Beneficial effects from beta-adrenergic blockade in elderly patients undergoing noncardiac surgery.
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.


CONCLUSIONS
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.
Zaugg
M
M
Department of Anesthesiology, The Mount Sinai School of Medicine, New York, New York 10029-6574, USA.
Tagliente
T
T
Lucchinetti
E
E
Jacobs
E
E
Krol
M
M
Bodian
C
C
Reich
D L
DL
Silverstein
J H
JH
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000368:Aged; D000369:Aged, 80 and over; D000465:Algorithms; D001262:Atenolol / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D004562:Electrocardiography; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006728:Hormones / Q000097:blood; D006801:Humans; D008297:Male; D008991:Monitoring, Physiologic; D009203:Myocardial Infarction / Q000097:blood / Q000517:prevention & control; D009490:Neurosecretory Systems / Q000503:physiopathology; D011183:Postoperative Complications / Q000517:prevention & control*; D013312:Stress, Physiological / Q000503:physiopathology / Q000517:prevention & control; D013514:Surgical Procedures, Operative / Q000009:adverse effects*; D019210:Troponin I / Q000097:blood
D000319:Adrenergic beta-Antagonists; D006728:Hormones; D019210:Troponin I; D001262:Atenolol