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Published on: September 15, 2018
Retinal findings in familial hypercholesterolemia: An exploratory case-control study
Gisle Langslet1, Synne Kollstad2, Øystein Kalsnes Jørstad3,4
1Lipid Clinic, Oslo University Hospital, Oslo, Norway.
Insights
Patients with familial hypercholesterolemia (FH) do not show increased retinal arteriolosclerosis. This study found no link between FH, high LDL-C, and damage to small arteries in the retina.
Area of Science:
- Ophthalmology
- Cardiology
- Genetics
Background:
- Familial hypercholesterolemia (FH) causes high LDL-C from birth, increasing cardiovascular risk via atherosclerosis.
- The impact of elevated LDL-C on smaller arteries, like retinal arterioles, is less understood.
- Retinal arterioles may stiffen and thicken due to high LDL-C.
Purpose of the Study:
- To investigate retinal arteriolosclerosis in FH patients versus controls.
- To explore associations between retinal arteriolosclerosis and lipid levels, demographics, and treatment duration.
Main Methods:
- Compared 50 FH patients (40-70 yrs, normotensive, non-smokers) with 30 controls.
- Excluded participants with diabetes or vascular retinal disease.
- Assessed retinal arteriolosclerosis using Scheie classification on fundus photographs.
Main Results:
- No significant difference in retinal arteriolosclerosis prevalence between FH patients and controls.
- Current lipid levels, age, sex, statin use, or duration of lipid-lowering treatment did not correlate with retinal arteriolosclerosis.
Conclusions:
- FH patients do not exhibit a higher prevalence of retinal arteriolosclerosis compared to individuals without FH.
- Elevated LDL-C in FH may not significantly impact retinal arteriolosclerosis in this cohort.
Background And Aims:
Patients with familial hypercholesterolemia (FH) have elevated LDL-C levels from birth and increased risk of cardiovascular disease due to atherosclerosis, mostly affecting larger arteries. Less is known about effects of elevated LDL-cholesterol on smaller arteries. Retinal arterioles are prone to damage in the form of stiffening and thickening. We therefore explored the occurrence of retinal arteriolosclerosis in patients with genetically verified FH, and in a control group. Associations between retinal arteriolosclerosis and current serum lipid values, sex, age, statin treatment, and years on lipid-lowering treatment were also investigated.
Methods:
Eligible patients were 40 to 70 years of age, normotensive, and non-smokers. Exclusion criteria were diabetes and vascular retinal disease. Control subjects had to have normal lipid levels and no history of cardiovascular disease. Lipid measurements were collected prior to the visit, and at the visit retinal fundus photographs of both eyes were taken. The fundus photographs were graded by two ophthalmologists according to the Scheie classification for retinal arteriolosclerosis.
Results:
Fifty patients with FH and 30 control subjects participated. Mean duration of lipid-lowering medication for the patient group was 17.0 years. The control group had higher total cholesterol, LDL-C and HDL-C, ApoB and ApoA1 levels than the patient group. There were no differences in the occurrence of retinal arteriolosclerosis between the two groups, and no associations were found between current lipid levels, age, sex, statin treatment, years on LLT and retinal arteriolosclerosis.
Conclusion:
Patients with FH did not have increased prevalence of retinal arteriolosclerosis compared to controls.
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