Catecholamines, infection, and death in acute ischemic stroke

Experimental studies have recently suggested that acute ischemia may facilitate the appearance of fatal infections as part of a brain-induced immunodepression syndrome. However, the mechanisms and neurological consequences of infections complicating acute ischemic stroke have received much less attention at the bedside. The incidence of infection and death after non-septic stroke was compared in this prospective study with longitudinal changes of cytokines, leukocytes, normetanephrine (NMN) and metanephrine (MN) in 75 consecutive patients. In multivariate analysis, infection, n = 13 (17%), was associated with the upper quartile of MN (OR 3.51, 95% CI 1.30–9.51), neurological impairment (NIHSS) on admission (OR 3.99, 95% CI 1.34–11.8), monocyte count (OR 1.78, 95% CI 1.13–2.79), and increased interleukin (IL)-10 (OR 1.54, 95% CI 1.00–2.38). Mortality at 3 months, n = 16 (21%), was associated with increased levels of NMN on admission (OR 2.34 95% CI 1.15–4.76), NIHSS score (OR 2.57, 95% CI 1.29–5.11), and higher IL-6 levels (OR 1.29, 95% 1.00–1.67). These findings suggest that acute ischemic stroke is associated with an early activation of the sympathetic adrenomedullar pathway that lowers the threshold of infection and increases the risk of death. Moreover, these findings are independent of the blood borne effects of pro- and anti-inflammatory cytokines, and circulating leukocytes.