| Literature DB >> 27246162 |
Raul D Santos1, Samuel S Gidding2, Robert A Hegele3, Marina A Cuchel4, Philip J Barter5, Gerald F Watts6, Seth J Baum7, Alberico L Catapano8, M John Chapman9, Joep C Defesche10, Emanuela Folco11, Tomas Freiberger12, Jacques Genest13, G Kees Hovingh10, Mariko Harada-Shiba14, Steve E Humphries15, Ann S Jackson16, Pedro Mata17, Patrick M Moriarty18, Frederick J Raal19, Khalid Al-Rasadi20, Kausik K Ray21, Zelijko Reiner22, Eric J G Sijbrands23, Shizuya Yamashita24.
Abstract
Familial hypercholesterolaemia is common in individuals who had a myocardial infarction at a young age. As many as one in 200 people could have heterozygous familial hypercholesterolaemia, and up to one in 300 000 individuals could be homozygous. The phenotypes of heterozygous and homozygous familial hypercholesterolaemia overlap considerably; the response to treatment is also heterogeneous. In this Review, we aim to define a phenotype for severe familial hypercholesterolaemia and identify people at highest risk for cardiovascular disease, based on the concentration of LDL cholesterol in blood and individuals' responsiveness to conventional lipid-lowering treatment. We assess the importance of molecular characterisation and define the role of other cardiovascular risk factors and advanced subclinical coronary atherosclerosis in risk stratification. Individuals with severe familial hypercholesterolaemia might benefit in particular from early and more aggressive cholesterol-lowering treatment (eg, with PCSK9 inhibitors). In addition to better tailored therapy, more precise characterisation of individuals with severe familial hypercholesterolaemia could improve resource use.Entities:
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Year: 2016 PMID: 27246162 DOI: 10.1016/S2213-8587(16)30041-9
Source DB: PubMed Journal: Lancet Diabetes Endocrinol ISSN: 2213-8587 Impact factor: 32.069