BACKGROUND: Perioperative beta-blockade has been shown to improve long-term cardiac outcome in noncardiac surgical patients. A possible mechanism for the reduced risk of perioperative myocardial infarction is the attenuation of the excitotoxic effects of catecholamine surges by beta-blockade. It was hypothesized that beta-blocker-induced alteration of the stress response was responsible for the reported improvements in cardiovascular outcome. Several variables associated with the perioperative use of beta-blockade were also evaluated. METHODS:Sixty-three patients were randomly assigned to one of three groups: group I, no atenolol; group II, pre- and postoperative atenolol; group III, intraoperative atenolol. Hormonal markers of the stress response (neuropeptide Y, epinephrine, norepinephrine, cortisol, and adrenocorticotropic hormone) were evaluated preoperatively and for 72 h after surgery. RESULTS: Perioperative beta-blockade did not significantly alter the hormonal stress response. However, the beta-blocked patients showed improved hemodynamic stability during emergence and postoperatively. They also received less fentanyl intraoperatively (27.7%, P < 0.0001), experienced faster early recovery, had lower pain scores, and required less analgesia in the postanesthesia care unit. Cardiac troponin I release was detected in 8 of 19, 4 of 20, and 5 of 20 patients in groups I, II, and III, respectively (not significant). Three patients in group I had cardiac troponin I levels consistent with myocardial infarction. CONCLUSION: Beta-blockade does not reduce the neuroendocrine stress response, suggesting that this mechanism is not responsible for the previously reported improved cardiovascular outcome. However, it confers several advantages, including decreased analgesic requirements, faster recovery from anesthesia, and improved hemodynamic stability. The release of cardiac troponin I suggests the occurrence of perioperative myocardial damage in this elderly population, which appears to be independent of the neuroendocrine stress response.
RCT Entities:
BACKGROUND: Perioperative beta-blockade has been shown to improve long-term cardiac outcome in noncardiac surgical patients. A possible mechanism for the reduced risk of perioperative myocardial infarction is the attenuation of the excitotoxic effects of catecholamine surges by beta-blockade. It was hypothesized that beta-blocker-induced alteration of the stress response was responsible for the reported improvements in cardiovascular outcome. Several variables associated with the perioperative use of beta-blockade were also evaluated. METHODS: Sixty-three patients were randomly assigned to one of three groups: group I, no atenolol; group II, pre- and postoperative atenolol; group III, intraoperative atenolol. Hormonal markers of the stress response (neuropeptide Y, epinephrine, norepinephrine, cortisol, and adrenocorticotropic hormone) were evaluated preoperatively and for 72 h after surgery. RESULTS: Perioperative beta-blockade did not significantly alter the hormonal stress response. However, the beta-blocked patients showed improved hemodynamic stability during emergence and postoperatively. They also received less fentanyl intraoperatively (27.7%, P < 0.0001), experienced faster early recovery, had lower pain scores, and required less analgesia in the postanesthesia care unit. Cardiac troponin I release was detected in 8 of 19, 4 of 20, and 5 of 20 patients in groups I, II, and III, respectively (not significant). Three patients in group I had cardiac troponin I levels consistent with myocardial infarction. CONCLUSION: Beta-blockade does not reduce the neuroendocrine stress response, suggesting that this mechanism is not responsible for the previously reported improved cardiovascular outcome. However, it confers several advantages, including decreased analgesic requirements, faster recovery from anesthesia, and improved hemodynamic stability. The release of cardiac troponin I suggests the occurrence of perioperative myocardial damage in this elderly population, which appears to be independent of the neuroendocrine stress response.
Authors: P J Devereaux; W Scott Beattie; Peter T-L Choi; Neal H Badner; Gordon H Guyatt; Juan C Villar; Claudio S Cinà; Kate Leslie; Michael J Jacka; Victor M Montori; Mohit Bhandari; Alvaro Avezum; Alexandre B Cavalcanti; Julian W Giles; Thomas Schricker; Homer Yang; Carl-Johan Jakobsen; Salim Yusuf Journal: BMJ Date: 2005-07-04
Authors: Hermann Blessberger; Sharon R Lewis; Michael W Pritchard; Lizzy J Fawcett; Hans Domanovits; Oliver Schlager; Brigitte Wildner; Juergen Kammler; Clemens Steinwender Journal: Cochrane Database Syst Rev Date: 2019-09-26
Authors: Jason B O'Neal; Frederic T Billings; Xulei Liu; Matthew S Shotwell; Yafen Liang; Ashish S Shah; Jesse M Ehrenfeld; Jonathan P Wanderer; Andrew D Shaw Journal: Am J Cardiol Date: 2017-07-24 Impact factor: 2.778