Inflammation as a risk factor for stroke: evidence from experimental models

Abstract

The association of preceding systemic infection and ischemic stroke has long been recognized by clinicians [1–7]. In a retrospective study of ischemic stroke in Sweden, stroke incidence exhibited seasonal variability with higher incidence in the colder winter months [1]. Infection was suggested to underlie the increased stroke incidence during winter since, in young adults without established stroke-risk factors, evidence of infection was seen concomitantly with the onset of stroke [1>]. Seasonal variability of plasma fibrinogen and factor VII activity in an elderly population in England with increased levels during winter was also related to respiratory infections [8]. Syrjanen et al. [4] demonstrated in Finland that young to middle-aged patients presenting with acute ischemic stroke had a significantly higher prevalence of febrile infections 1 month preceding the stroke. A similar association of ischemic stroke and dental infection in the preceding month was further established in young Finnish men [9]. Evidence of infection less than 1 month before onset of stroke was also reported in 34% of stroke patients of all age groups in southern California by Ameriso et al. [10]. Several case-control studies that have also included older patients, revealed that infection within 1 week before onset of stroke or examination was significantly more common among stroke patients than in control subjects [5–7]. An inflammatory response may also explain why chronic infection with Chlamydia pneumoniae is a predisposing risk factor for carotid atherosclerosis and cerebrovascular disease [11–16].