Abstract
We investigated the hemorheological changes and correlations among aging, cerebral atrophy, and silent infarct lesions in patients with silent cerebral infarctions (n=46) and in patients with symptomatic cerebral infarctions. We measured the whole blood viscosity, corrected blood viscosity at a standard hematocrit level of 45%, plasma viscosity, plasma fibrinogen concentration, fibrinogen/albumin ratio, and yield shear stress index as hemorheological parameters. For the evaluation of cerebral atrophy, the parenchyma/skull-volume ratio and parenchyma/ (ventricles + subarachnoid space) -volume ratio were estimated using a planimeter or digitizer.
The patients with silent cerebral infarctions (n=36) revealed significantly lower values for the corrected blood viscosity, plasma fibrinogen concentration, fibrinogen/albumin ratio, and yield shear stress index than those in patients with chronic cerebral infarction (n=25) (4.36 vs. 4.63 mPa·s, p<0.05 ; 280.0 vs. 379.0 mg/dl, p<0.05; 71.2 vs. 105.0 p<0.05; and 0.056 vs. 0.080, p<0.01, respectively). Among the patients with silent cerebral infarct lesions, those with more progressive lesions showed significantly higher plasma fibrinogen concentrations and fibrinogen/albumin ratios than those with less progressive lesions (P<0.010.05).
The increase in numbers of silent white matter lesions (WML) was significantly correlated with aging and severity of cerebral atrophy (p<0.050.01). In patients with silent infarctions, the severity of periventricular hyperintensity (PVH) was significantly correlated only with the increase in numbers of WML (p<0.010.05). In patients with silent infarctions together with patients with symptomatic cerebral infarctions of perforating arteries (n=16), the severity of PVH became significantly correlated with the increase in numbers of WML, aging, and severity of cerebral atrophy (p<0.010.05).
It is suggested that increases in plasma fibrinogen concentration might play a role in the progression of silent cerebral infarct lesions, and extensions of the silent cerebral infarct lesions may be significantly correlated with aging and cerebral atrophy.
