Use Of Non-selective Beta-blockers Research Articles

Genetic Variation in the β2-Adrenocepter Gene Is Associated with Susceptibility to Bacterial Meningitis in Adults

Recently, the biased β2-adrenoceptor/β-arrestin pathway was shown to play a pivotal role in crossing of the blood brain barrier by Neisseria meningitidis. We hypothesized that genetic variation in the β2-adrenoceptor gene (ADRB2) may influence susceptibility to bacterial meningitis. In a prospective genetic association study we genotyped 542 patients with CSF culture proven community acquired bacterial meningitis and 376 matched controls for 2 functional single nucleotide polymorphisms in the β2-adrenoceptor gene (ADRB2). Furthermore, we analyzed if the use of non-selective beta-blockers, which bind to the β2-adrenoceptor, influenced the risk of bacterial meningitis. We identified a functional polymorphism in ADRB2 (rs1042714) to be associated with an increased risk for bacterial meningitis (Odds ratio [OR] 1.35, 95% confidence interval [CI] 1.04–1.76; p = 0.026). The association remained significant after correction for age and was more prominent in patients with pneumococcal meningitis (OR 1.52, 95% CI 1.12–2.07; p = 0.007). For meningococcal meningitis the difference in genotype frequencies between patients and controls was similar to that in pneumococcal meningitis, but this was not statistically significant (OR 1.43, 95% CI 0.60–3.38; p = 0.72). Patients with bacterial meningitis had a lower frequency of non-selective beta-blockers use compared to the age matched population (0.9% vs. 1.8%), although this did not reach statistical significance (OR 1.96 [95% CI 0.88–4.39]; p = 0.09). In conclusion, we identified an association between a genetic variant in the β2-adrenoceptor and increased susceptibility to bacterial meningitis. The potential benefit of pharmacological treatment targeting the β2-adrenoceptor to prevent bacterial meningitis in the general population or patients with bacteraemia should be further studied in both experimental studies and observational cohorts.

Non‐selective vs. selective beta‐blocker treatment and the risk of thrombo‐embolic events in patients with heart failure

Heart failure (HF) is associated with a prothrombotic state, resulting in an increased risk for thrombo-embolic events. Studies suggest a reduced prothrombotic state when non-selective beta-blockers relative to selective beta-blockers are given. We studied the influence of non-selective beta-blockers compared with selective beta-blockers on the occurrence of arterial and venous thrombo-embolic events in patients with HF. Data were obtained from the PHARMO Record Linkage System, a population-based registry of pharmacy records linked with hospital discharge records in The Netherlands. In the period of 1998-2007, 20 870 patients were hospitalized for HF. We used Cox regression analysis with time-varying beta-blocker covariate to assess the difference in the incidence of thrombo-embolic events [acute coronary syndrome (ACS), stroke, or pulmonary embolism] among patients. Median follow-up was 2.0 years (inter-quartile range: 0.7-4.1). Directly after discharge, 6558 patients were prescribed a selective beta-blocker and 2202 patients a non-selective beta-blocker. The hazard ratio (HR) for any thrombo-embolic event for non-selective beta-blockers compared with selective beta-blockers was 0.76 [95% confidence interval (CI): 0.64-0.89]. After adjustment, the difference remained (HR 0.84, 95% CI: 0.72-0.99). The effect was most prominent for ACS (HR 0.78, 95% CI: 0.65-0.93), and not clear for stroke (HR 1.00, 95% CI: 0.67-1.50) or pulmonary embolism (HR 1.33, 95% CI: 0.66-2.71). In patients with HF, the use of non-selective beta-blockers was associated with a lower risk of thrombo-embolic events than selective beta-blockers. Whether this beneficial effect is caused by the additional beta2-receptor blockade remains to be elucidated. These findings need to be validated in a well-designed randomized study.

Rates of Hospitalizations and Emergency Department Visits in Patients with Asthma and Chronic Obstructive Pulmonary Disease Taking β‐Blockers

To determine the rates of hospitalizations and emergency department (ED) visits during cardioselective and nonselective beta-blocker therapy in patients with asthma and/or chronic obstructive pulmonary disease (COPD). Retrospective, observational cohort study. Electronic medical records database. A total of 11,592 adult patients with asthma and/or COPD, identified from August 1, 1997-December 31, 2005, who were taking beta-blockers for at least 30 days or had never received a beta-blocker (controls). Of these patients, 3062 were taking cardioselective and 690 nonselective beta-blockers; 7840 were controls. The primary end point for the beta-blocker groups was the rate of hospitalizations and ED visits/patient-year of beta-blocker therapy relative to the control group. In patients with asthma with or without concomitant COPD, cardioselective beta-blockers were associated with a relative risk of 0.89 (95% confidence interval [CI] 0.53-1.50) for hospitalizations and 1.40 (95% CI 1.20-1.62) for ED visits compared with controls. Nonselective beta-blockers were associated with a relative risk of 2.47 (95% CI 1.37-4.48) for hospitalizations and 1.21 (95% CI 0.91-1.62) for ED visits. In patients with COPD only, cardioselective beta-blockers were associated with a relative risk of 0.64 (95% CI 0.43-0.96) for hospitalizations and 1.19 (95% CI 1.02-1.39) for ED visits. Nonselective beta-blockers were associated with a relative risk of 1.02 (95% CI 0.52-2.02) for hospitalizations and 0.51 (95% CI 0.33-0.80) for ED visits. In patients with asthma with or without COPD, both cardioselective and nonselective beta-blocker use increased hospitalizations and ED visits compared with controls. Thus, these patients should receive beta-blocker therapy only if their cardiac risk exceeds their pulmonary risk and if they have concomitant cardiac disease for which beta-blockers decrease mortality, such as previous acute myocardial infarction or chronic heart failure. In patients with COPD only, cardioselective beta-blockers slightly increased the risk of ED visits but reduced the risk of hospitalizations. Nonselective beta-blocker therapy in these patients reduced the rate of ED visits and total visits. These findings suggest a larger safety margin with beta-blocker therapy in patients with COPD only than in those with asthma with or without COPD.

Prophylaxis with beta blockers as a performance measure of quality health care in cirrhosis

Prophylaxis with beta blockers as a performance measure of quality health care in cirrhosis

Circadian variation in portal pressure: appropriate use of non-selective beta blockers in the prevention of variceal bleed

The circadian variation in some biologic functions may have clinical, fiscal and therapeutic implications. The authors discuss circadian variation in portal pressure in cirrhotic patients and nocturnal occurrence of bleeding from varices in these patients. The pathogenesis of the diurnal variation in portal pressure is presented. The authors submit the hypothesis that an optimal dosing regimen for non-selective beta blocker therapy in the prevention of variceal bleed must include an evening dose of beta blocker medication. In studies reporting comparative efficacy of beta blocker therapy with other modalities in the prevention of variceal bleeding, the optimal dosing schedule for beta blocker therapy must be emphasized.

Serum Magnesium and Potassium in Acute Myocardial Infarction: Relationship to Existing β-Blockade and Infarct Size

Patients (n = 314) with acute myocardial infarction (AMI) were divided into three groups according to the time elapsed from onset of chest pain to when the first sample for determination of magnesium (s-Mg1) and potassium (s-K1) was drawn (A: hours 0-6; B: hours 6-10, and C: hours 10-24). Potassium and Mg were also measured in a second sample drawn three to twelve days (mean 6.3 days) later (s-Mg2, s-K2). Whereas s-Mg1 was lower than s-Mg2 in all three groups, s-K1 was reduced only in group A. Ten patients in group A receiving nonselective beta-blockers had an attenuated drop in s-Mg1, whereas the drop in s-K1 was completely inhibited. The differences between s-Mg2 and s-Mg1 (delta s-Mg) in all groups, and between s-K2 and s-K1 (delta s-K) in group A, increased with increasing mean peak creatine kinase (CKmax) levels to approximately 1300-1800 U/L. In conclusion, these observations suggest that the initial drop in s-Mg and s-K in the early phase of AMI is due to increased stimulation of beta 2-adrenergic receptors; these changes can be prevented partly or completely by the use of nonselective beta-blockers.