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Low and high density lipoprotein metabolism in atherothrombotic brain infarction
Insights
Altered metabolism of low density lipoprotein (LDL) and high density lipoprotein (HDL) is linked to carotid stenosis. Metabolic rates, not just concentrations, are key predictors of stroke risk.
Area of Science:
- Cardiovascular Medicine
- Metabolic Research
- Neurology
Background:
- Elevated low density lipoprotein (LDL) and reduced high density lipoprotein (HDL) cholesterol are potential risk factors for atherothrombotic brain infarction.
- The precise metabolic mechanisms underlying this association remain incompletely understood.
Purpose of the Study:
- To investigate the kinetic parameters of LDL and HDL metabolism in individuals with atherothrombotic brain infarction or extracranial occlusive disease.
- To elucidate the relationship between lipoprotein metabolism and the pathogenesis of carotid stenosis.
Main Methods:
- Studied nine subjects with atherothrombotic brain infarction/occlusive disease and 12 controls.
- Injected autologous iodine-125-labeled lipoproteins and monitored decay curves over 10 days.
- Calculated kinetic parameters, including fractional catabolic rates, from blood samples.
Main Results:
- Stroke-risk group had higher triglycerides, total cholesterol, and LDL cholesterol.
- Significantly lower fractional catabolic rate of LDL and higher rate of HDL in the stroke-risk group.
- Carotid stenosis correlated significantly with triglyceride, LDL cholesterol, and LDL fractional catabolic rate.
Conclusions:
- Altered LDL and HDL metabolism plays a role in carotid stenosis pathogenesis.
- Metabolic rates of serum lipoproteins are more significantly associated with carotid stenosis than their concentrations.
- Metabolic parameters may be more crucial for predicting stroke risk than serum lipoprotein levels alone.
Background And Purpose:
Elevated low density lipoprotein and reduced high density lipoprotein cholesterol may increase the risk of atherothrombotic brain infarction, but the metabolic mechanisms accounting for this relation are poorly understood.
Methods:
The kinetic parameters of low density and high density lipoprotein were studied in nine subjects with atherothrombotic brain infarction or identifiable (by noninvasive testing) extracranial occlusive disease and in 12 control subjects. Autologous iodine-125-labeled lipoproteins were injected intravenously. Blood samples were drawn 10 minutes after injection and periodically thereafter for 10 days. Kinetic parameters were calculated from the decay curves.
Results:
The stroke-risk group showed significantly higher triglyceride (p less than 0.05), total cholesterol (p less than 0.02), and low density lipoprotein cholesterol (p less than 0.01). The fractional catabolic rate of low density lipoprotein was significantly lower (p less than 0.001) and the high density lipoprotein rate higher (p less than 0.02) in the stroke-risk group than in the control group. Regression analysis (using all subjects) of serum lipoproteins and their respective fractional catabolic rates correlated significantly (for low density lipoprotein, r = 0.684, p less than 0.001; for high density lipoprotein, r = 0.595, p less than 0.002). Mean percent stenosis showed a significant relation with triglyceride level (r = 0.678, p less than 0.01) and low density lipoprotein cholesterol (r = 0.535, p less than 0.02) but not with high density lipoprotein cholesterol. Mean percent stenosis also showed correlation with both fractional catabolic rate of low density lipoprotein (r = 0.667, p less than 0.002) and with serum high density lipoprotein levels (r = 0.504, p less than 0.02).
Conclusions:
Our study provides insights into the role of altered low and high density lipoprotein metabolism in the pathogenesis of carotid stenosis. The statistically significant association of serum lipoprotein metabolic rates with carotid stenosis, rather than their respective serum concentrations, implies that metabolic parameters may be more important in predicting stroke risk.