Faculty Bibliography

BACKGROUND: American College of Cardiology and American Heart Association (ACC/AHA) guidelines on perioperative assessment recommend perioperative beta blockers for non-cardiac surgery, although results of some clinical trials seem not to support this recommendation. We aimed to critically review the evidence to assess the use of perioperative beta blockers in patients having non-cardiac surgery. METHODS: We searched Pubmed and Embase for randomised controlled trials investigating the use of beta blockers in non-cardiac surgery. We extracted data for 30-day all-cause mortality, cardiovascular mortality, non-fatal myocardial infarction, non-fatal stroke, heart failure, and myocardial ischaemia, safety outcomes of perioperative bradycardia, hypotension, and bronchospasm. FINDINGS: 33 trials included 12 306 patients. beta blockers were not associated with any significant reduction in the risk of all-cause mortality, cardiovascular mortality, or heart failure, but were associated with a decrease (odds ratio [OR] 0.65, 95% CI 0.54-0.79) in non-fatal myocardial infarction (number needed to treat [NNT] 63) and decrease (OR 0.36, 0.26-0.50) in myocardial ischaemia (NNT 16) at the expense of an increase (OR 2.01, 1.27-3.68) in non-fatal strokes (number needed to harm [NNH] 293). The beneficial effects were driven mainly by trials with high risk of bias. For the safety outcomes, beta blockers were associated with a high risk of perioperative bradycardia requiring treatment (NNH 22), and perioperative hypotension requiring treatment (NNH 17). We recorded no increased risk of bronchospasm. INTERPRETATION: Evidence does not support the use of beta-blocker therapy for the prevention of perioperative clinical outcomes in patients having non-cardiac surgery. The ACC/AHA guidelines committee should soften their advocacy for this intervention until conclusive evidence is available

OBJECTIVES: The purpose of this study was to evaluate the role of heart rate reduction with beta-blockers on the risk of cardiovascular events in patients with hypertension. BACKGROUND: Resting heart rate has been shown to be a risk factor for cardiovascular morbidity and mortality in the general population and in patients with heart disease such as hypertension, myocardial infarction, and heart failure. Conversely, pharmacological reduction of heart rate is beneficial for patients with heart disease. However, the role of pharmacological reduction of heart rate using beta-blockers in preventing cardiovascular events in patients with hypertension is not known. METHODS: We conducted a MEDLINE/EMBASE/CENTRAL database search of studies from 1966 to May 2008. We included randomized controlled trials that evaluated beta-blockers as first-line therapy for hypertension with follow-up for at least 1 year and with data on heart rate. We extracted the baseline characteristics, the blood pressure response, heart rate at the baseline and end of trial, and cardiovascular outcomes from each trial. RESULTS: Of 22 randomized controlled trials evaluating beta-blockers for hypertension, 9 studies reported heart rate data. The 9 studies evaluated 34,096 patients taking beta-blockers against 30,139 patients taking other antihypertensive agents and 3,987 patients receiving placebo. Paradoxically, a lower heart rate (as attained in the beta-blocker group at study end) was associated with a greater risk for the end points of all-cause mortality (r = -0.51; p < 0.0001), cardiovascular mortality (r = -0.61; p < 0.0001), myocardial infarction (r = -0.85; p < 0.0001), stroke (r = -0.20; p = 0.06), or heart failure (r = -0.64; p < 0.0001). The same was true when the heart rate difference between the 2 treatment modalities at the end of the study was compared with the relative risk reduction for cardiovascular events. CONCLUSIONS: In contrast to patients with myocardial infarction and heart failure, beta-blocker-associated reduction in heart rate increased the risk of cardiovascular events and death for hypertensive patients

BACKGROUND: Obesity has been shown to be associated with atrial enlargement and ventricular diastolic dysfunction, both of which are risk factors for atrial fibrillation (AF). However, the role of obesity as a risk factor for the development of AF is unknown. The study aims to evaluate the role of obesity as a risk factor for the development of AF. METHODS: The MEDLINE/ PUBMED and Cochrane databases were searched for studies in human subjects published in English language between 1966 and May 2007. Studies were included in our analyses if they were population-based cohort or postcardiac surgery cohort and investigated the incidence of AF in relation to the body mass index (BMI) categories. RESULTS: Of the 468 articles identified, 16 studies that enrolled a total of 123,249 individuals met the inclusion criteria. These 16 articles included 5 population-based cohort studies that enrolled 78,602 adult individuals from the United States and 3 European countries and 11 postcardiac surgery studies that enrolled 44,647 patients. Based on the population-based cohort studies, obese individuals have an associated 49% increased risk of developing AF compared to nonobese individuals (relative risk 1.49, 95% CI 1.36-1.64). The risk of AF increased in parallel with greater BMI in this cohort. In contrast, in the postcardiac surgery studies, obese individuals do not have an associated increased risk of developing AF compared to nonobese individuals (relative risk 1.02, 95% CI 0.99-1.06). CONCLUSIONS: Our findings demonstrate that obesity increased the risk of developing AF by 49% in the general population, and the risk escalated in parallel with increased BMI. Thus, AF evolves as yet another pathogenetic factor by which obesity may increase cardiovascular and cerebrovascular events