Hemostasis and Vascular Dementia

Abstract

Vascular dementia (VaD) comprises a group of syndromes caused by vascular lesions in the brain. Cognitive impairment may follow a single cortical or lacunar infarct in a strategic area of the brain, multiple infarcts, small-vessel disease (leukoaraiosis), intracerebral hemorrhage, or any of these conditions coexisting with Alzheimer dementia (so-called mixed dementia). Depending on case mix and the type of observational study, 10% of patients already have dementia before their first stroke, 10% develop it soon after their first stroke, and more than 33% have dementia after a recurrent stroke.1 Typically, dementia develops at a rate of 3% per year after stroke, and it is the stroke, rather than its underlying risk factors, that appears to be the dominant cause of subsequent dementia.1 See accompanying articles on pages 599 and 605 Although VaD, including poststroke dementia, is associated with conventional risk factors, such as hypertension and hypercholesterolemia,2,3 their relationship with hemostatic factors is less clear. This contrasts with the relationship between hemostatic factors and stroke, which is well established and involves both soluble (eg, fibrinogen4) and cellular (eg, mean platelet volume5) biomarkers. Several hemostatic factors, including fibrinogen and fibrin d-dimer levels, are associated with subsequent cognitive impairment and dementia in observational studies (Table).6–10 This issue of Arteriosclerosis, Thrombosis, and Vascular Biology expands on this relationship between “sticky blood” and cognition.11 Two new studies are described. View this table: Table. Selected Hemostatic Factors With …