Anti-PCSK9 antibodies for the treatment of heterozygous familial hypercholesterolemia: Patient selection and perspectives

© 2017 Catapano et al. Heterozygous familial hypercholesterolemia (FH) is a genetic disorder characterized by high low-density lipoprotein cholesterol levels from birth, which exposes the arteries to high levels of atherogenic lipoproteins lifelong and results in a significantly increased risk of p...

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Main Authors: Catapano, A., Pirillo, A., Norata, Giuseppe
Format: Journal Article
Published: 2017
Online Access:http://hdl.handle.net/20.500.11937/63283
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author Catapano, A.
Pirillo, A.
Norata, Giuseppe
author_facet Catapano, A.
Pirillo, A.
Norata, Giuseppe
author_sort Catapano, A.
building Curtin Institutional Repository
collection Online Access
description © 2017 Catapano et al. Heterozygous familial hypercholesterolemia (FH) is a genetic disorder characterized by high low-density lipoprotein cholesterol levels from birth, which exposes the arteries to high levels of atherogenic lipoproteins lifelong and results in a significantly increased risk of premature cardiovascular events. The diagnosis of FH, followed by an appropriate and early treatment is critical to reduce the cardiovascular burden in this population. Phase I-III clinical trials showed the benefit of proprotein convertase subtilisin kexin 9 inhibitors, both alirocumab and evolocumab, in these patients with an average low-density lipoprotein cholesterol reduction ranging from −40% to −60%. The aim of this review is to address the unmet needs in cholesterol management, elucidate the biology and the clinical benefit of proprotein convertase subtilisin kexin 9 inhibition and finally discuss the open gaps and future directions in the treatment of patients with heterozygous FH.
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spelling curtin-20.500.11937-632832018-02-06T06:23:53Z Anti-PCSK9 antibodies for the treatment of heterozygous familial hypercholesterolemia: Patient selection and perspectives Catapano, A. Pirillo, A. Norata, Giuseppe © 2017 Catapano et al. Heterozygous familial hypercholesterolemia (FH) is a genetic disorder characterized by high low-density lipoprotein cholesterol levels from birth, which exposes the arteries to high levels of atherogenic lipoproteins lifelong and results in a significantly increased risk of premature cardiovascular events. The diagnosis of FH, followed by an appropriate and early treatment is critical to reduce the cardiovascular burden in this population. Phase I-III clinical trials showed the benefit of proprotein convertase subtilisin kexin 9 inhibitors, both alirocumab and evolocumab, in these patients with an average low-density lipoprotein cholesterol reduction ranging from −40% to −60%. The aim of this review is to address the unmet needs in cholesterol management, elucidate the biology and the clinical benefit of proprotein convertase subtilisin kexin 9 inhibition and finally discuss the open gaps and future directions in the treatment of patients with heterozygous FH. 2017 Journal Article http://hdl.handle.net/20.500.11937/63283 10.2147/VHRM.S130338 unknown
spellingShingle Catapano, A.
Pirillo, A.
Norata, Giuseppe
Anti-PCSK9 antibodies for the treatment of heterozygous familial hypercholesterolemia: Patient selection and perspectives
title Anti-PCSK9 antibodies for the treatment of heterozygous familial hypercholesterolemia: Patient selection and perspectives
title_full Anti-PCSK9 antibodies for the treatment of heterozygous familial hypercholesterolemia: Patient selection and perspectives
title_fullStr Anti-PCSK9 antibodies for the treatment of heterozygous familial hypercholesterolemia: Patient selection and perspectives
title_full_unstemmed Anti-PCSK9 antibodies for the treatment of heterozygous familial hypercholesterolemia: Patient selection and perspectives
title_short Anti-PCSK9 antibodies for the treatment of heterozygous familial hypercholesterolemia: Patient selection and perspectives
title_sort anti-pcsk9 antibodies for the treatment of heterozygous familial hypercholesterolemia: patient selection and perspectives
url http://hdl.handle.net/20.500.11937/63283