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Regional cerebral blood flow in familial hypercholesterolemia
G Rodriguez1, S Bertolini, F Nobili
1Department of Motor Science (Neurophysiopathology), University of Genova, Italy.
Insights
Sustained hypercholesterolemia did not significantly impair cerebral blood flow (CBF) or cerebrovascular reactivity in patients with familial hypercholesterolemia. However, higher LDL-C levels were associated with slightly reduced CBF, suggesting a minor role in intracranial atherosclerosis.
Area of Science:
- Neurology
- Cardiovascular Medicine
- Metabolic Disorders
Background:
- Epidemiologic studies investigate plasma lipid concentrations as stroke risk factors.
- Limited data exist on sustained hypercholesterolemia's impact on cerebral perfusion.
Purpose of the Study:
- To assess the effect of long-term hypercholesterolemia on cerebral blood flow (CBF) and cerebrovascular reactivity.
- To correlate CBF with lipid levels and clinical features in familial hypercholesterolemia patients.
Main Methods:
- Regional CBF measured using the 133Xe inhalation method in 25 familial hypercholesterolemia patients.
- Cerebrovascular reactivity assessed via acetazolamide challenge in 15 patients.
- Statistical analysis (ANOVA) correlated CBF with lipid profiles and clinical data.
Main Results:
- Basal CBF and cerebrovascular reactivity were generally normal compared to controls.
- CBF showed significant dependence on pretreatment low-density lipoprotein cholesterol (LDL-C) (P=.005) and ischemic heart disease (P=.015).
- CBF was not dependent on lipoprotein(a) or current LDL-C; no differences between treated/untreated patients.
Conclusions:
- Cerebral perfusion and reactivity remain normal despite severe, long-lasting hypercholesterolemia.
- Highest LDL-C levels correlated with slightly reduced CBF.
- Findings align with epidemiologic data suggesting hypercholesterolemia is a minor risk factor for intracranial atherosclerosis and ischemic stroke.
Background And Purpose:
Although epidemiologic investigations are trying to clarify the role of plasma lipid concentrations (primarily cholesterol and its subfractions) as risk factors for both ischemic and hemorrhagic stroke, little information is available regarding the effect of sustained hypercholesterolemia on cerebral perfusion.
Methods:
Regional cerebral blood flow (CBF) was measured by the 133Xe inhalation method in 25 heterozygous patients (four untreated) affected with familial hypercholesterolemia. In 15 patients regional CBF was repeated 20 minutes after intravenous administration of acetazolamide (10 mg/kg body wt) to evaluate cerebrovascular reactivity. Correlations among cerebral perfusion data, present or pretreatment plasma lipid concentrations, and certain other clinical features were assessed by ANOVA.
Results:
Both basal regional CBF and cerebrovascular reactivity were normal in the vast majority of patients compared with age- and sex-matched normal control subjects. CBF was significantly dependent on pretreatment low-density lipoprotein cholesterol (LDL-C) concentration (P = .005) and the presence of symptomatic ischemic heart disease (P = .015). CBF was only slightly dependent on age (P = .05) and was not dependent on either lipoprotein(a) or present LDL-C concentration. CBF did not differ between treated and untreated patients, and the perfusional increase induced by acetazolamide was not related to any other variable.
Conclusions:
Cerebral perfusion and cerebrovascular reactivity were maintained within the normal range despite long-lasting, severe hypercholesterolemia, even if a somewhat lower CBF was found in those patients with the highest LDL-C pretreatment levels. These results are in accord with the epidemiologic data that implicate hypercholesterolemia as a minor risk factor, if a risk factor at all, for intracranial atherosclerosis and ischemic stroke.