Article Archive
How low should LDL cholesterol be lowered – and for how long?
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PCSK9 plasma transport and lipoprotein association
Hagai Tavori, PhD, and Sergio Fazio, MD, PhD. Knight Cardiovascular Institute, Center of Preventive Cardiology, Oregon Health and Science University, Portland, OR. PCSK9 and LDL are ligands for the LDL receptor (LDLR). The fate of the ligand-receptor complex is dependent on the ligand, with both…
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Overturning the 1%…Bridging the gaps in care
2014 FH Global Summit: 13-14 October, New York, USA: Familial hypercholesterolaemia (FH) is a major clinical challenge for the 21st century. The European Atherosclerosis Society Consensus Panel has already made the case for FH being one of the most common inherited conditions, affecting about one…
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RUTHERFORD-2 in brief
RUTHERFORD-2 was a large, randomised, placebo-controlled trial of the PCSK9 inhibitor, evolocumab, in 331 patients with heterozygous familial hypercholesterolaemia (mean LDL-C at baseline 3.9-4.2 mmol/L). All were on statins and 62% were also on ezetimibe. FH-causing mutations were identified in 80% of patients, most were…
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Why new NLA guidelines for dyslipidaemia? A view from the authors
The US National Lipid Association (NLA) has just released recommendations for management of dyslipidaemia. Matthew K. Ito, Professor of Pharmacy Practice, Portland, Oregon and one of the lead authors, discusses thinking behind these recommendations, and what are the implications for clinicians. • Why has the…
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Missing FH: How can we improve FH referral and diagnosis?
Heterozygous familial hypercholesterolemia (FH) is neither a rare disease nor a sentence to a life full of complications and early death. Recent evidence shows that even when founder effects are taken into account, heterozygous FH affects around 1/200-300 people instead of the historical estimate of…
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Will the PCSK9 monoclonal antibodies replace other lipid lowering treatments currently used with statins?
Where will the new PCSK9 inhibitors fit into the treatment of people whose raised low density lipoprotein cholesterol (LDL-C) puts them at high risk of cardiovascular disease? Leading researcher, Professor Frederick Raal discusses this important question.
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In your opinion, what are the optimum patient populations for PCSK9 monoclonal antibody therapy?
PCSK9 monoclonal antibodies offer very important new treatments to lowed low density lipoprotein cholesterol (LDL-C) in patients who cannot tolerate statins or whose LDL-C is inadequately reduced as well as those people with high LDL-C caused by Familial Hypercholesterolemia.
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Not only lower BUT but SOONER is better
2014 FH Global Summit: 13-14 October, New York, USA FH is highly treatable: lowering LDL-C helps in managing the disease process. Clearly, the focus for FH care needs to move from the acute setting to prevention. Identifying FH sooner rather than later is optimal for…
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PCSK9 inhibitors and FH: future for standard of care?
Two recent trials in FH patients – RUTHERFORD-2 and TESLA – have raised the focus of the PCSK9 inhibitors in FH. In an accompanying Lancet editorial, Profs. Raul Santos (Sao Paulo, Brazil) and Gerald Watts (Perth, Australia) have intimidated that PCSK9 inhibitors might represent the…
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How can we optimise PCSK9-targeted therapies?
Highly relevant to these discussions was how to optimise the use of PCSK9-targeted therapies, discussed from both European (Professor Luís Masana, University Rovira and Virgili, Reus-Tarragona, Spain) and North American (Professor Henry Ginsberg, Columbia University, New York, USA) perspectives, from the guidelines perspectives. There are…
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RUTHERFORD-2 slide deck now available
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Alirocumab
A 24-Week Study of Alirocumab as Monotherapy versus Ezetimibe: The First Phase 3 Data of a Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitor One Year Open-Label Treatment with Alirocumab 150 mg Every Two Weeks in Heterozygous Familial Hypercholesterolemic Patients Effects of Alirocumab, a Fully Human Monoclonal…
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Will PCSK9 monoclonal antibody therapy replace other classes of drug currently used in combination therapy both in FH and non-FH indications?
Frederick J. Raal FRCP, FRCPC, FCP(SA), Cert Endo, MMED, PhD Professor and Head, Division of Endocrinology & Metabolism Director, Carbohydrate and Lipid Metabolism Research Unit University of the Witwatersrand, South Africa Elevated LDL-cholesterol(LDL-C) is considered to be the pivotal causative factor for atherosclerosis and LDL-C…
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Mind the Gap: How can we address the challenges in FH?
2014 FH Global Summit: 13-14 October, New York, USA Screening for FH needs new impetus. Family history and an elevated LDL-C are the two key screening criteria for suspected FH. The obvious role for screening for suspected FH lies with primary care. Insights from the…
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Heterogeneity in FH: What are the implications for management?
According to Professor Frederick Raal, South Africa, irrespective of genotype, what matters is reducing the LDL-C burden with lipid-lowering therapy. Familial hypercholesterolemia (FH) is an autosomal co-dominant disorder usually resulting from mutations in the LDL receptor (LDLR) gene characterised by elevated levels of LDL-cholesterol (LDL-C)…
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PCSK9 inhibition in diabetes and metabolic syndrome: an analysis from OSLER
New findings, reported at the 2014 American Diabetes Association 74th Scientific Sessions,1 show thattreatment with the PCSK9 monoclonal antibody evolocumab reduced plasma levels of low-density lipoprotein cholesterol (LDL-C) in hypercholesterolaemic patients with dysglycaemia or metabolic syndrome, without worsening glucose control. Lead author, Dr Robert R…
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Rationale and Design of the Familial Hypercholesterolemia Foundation CAscade SCreening for Awareness and Detection
Familial hypercholesterolemia (FH) is a hereditary condition caused by various genetic mutations that lead to significantly elevated low-density lipoprotein cholesterol levels and resulting in a 20-fold increased lifetime risk for premature cardiovascular disease. Although its prevalence in the United States is 1 in 300 to…
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