title: Increased infections with β-blocker use in ischemic stroke, a β2-receptor mediated process?
abstract: Strokes promote immunosuppression, partially from increased sympathetic activity. Altering sympathetic drive with β-blockers has variably been shown to improve stroke outcomes. This study adds to this literature using propensity score matching to limit confounding and by examining the effects of selective and non-selective β-blockers. Prospective data from acute ischemic stroke admissions at a single center from July 2010-June 2015 were analyzed. Outcomes included infection (urinary tract infection [UTI], pneumonia, or bacteremia), discharge modified Rankin Score (mRS), and in-hospital death. Any selective and non-selective β-blocker use during the first 3 days of admission were investigated with propensity score matching. A sensitivity analysis was also performed. This study included 1431 admissions. Any β-blocker use was associated with increased infections (16.4 vs. 10.7%, p = 0.030). Non-selective β-blocker use was associated with increased infections (18.9 vs. 9.7%, p = 0.005) and UTIs (13.0 vs. 5.5%, p = 0.009). Selective β-blocker use was not associated with infection. There were no associations between β-blocker use and in-hospital death or discharge mRS. In the sensitivity analysis, the association between non-selective β-blocker use and urinary tract infections persisted (12.5 vs. 4.2%, p = 0.044). No associations with death or mRS were found. Early β-blocker use after ischemic stroke may increase the risk of infection but did not change disability or mortality risk. The mechanism may be mediated by β2-adrenergic receptor antagonism given the different effects seen with selective versus non-selective β-blocker use.
authors.affiliation: Department of Anesthesiology and Pain Medicine, University of Washington, Box 356540, Seattle, WA, 98195-6540, USA. jordanbstarr@gmail.com.
authors.forename: Jordan B
authors.initials: JB
authors.lastname: Starr
authors.affiliation: Department of Neurology, University of Washington, Seattle, WA, USA.
authors.forename: David L
authors.initials: DL
authors.lastname: Tirschwell
authors.affiliation: Department of Neurology, University of Washington, Seattle, WA, USA.
authors.forename: Kyra J
authors.initials: KJ
authors.lastname: Becker
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000368:Aged; D002545:Brain Ischemia / Q000188:drug therapy* / Q000453:epidemiology* / Q000378:metabolism; D004185:Disability Evaluation; D005260:Female; D006801:Humans; D007239:Infections / Q000453:epidemiology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010343:Patient Admission; D057216:Propensity Score; D011446:Prospective Studies; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism; D012307:Risk Factors; D020521:Stroke / Q000188:drug therapy* / Q000453:epidemiology* / Q000378:metabolism; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D000319:Adrenergic beta-Antagonists; D018343:Receptors, Adrenergic, beta-2
keywords: Adrenergic beta-antagonists; Infection; Outcome studies; Propensity score; Stroke