Abstract
BackgroundInfections are a frequent cause for prolonged hospitalization and increased mortality after stroke. Recent studies revealed a stroke-induced depression of the peripheral immune system associated with an increased susceptibility for infections. In a mice model for stroke, this immunosuppressive effect was reversible after beta-blocker administration. The aim of our study was to investigate the effect of beta-blocker therapy on the risk of infections and death after stroke in humans.Methods625 consecutive patients with ischemic or hemorrhagic stroke, admitted to a university hospital stroke unit, were included in this historical cohort study. The effect of beta-blocker therapy on post-stroke pneumonia, urinary tract infections and death was investigated using multivariable Poisson and Cox regression models.Results553 (88.3%) patients were admitted with ischemic stroke, the remaining 72 (11.7%) had a hemorrhagic stroke. Median baseline NIHSS was 8 (IQR 5–16) points. 301 (48.2%) patients received beta-blocker therapy. There was no difference in the risk of post-stroke pneumonia between patients with and without beta-blocker therapy (Rate Ratio = 1.00, 95%CI 0.77–1.30, p = 0.995). Patients with beta-blocker therapy showed a decreased risk for urinary tract infections (RR = 0.65, 95%CI 0.43–0.98, p = 0.040). 7-days mortality did not differ between groups (Hazard Ratio = 1.36, 95%CI 0.65–2.77, p = 0.425), while patients with beta-blocker therapy showed a higher 30-days mortality (HR = 1.93, 95%CI 1.20–3.10, p = 0.006).ConclusionsBeta-blocker therapy did not reduce the risk for post-stroke pneumonia, but significantly reduced the risk for urinary tract infections. Different immune mechanisms underlying both diseases might explain these findings that need to be confirmed in future studies.
Highlights
Systemic infections are associated with poor outcome and increased mortality after ischemic and hemorrhagic stroke [1,2,3]
Beta-blocker therapy did not reduce the risk for post-stroke pneumonia, but significantly reduced the risk for urinary tract infections
Recent experimental studies showed an active interaction between the central nervous system and the peripheral immune system, which can result in immunosuppression and increased susceptibility for systemic infections after stroke [5,6,7,8]
Summary
Systemic infections are associated with poor outcome and increased mortality after ischemic and hemorrhagic stroke [1,2,3]. Recent experimental studies showed an active interaction between the central nervous system and the peripheral immune system, which can result in immunosuppression and increased susceptibility for systemic infections after stroke [5,6,7,8] This effect is thought to be a compensatory response to protect the post-ischemic brain from overwhelming and damaging inflammatory response, which is caused by infiltration of immune cells in the ischemic brain area with oxidative stress, microglial and complement activation and damage of the blood brain barrier [9, 10]. The authors demonstrated a complete reversion of the anti-inflammatory phenotype, a complete inhibition of mortality after systemic administration of the nonspecific beta-blocker propranolol and a 50% reduction of mortality after chemical depletion of peripheral neuronal terminals containing noradrenaline 24 h after MCAO These data suggest a post-ischemic, noradrenergic immunosuppressive pathway and a central role of iNKT cells in the systemic immune reaction after stroke. The aim of our study was to investigate the effect of beta-blocker therapy on the risk of infections and death after stroke in humans
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