The origin and significance of blood hyperviscosity in subjects with acute stroke has been controversial. It has been argued that viscous abnormalities simply reflect either elevated hematocnt or an acute-phase response to the stroke itself. To address these issues, we measured the factors that determine blood viscosity in a cross-sectional study of 430 subjects, including 135 with acute stroke, 89 with acute transient ischemic attacks of the brain, 115 with recognized risk factors for stroke, and 91 healthy controls. The at-risk group was balanced with the acute stroke group for types of risk factors and medication usage, and all four groups were balanced for age. The viscosity of whole blood at low rates of shear and the plasma viscosity were significantly elevated in both groups with cerebrovascular symptoms and in the at-risk group compared with the healthy controls. The severity of hyperviscosity was stroke group > transient ischemic attack group > at-risk group > healthy controls. Increased viscosity of whole blood was associated with an elevated plasma fibrinogen concentration and with a decreased albumin/ globulin ratio. This study provides evidence that blood hyperviscosity is present not only in subjects with acute brain infarction, but also in those with risk factors for stroke, and that these abnormalities are, to a considerable degree, chronic (Stroke 1991^2:162-168)

Background and Purpose: In following patients initially recruited for a cross-sectional study of blood viscosity in ischemic cerebrovascular disease, it was noted that those having a low albumin-globulin ratio appeared to experience the majority of subsequent vascular events. Accordingly, a prospective study in which subjects were assigned to a high or low albumin-globulin cohort was undertaken to examine the relation between a low albumin-globulin ratio, the presence of clinical risk factors for stroke, and the occurrence of subsequent stroke, myocardial infarction, or vascular death.Methods: Three groups of subjects were followed for an average of 1.5±0.8 years to ascertain vascular end points. Group 1 consisted of 126 patients with acute ischemic stroke; group 2 included 109 subjects matched with group 1 for age, medications, and recognized clinical risk factors for stroke; and group 3 was composed of 84 healthy volunteers, matched for age with groups 1 and 2. The median albumin-globulin ratio for group 1 at enrollment, 1.45, was used to dichotomize patients into two cohorts: all subjects with an albumin-globulin ratio of 1.45 or less were assigned to the "low" albumin-globulin cohort; those whose ratio was greater than 1.45 were assigned to the "high" albumin-globulin cohort. The occurrence of vascular end points was verified during subsequent hospitalizations and outpatient clinic visits and by telephone interviews of patients and providers.Results: A total of 51 vascular events occurred, including 39 in group 1, 8 in group 2, and 4 in group 3. Subjects in either group 1 or 2 who were in the low albumin-globulin cohort had at least double the risk for a subsequent vascular event compared with their counterparts in the high albumin-globulin cohort (P<.01 and P<.03, respectively). In comparison with the high albumin-globulin cohort, significantly more patients in the low albumin-globulin cohort in group 1 had a history of prior stroke (P<.03). When groups 1 and 2 were combined, both a low albumin-globulin ratio and diabetes had a significant independent association with increased risk for subsequent vascular events in a Cox proportional-hazards model (P<.01 and P<.03, respectively).Conclusions: The results of this study indicate that significantly increased risk for subsequent vascular events in stroke patients and in subjects with clinical risk factors for stroke is associated with a shift in the concentrations of blood proteins to a prothrombotic environment characterized by lower levels of albumin and an increased concentration of globulins and fibrinogen.

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