Of cholesterol-fed rabbits and LDL receptor-deficient men

      The lipid hypothesis, born in St Petersburg 100 years ago, was based upon Anitschkow's production of atherosclerosis in rabbits by diet-induced hypercholesterolaemia. Withdrawal of the diet reversed the hypercholesterolaemia and reduced the severity of aortic lesions. Striking similarities exist between the location and composition of atheromatous plaques in this animal model and lesions in humans with familial hypercholesterolaemia (FH). Retrospective analysis of angiographic trials suggests that cholesterol-lowering by statins and/or apheresis results in regression of coronary lesions in FH but only reduces their progression in non-FH subjects, despite similar percentage reductions in LDL cholesterol (C). This apparent discrepancy has been explored prospectively using serial carotid ultrasound to measure carotid plaque thickness in 10 FH patients and 21 with non-FH (mixed dyslipidaemia) treated with rosuvastatin ± ezetimibe for 2-9 (mean=4) years. Despite similar decreases in LDL-C (60% v 57%) increases in carotid plaque thickness were less in FH than in non-FH patients (0.013 mm/yr v 0.032 mm/yr, P= 0.02) These findings indicate that LDL-lowering has a greater anti-atherosclerotic effect in FH patients than in non-FH patients with multiple risk factors, presumably reflecting the monofactorial basis of atherosclerosis in FH, analogous to Anitschkow's hypercholesterolaemic rabbits.
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