study, authors indicate that epidural catheter was introduced at thoracic level T6–T10 and epidural analgesia was started after opening the aortic cross-clamp in the two groups of patients.

In our opinion, the use of thoracic epidural analgesia (TEA) in the two groups of patients included in this trial could be an important issue regarding the obtained results. It has been suggested that intraoperative combination of general and epidural anesthesia with continuing postoperative epidural analgesia could be beneficial in high-risk surgical patients undergoing major noncardiac surgery.²  The effects of TEA are produced by the blockade of cardiac sympathetic efferent nerve fibers that have their origin in segments T1–T5.³  Activation of these fibers results in the stimulation of α- and β-adrenergic receptors, leading to an increased inotropy, chronotropy, vasoconstriction of epicardial coronary arteries, and systemic vasoconstriction, increasing myocardial oxygen demand. Previous studies have shown that combination of TEA and general anesthesia decreases heart rate, myocardial contractility, and systemic vascular resistance, resulting in potential benefits such as an improved balance of myocardial oxygen supply demand and greater intraoperative hemodynamic stability in patients with coronary artery disease undergoing surgery.^3,4  TEA has been reported to improve the status of nonsurgical patients with unstable angina and myocardial ischemia,⁵  but we must note that studies on cardiac surgery have failed to find significant differences in troponin levels after TEA although this difference could be explained by the varying etiology and pathophysiology of the perioperative ischemia during coronary artery bypass graft surgery.⁶  To this way, Jackobsen et al.⁷  found that thoracic epidural anesthesia patients had higher stroke volume index, higher cardiac index, higher venous pressures, and lower systemic vascular resistance index perioperatively and postoperatively in cardiac surgical patients. Therefore, it seems logical to suggest that TEA could have decreased myocardial ischemia in patients included in the two groups of this intersesting study and this may have biased the results of this trial. We wonder that what would had happened to the results whether thoracic epidural anesthesia had not been added to the patients included in the two groups of this trial.

The authors declare no competing interests.