Increased infections with β-blocker use in ischemic stroke, a β₂-receptor mediated process?

Area of Science:

• Neurology
• Pharmacology
• Immunology

Background:

• Strokes can lead to immunosuppression due to increased sympathetic activity.
• Beta-blockers, which modulate sympathetic drive, have shown variable effects on stroke outcomes.
• Understanding the differential impact of selective and non-selective beta-blockers is crucial.

Purpose of the Study:

• To investigate the association between early beta-blocker use and post-stroke outcomes, including infection, disability, and mortality.
• To differentiate the effects of selective versus non-selective beta-blockers on stroke recovery.
• To limit confounding factors using propensity score matching.

Main Methods:

• Analysis of prospective data from 1431 acute ischemic stroke admissions (July 2010-June 2015).
• Propensity score matching was employed to compare outcomes between beta-blocker users and non-users within the first 3 days of admission.
• Outcomes assessed included infection (UTI, pneumonia, bacteremia), modified Rankin Score (mRS), and in-hospital death. A sensitivity analysis was also conducted.

Main Results:

• Overall beta-blocker use was linked to a higher incidence of infections (16.4% vs. 10.7%).
• Non-selective beta-blocker use showed a significant association with increased infections (18.9% vs. 9.7%) and urinary tract infections (UTIs) (13.0% vs. 5.5%).
• Selective beta-blocker use was not associated with infection. No significant associations were found between any beta-blocker use and in-hospital death or discharge mRS.

Conclusions:

• Early administration of beta-blockers post-ischemic stroke may elevate the risk of infection, particularly UTIs with non-selective agents.
• Beta-blocker use did not appear to influence long-term disability or mortality after stroke.
• The observed differences suggest a potential mechanism mediated by beta2-adrenergic receptor antagonism.