Hyperinsulinemia and hemostatic abnormalities are associated with silent lacunar cerebral infarcts in elderly hypertensive subjects.
OBJECTIVE
We sought to study the association of the silent cerebral infarct (SCI), a predisposing condition of stroke, with hyperinsulinemia and hemostatic abnormalities in older hypertensive subjects.


BACKGROUND
Hypertension is a powerful risk factor for stroke. However, the role of other risk factors for stroke in hypertensive subjects remains incompletely understood.


METHODS
We performed brain magnetic resonance imaging and measured cardiovascular risk factors, by administering the 75-g oral glucose tolerance test and measuring plasma insulin and hemostatic variables, in 123 asymptomatic hypertensive subjects (mean age 69 years).


RESULTS
At least one SCI was detected in 80 subjects (65%), and multiple SCIs were found in 48 subjects (39%). The presence of SCIs was associated with older age, higher levels of 24-h systolic blood pressure, 2-h insulin, thrombin-generation markers (prothrombin fragment 1+2 and thrombin-antithrombin complexes), plasminogen activator inhibitor-1 (PAI-1), D-dimer and von Willebrand factor (vWF), but not with plasmin-alpha2-plasmin complex (PIC) levels. The 2-h insulin area under the curve (AUC) was positively correlated with PAI-1 and vWF levels (p < 0.01), and the PAI-1 level was negatively correlated with the PIC level (p < 0.02). Multiple logistic regression analysis revealed that age and the 2-h insulin AUC were significantly associated with SCIs, particularly those located in the subcortical white matter, and hemostatic abnormalities were significantly associated with the presence of multiple SCIs, particularly those located in the basal ganglia.


CONCLUSIONS
In older asymptomatic hypertensive subjects, hyperinsulinemia appears to be associated with lacunar-type SCIs, particularly those located in the subcortical white matter, and hemostatic abnormalities show an association with the presence of multiple SCIs, particularly those located in the basal ganglia.
Kario
K
K
Department of Cardiology, Jichi Medical School, Tochigi, Japan. tkario@kdd.net
Matsuo
T
T
Kobayashi
H
H
Hoshide
S
S
Shimada
K
K
D000368:Aged; D000369:Aged, 80 and over; D001479:Basal Ganglia / Q000473:pathology; D001921:Brain / Q000473:pathology; D002544:Cerebral Infarction / Q000097:blood* / Q000453:epidemiology* / Q000473:pathology; D005260:Female; D005951:Glucose Tolerance Test; D006487:Hemostasis; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood* / Q000453:epidemiology*; D006973:Hypertension / Q000097:blood* / Q000453:epidemiology*; D016015:Logistic Models; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D012307:Risk Factors; D010959:Tissue Plasminogen Activator / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
D017395:Plasminogen Activator Inhibitor 1; D014841:von Willebrand Factor; D010959:Tissue Plasminogen Activator