Maier Ilko L, Karch André, Mikolajczyk Rafael, Bähr Mathias, Liman Jan
Department of Neurology, University Medicine Göttingen, Göttingen, Germany.
Research group Epidemiological and Statistical Methods (ESME), Department of Epidemiology, Helmholtz Centre for Infection Research, Braunschweig, Germany; German Center for Infection Research (DZIF), Braunschweig site, Braunschweig, Germany.
PLoS One. 2015 Feb 2;10(2):e0116836. doi: 10.1371/journal.pone.0116836. eCollection 2015.
Infections 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.
625 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.
553 (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).
Beta-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.
感染是导致中风后住院时间延长和死亡率增加的常见原因。最近的研究表明,中风会导致外周免疫系统抑制,从而增加感染易感性。在中风小鼠模型中,β受体阻滞剂给药后这种免疫抑制作用是可逆的。我们研究的目的是调查β受体阻滞剂治疗对人类中风后感染风险和死亡风险的影响。
本历史队列研究纳入了连续625例入住大学医院中风单元的缺血性或出血性中风患者。使用多变量泊松回归模型和Cox回归模型研究β受体阻滞剂治疗对中风后肺炎、尿路感染和死亡的影响。
553例(88.3%)患者因缺血性中风入院,其余72例(11.7%)为出血性中风。基线NIHSS中位数为8分(四分位间距5 - 16分)。301例(48.2%)患者接受了β受体阻滞剂治疗。接受β受体阻滞剂治疗和未接受治疗的患者中风后肺炎风险没有差异(率比 = 1.00,95%置信区间0.77 - 1.30,p = 0.995)。接受β受体阻滞剂治疗的患者尿路感染风险降低(RR = 0.65,95%置信区间0.43 - 0.98,p = 0.040)。两组间7天死亡率无差异(风险比 = 1.36,95%置信区间0.65 - 2.77,p = 0.425),而接受β受体阻滞剂治疗的患者30天死亡率更高(HR = 1.93,95%置信区间1.20 - 3.10,p = 0.006)。
β受体阻滞剂治疗并未降低中风后肺炎风险,但显著降低了尿路感染风险。两种疾病潜在的不同免疫机制可能解释了这些发现,这需要在未来的研究中得到证实。