Very low levels of HDL cholesterol and atherosclerosis, a variable relationship – a review of LCAT deficiency Full Text
Vascular Health and Risk Management, 06/07/2012
Savel J et al. - The authors present a case study of one patient, referred for evaluation of global cardiovascular risk in the presence of a low HDL cholesterol level, who was diagnosed with LCAT gene mutations.
- A number of epidemiological and clinical studies have demonstrated that plasma high-density lipoprotein (HDL) level is a strong inverse predictor of cardiovascular events.
- HDL is believed to retard the formation of atherosclerotic lesions by removing excess cholesterol from cells and preventing endothelial dysfunction.
- Lecithin cholesterol acyltransferase (LCAT) plays a central role in the formation and maturation of HDL, and in the intravascular stage of reverse cholesterol transport: a major mechanism by which HDL modulates the development and progression of atherosclerosis.
- A defect in LCAT function would be expected to enhance atherosclerosis, by interfering with the reverse cholesterol transport step.
- As such, one would expect to find more atherosclerosis and cardiovascular events in LCAT-deficient patients.
- But this relationship is not always evident.
- The authors discuss the paradoxical finding of severe high-density lipoprotein (HDL) deficiency and an absence of subclinical atherosclerosis in Lecithin cholesterol acyltransferase (LCAT)-deficient patients, which has been used to reject the hypothesis that HDL level is important in the protection against atherosclerosis.