The study was limited by the fact that the control group did not include patients who were on a beta blocker at home, thus potentially increasing the number of events in this group. The discontinuation beta blocker group had an increased baseline risk for POMI. The reason for discontinuing the beta blocker was not known, and cessation of beta blocker could have been due to an acute event.
Bottom line: This study adds support to the American College of Cardiology and American Heart Association (ACC/AHA) guidelines, which recommend continuation of beta-blocker therapy in the perioperative period.
Citation: Van Klei WA, Bryson GL, Yang H, Forster AJ. Effect of beta-blocker prescription on the incidence of postoperative myocardial infarction after hip and knee arthroplasty. Anesthesiology. 2009;111(4):717-724.
Lower Perioperative Mortality with Endovascular Vs. Open Abdominal Aortic Aneurysm Repair
Clinical question: How do perioperative and long-term morbidity and mortality compare in endovascular and open repair of abdominal aortic aneurysm (AAA)?
Background: Open AAA repair has relatively high perioperative mortality. Endovascular repair was developed as a less-invasive option and has been shown to reduce inpatient perioperative mortality, length of hospital stay, and ICU requirement. However, data suggest it leads to more frequent reinterventions and the same mortality rate as open repair at two years.
Study design: Randomized clinical trial.
Setting: Veterans Affairs medical centers.
Synopsis: The study randomized 881 veterans who planned to have elective AAA repair and were eligible for both endovascular and open repair. This is a planned, two-year interim report in a nine-year study.
Perioperative mortality was 0.5% in the endovascular repair group, compared with 3.0% in the open repair group. However, this difference in mortality was not statistically significant at two years. The endovascular repair group experienced shorter procedure and mechanical ventilation time, decreased hospital and ICU stay, and lower rate of blood transfusions.
Overall, there was no difference between the groups for major morbidity, procedure failure, need for secondary therapeutic intervention, quality of life, or erectile dysfunction. More data on long-term comparison of these two interventions will be available at the conclusion of this study.
Bottom line: Endovascular repair of AAA has lower perioperative mortality than open repair but did not lead to improved morbidity or mortality at two years.
Citation: Lederle FA, Freischlag JA, Kyriakides TC, et al. Outcomes following endovascular vs. open repair of abdominal aortic aneurysm: a randomized trial. JAMA. 2009;302 (14):1535-1542.
OTC Analgesics Not Associated with Acute Decompensation in Cirrhotic Patients
Clinical question: Do over-the-counter (OTC) analgesics lead to acute hepatic decompensation among patients with cirrhosis?
Background: In theory, intake of acetaminophen and/or nonsteroidal anti-inflammatory drugs (NSAIDs) can worsen hepatic function and lead to complications among cirrhotic patients. The role of OTC analgesics in potentially triggering acute hepatic decompensation among cirrhotic patients has not been studied.
Study design: Prospective case-control study.
Setting: Two tertiary-care hospitals.
Synopsis: Cirrhotic patients hospitalized for acute liver decompensation were compared with compensated cirrhotic patients in the liver clinic (cirrhotic controls) and with randomly selected, noncirrhotic patients who were simultaneously hospitalized (noncirrhotic controls). Data collected through questionnaires included quantity and dose of OTC analgesics used and alcohol consumption in the past 30 days.
Thirty-five percent of the hospitalized cirrhotic patients, 52% of the cirrhotic controls, and 70% of the noncirrhotic controls used OTC analgesics. At doses lower than those recommended, acetaminophen is not associated with acute liver decompensation among cirrhotic patients, even with recent alcohol use. However, NSAIDs taken by the cirrhotic patients, when compared to control subjects, were in larger doses and used for a longer duration, suggesting NSAIDs may have contributed to the acute decompensation.