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Hypercholesterolemia: HELP
Articles from Paris
Based on 201 articles published since 2010
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These are the 201 published articles about Hypercholesterolemia that originated from Paris during 2010-2020.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9
1 Guideline [Recommendations for children with hypercholesterolemia]. 2011

Girardet, J-P / Luc, G / Rieu, D / Bruckert, E / Darmaun, D / Farnier, M / Anonymous2240681 / Anonymous2250681. ·Comité de nutrition de la Société française de pédiatrie, 75012 Paris, France. jean-philippe.girardet@trs.aphp.fr ·Arch Pediatr · Pubmed #21145715.

ABSTRACT: Some cases of hypercholesterolemia observed in childhood present a high risk of premature cardiovascular disease, such as in monogenic dominantly inherited hypercholesterolemia, particularly familial hypercholesterolemia due to mutations on the LDL receptor gene. This article, jointly written by the Société Française de Pédiatrie Nutrition Committee and the Nouvelle Société Française d'Athérosclérose, proposes recommendations for a screening strategy and management of childhood hypercholesterolemia. A practical approach to high-risk cases of inherited hypercholesterolemia is detailed and the dietary management, indications, and supervision of lipid-lowering drug therapy in children are discussed.

2 Editorial Evolocumab Treatment of Hypercholesterolemia in OSLER-1: Enduring Efficacy, Tolerability, and Safety Over 5 Years. 2019

Chapman, M John / Ginsberg, Henry N. ·Endocrinology-Metabolism Division, Pitié-Salpetriere Hospital, Sorbonne University and National Institute for Health and Medical Research (INSERM), Paris, France. Electronic address: john.chapman@upmc.fr. · Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York. ·J Am Coll Cardiol · Pubmed #31648706.

ABSTRACT: -- No abstract --

3 Editorial [Statin treatment must be personalized]. 2019

Bruckert, E / Gallo, A. ·Service endocrinologie métabolisme et prévention cardiovasculaire, Institut E3M et IHU cardiométabolique, hôpital Pitié-Salpêtrière, 75013Paris, France. Electronic address: eric.bruckert@aphp.fr. · Service endocrinologie métabolisme et prévention cardiovasculaire, Institut E3M et IHU cardiométabolique, hôpital Pitié-Salpêtrière, 75013Paris, France. ·Rev Med Interne · Pubmed #29510859.

ABSTRACT: -- No abstract --

4 Editorial Hypercholesterolemia in children: Why and how to screen for it? 2018

Girardet, J-P / Bocquet, A / Chouraqui, J P / Darmaun, D / Feillet, F / Frelut, M-L / Hankard, R / Rozé, J-C / Simeoni, U / Turck, D / Briend, A / Dupont, C / Anonymous1720940. ·Université Pierre et Marie Curie-Paris 6, 75005 Paris, France. Electronic address: girardetjph@gmail.com. · Université de Franche-Comté, 25000 Besançon, France. · Université Joseph-Fourier, 38000 Grenoble, France. · Université Nantes-Atlantique, 44300 Nantes, France. · Université de Lorraine, 54000 Nancy, France. · Endocrinologie-diabète de l'enfant, CHU de Bicêtre, 74270 Le Kremlin-Bicêtre, France. · Inserm U 1069, Université de Tours, 37000 Tours, France. · Université de Lausanne, 1011 Lausanne, Suisse. · Université Lille 2, 59000 Lille, France. · Institut de recherche pour le développement, 13572 Marseille, France. · Université Paris-Descartes, 75006 Paris, France. ·Arch Pediatr · Pubmed #29548557.

ABSTRACT: -- No abstract --

5 Editorial Is lomitapide a life-saving drug in homozygous familial hypercholesterolemia. 2017

Bruckert, Eric / Gallo, Antonio. ·Department of Endocrinology and Cardiovascular Disease Prevention, Hôpital Pitié-Salpêtrière, France. ·Eur J Prev Cardiol · Pubmed #28952803.

ABSTRACT: -- No abstract --

6 Review [Myalgia and statins: Separating the true from the false]. 2019

Blacher, Jacques / Bruckert, Eric / Farnier, Michel / Ferrières, Jean / Henry, Patrick / Krempf, Michel / Mourad, Jean-Jacques. ·AP-HP, université Paris-Descartes, Hôtel-Dieu, Centre de diagnostic et de thérapeutique, 75004 Paris, France. Electronic address: jacques.blacher@aphp.fr. · Institut E3M et IHU cardiométabolique (ICAN), hôpital Pitié Salpêtrière, endocrinologie métabolisme et prévention cardiovasculaire, 75013 Paris, France. · CHU Dijon-Bourgogne, point médical et service de cardiologie, 21000 Dijon, France. · CHU de Toulouse, Fédération de cardiologie, Inserm UMR 1027, 30159 Toulouse, France. · AP-HP, université Paris VII, hôpital Lariboisière, pôle urgences, cardiologie, 75010 Paris, France. · CHU, hôpital Laennec, service endocrinologie-diabétologie-nutrition, 44093 Nantes cedex, France. · Hôpital Saint-Joseph, service de médecine interne, 75014 Paris, France. ·Presse Med · Pubmed #31473026.

ABSTRACT: In therapeutic trials, the incidence of adverse muscle effects under statin is low, exceptional for some authors,<5% for others. In observational studies, however, this incidence is much higher, up to 20% of patients. These adverse effects are drug-dependent and dose-dependent. It is often complex to distinguish between a real adverse effect and a nocebo effect. Causality is more likely if the symptoms are symmetrical and affect the large muscle masses dependent on the large joints, occur within one month of the introduction of the statin and disappear quickly, within a few weeks after discontinuation of treatment. It seems important not to waste time trying to convince the patient that the alleged muscle symptoms are unrelated to statin therapy. In these patients with suspected statin intolerance, therapeutic impasse is rare and there is a need to attempt dosage reductions, experiment different statins or even prescribe other cholesterol-lowering agents.

7 Review The role of red yeast rice (RYR) supplementation in plasma cholesterol control: A review and expert opinion. 2019

Banach, Maciej / Bruckert, Eric / Descamps, Olivier S / Ellegård, Lars / Ezhov, Marat / Föger, Bernhard / Fras, Zlatko / Kovanen, Petri T / Latkovskis, Gustavs / März, Winfried / Panagiotakos, Demosthenes B / Paragh, György / Pella, Daniel / Pirillo, Angela / Poli, Andrea / Reiner, Željko / Silbernagel, Günter / Viigimaa, Margus / Vrablík, Michal / Catapano, Alberico L. ·Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland; Polish Mother's Memorial Hospital Research Institute (PMMHRI), Lodz, Poland; Cardiovascular Research Centre, University of Zielona Gora, Zielona Gora, Poland. · Endocrinologie Métabolisme et Prévention Cardiovasculaire, Institut E3M et IHU Cardiométabolique (ICAN), Hôpital Pitié Salpêtrière, Paris, France; Sorbonne University, Paris, France. · Department of Internal Medicine, Centres Hospitaliers Jolimont, La Louvière and Department of Cardiology, Cliniques Universitaires Saint-Luc (UCLouvain), Bruxelles, Belgium. · Department of Internal medicine and clinical nutrition, Sahlgrenska Academy at the University of Gothenburg, Sahlgrenska University Hospital, Sweden. · National Medical Research Center of Cardiology of the Ministry of Health, Moscow, Russia. · Department of Internal Medicine, Medical University Innsbruck, Innsbruck, Austria; Department of Internal Medicine, Landeskrankenhaus Bregenz, Austria. · Division of Internal Medicine, University Medical Centre Ljubljana Professor of Internal Medicine, Medical Faculty, University of Ljubljana, Slovenia. · Wihuri Research Institute, Helsinki, Finland. · Institute of Cardiology and Regenerative Medicine, Faculty of Medicine, University of Latvia, Latvia; Pauls Stradins Clinical University Hospital, Riga, Latvia. · Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria; Medical Clinic V, Medical Faculty Mannheim, University of Heidelberg, Germany; SYNLAB Academy, SYNLAB Holding Deutschland GmbH, Mannheim and Augsburg, Germany. · Department of Nutrition - Dietetics, Harokopio University, Athens, Greece. · Department of Internal Medicine, University of Debrecen Faculty of Medicine, Debrecen, Hungary. · 2nd Department of Cardiology of the East Slovak Institute of Cardiovascular Disease and Faculty of Medicine PJ Safarik University, Kosice, Slovak Republic. · Center for the Study of Atherosclerosis, E. Bassini Hospital, Cinisello Balsamo, Milan, Italy; IRCCS MultiMedica, Sesto S. Giovanni, Milan, Italy. · Nutrition Foundation of Italy (NFI), Milan, Italy. · Department of Internal Medicine, University Hospital Center Zagreb, School of Medicine University of Zagreb, Zagreb, Croatia. · Department of Cardiology, Charité Berlin (CBF), Berlin Institute of Health (BIH), And DZHK (German Research Centre for Cardiovascular Research), Partner Site Berlin, Hindenburgdamm 30, 12203, Berlin, Germany; Division of Angiology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria. · Tallinn University of Technology, School of Information Technologies, Department of Health Technologies, Estonia. · 3rd Department of Medicine, Charles University and General University Hospital, Prague, Czech Republic. · Department of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy; Multimedica IRCCS, Milano, Italy. Electronic address: alberico.catapano@unimi.it. ·Atheroscler Suppl · Pubmed #31451336.

ABSTRACT: -- No abstract --

8 Review [PCSK9 inhibitors: What place in the management of dyslipidemia?] 2019

Sabouret, Pierre / Farnier, Michel / Puymirat, Etienne. ·Pitié-Salpétrière Hospital and ACTION-Group, Heart Institute, Cardiology Department, 47-83, boulevard de l'Hôpital, 75013 Paris, France. · Lipid Clinic, Point Médical, rond-point de la Nation, 21000 Dijon, France; CHU Dijon-Bourgogne, Cardiology Department, 5, boulevard Jeanne-d'Arc, 21000 Dijon, France. · AP-HP, Hôpital Européen Georges Pompidou, Cardiology Department, 20, rue Leblanc, 75015 Paris, France; Université Paris Descartes, 75015 Paris, France. ·Presse Med · Pubmed #30853281.

ABSTRACT: PCSK9 protein is a key regulator of LDL receptor activity. Gain-of-function mutations in PCSK9 are one of the genetic causes of familial hypercholesterolemia. Conversely, loss-of-function mutations are associated with lower levels of LDL cholesterol and reduced coronary heart disease. Monoclonal antibodies targeting PCSK9 are highly efficacious in lowering LDL-C levels, with a good tolerability and safety profile. Two PCSK9 inhibitors, alirocumab and evolocumab, have demonstrated a cardiovascular benefit in addition to statin therapy in patients with established cardiovascular disease. A recent European consensus has defined the candidates for PCSK9 inhibitors, e.g., patients with established cardiovascular disease and patients with familial hypercholesterolemia in primary prevention, with substantially elevated LDL-C levels despite maximally tolerated statin with or without ezetimibe therapy.

9 Review Microbial impact on cholesterol and bile acid metabolism: current status and future prospects. 2019

Kriaa, Aicha / Bourgin, Mélanie / Potiron, Aline / Mkaouar, Héla / Jablaoui, Amin / Gérard, Philippe / Maguin, Emmanuelle / Rhimi, Moez. ·UMR 1319 Micalis, INRA, Microbiota Interaction with Human and Animal Team (MIHA), AgroParisTech, Université Paris-Saclay, F-78350 Jouy-en-Josas, France. · UMR 1319 Micalis, INRA, Microbiota Interaction with Human and Animal Team (MIHA), AgroParisTech, Université Paris-Saclay, F-78350 Jouy-en-Josas, France moez.rhimi@inra.fr. ·J Lipid Res · Pubmed #30487175.

ABSTRACT: Recently, the gut microbiota has emerged as a crucial factor that influences cholesterol metabolism. Ever since, significant interest has been shown in investigating these host-microbiome interactions to uncover microbiome-mediated functions on cholesterol and bile acid (BA) metabolism. Indeed, changes in gut microbiota composition and, hence, its derived metabolites have been previously reported to subsequently impact the metabolic processes and have been linked to several diseases. In this context, associations between a disrupted gut microbiome, impaired BA metabolism, and cholesterol dysregulation have been highlighted. Extensive advances in metagenomic and metabolomic studies in this field have allowed us to further our understanding of the role of intestinal bacteria in metabolic health and disease. However, only a few have provided mechanistic insights into their impact on cholesterol metabolism. Identifying the myriad functions and interactions of these bacteria to maintain cholesterol homeostasis remain an important challenge in such a field of research. In this review, we discuss the impact of gut microbiota on cholesterol metabolism, its association with disease settings, and the potential of modulating gut microbiota as a promising therapeutic target to lower hypercholesterolemia.

10 Review Clinical Genetic Testing for Familial Hypercholesterolemia: JACC Scientific Expert Panel. 2018

Sturm, Amy C / Knowles, Joshua W / Gidding, Samuel S / Ahmad, Zahid S / Ahmed, Catherine D / Ballantyne, Christie M / Baum, Seth J / Bourbon, Mafalda / Carrié, Alain / Cuchel, Marina / de Ferranti, Sarah D / Defesche, Joep C / Freiberger, Tomas / Hershberger, Ray E / Hovingh, G Kees / Karayan, Lala / Kastelein, Johannes Jacob Pieter / Kindt, Iris / Lane, Stacey R / Leigh, Sarah E / Linton, MacRae F / Mata, Pedro / Neal, William A / Nordestgaard, Børge G / Santos, Raul D / Harada-Shiba, Mariko / Sijbrands, Eric J / Stitziel, Nathan O / Yamashita, Shizuya / Wilemon, Katherine A / Ledbetter, David H / Rader, Daniel J / Anonymous750957. ·Genomic Medicine Institute, Geisinger, Danville, Pennsylvania. Electronic address: asturm@geisinger.edu. · Department of Medicine, Division of Cardiovascular Medicine, and Cardiovascular Institute, Stanford University, Stanford California; The Familial Hypercholesterolemia Foundation, Pasadena, California. · Nemours Cardiac Center, A.I. DuPont Hospital for Children, Wilmington, Delaware. · Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas. · The Familial Hypercholesterolemia Foundation, Pasadena, California. · Department of Medicine, Baylor College of Medicine, Houston, Texas. · The Familial Hypercholesterolemia Foundation, Pasadena, California; Department of Integrated Medical Sciences, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, Florida. · Unidade I&D, Grupo de Investigação Cardiovascular, Departamento de Promoção da Saúde e Doenças Não Transmissíveis, Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisboa, Portugal; University of Lisboa, Faculty of Sciences, BioISI-Biosystems & Integrative Sciences Institute, Lisboa, Portugal. · Sorbonne Université and Centre de Génétique Moléculaire et Chromosomique, unité de Génétique de l'Obésitéet des dyslipidémies, Hôpital de la Pitié-Salpêtrière, Paris, France. · Division of Translational Medicine and Human Genetics, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania. · Department of Cardiology, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts. · Department of Clinical Genetics, Academic Medical Center at the University of Amsterdam, Amsterdam, the Netherlands. · Central European Institute of Technology, Masaryk University, Brno, Czech Republic; Centre for Cardiovascular Surgery and Transplantation, Brno, Czech Republic. · Department of Internal Medicine, Wexner Medical Center at The Ohio State University, Columbus, Ohio. · Department of Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands. · Bioinformatics, Genomics England, Queen Mary University of London, London, United Kingdom. · Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee. · Fundación Hipercolesterolemia Familiar, Madrid, Spain. · The Familial Hypercholesterolemia Foundation, Pasadena, California; Department of Pediatrics (Cardiology), West Virginia University, Morgantown, West Virginia. · Department of Clinical Biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. · Lipid Clinic Heart Institute (InCor) University of São Paulo Medical School Hospital and Hospital Israelita Albert Einstein, São Paulo, Brazil. · Department of Molecular Innovation in Lipidology, National Cerebral and Cardiovascular Center Research Institute, Osaka, Japan. · Department of Internal Medicine, Erasmus Medical Center, Rotterdam, the Netherlands. · Department of Medicine, Division of Cardiology, Department of Genetics, McDonnell Genome Institute, Washington University School of Medicine, St. Louis, Missouri. · Department of Cardiovascular Medicine, Rinku General Medical Center, Osaka, Japan; Departments of Community Medicine and Cardiovascular Medicine, Osaka University Graduate School of Medicine, Osaka, Japan. · Genomic Medicine Institute, Geisinger, Danville, Pennsylvania. · The Familial Hypercholesterolemia Foundation, Pasadena, California; Departments of Genetics, Medicine, and Pediatrics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania. ·J Am Coll Cardiol · Pubmed #30071997.

ABSTRACT: Although awareness of familial hypercholesterolemia (FH) is increasing, this common, potentially fatal, treatable condition remains underdiagnosed. Despite FH being a genetic disorder, genetic testing is rarely used. The Familial Hypercholesterolemia Foundation convened an international expert panel to assess the utility of FH genetic testing. The rationale includes the following: 1) facilitation of definitive diagnosis; 2) pathogenic variants indicate higher cardiovascular risk, which indicates the potential need for more aggressive lipid lowering; 3) increase in initiation of and adherence to therapy; and 4) cascade testing of at-risk relatives. The Expert Consensus Panel recommends that FH genetic testing become the standard of care for patients with definite or probable FH, as well as for their at-risk relatives. Testing should include the genes encoding the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase subtilisin/kexin 9 (PCSK9); other genes may also need to be considered for analysis based on patient phenotype. Expected outcomes include greater diagnoses, more effective cascade testing, initiation of therapies at earlier ages, and more accurate risk stratification.

11 Review Processing of oat: the impact on oat's cholesterol lowering effect. 2018

Grundy, Myriam M-L / Fardet, Anthony / Tosh, Susan M / Rich, Gillian T / Wilde, Peter J. ·Food and Health Programme, Quadram Institute Bioscience, Norwich Research Park, NR4 7UA, UK. myriam.grundy@quadram.ac.uk wildongillian@gmail.com peter.wilde@quadram.ac.uk. · INRA, JRU 1019, UNH, CRNH Auvergne, F-63000 Clermont-Ferrand & Université de Clermont, Université d'Auvergne, Unité de Nutrition Humaine, BP 10448, F-63000 Clermont-Ferrand, France. anthony.fardet@inra.fr. · University of Ottawa, Université, Salle 118, Ottawa, ON K1N 6N5 Canada. Susan.Tosh@uottawa.ca. ·Food Funct · Pubmed #29431835.

ABSTRACT: Epidemiological and interventional studies have clearly demonstrated the beneficial impact of consuming oat and oat-based products on serum cholesterol and other markers of cardiovascular disease. The cholesterol-lowering effect of oat is thought to be associated with the β-glucan it contains. However, not all food products containing β-glucan seem to lead to the same health outcome. Overall, highly processed β-glucan sources (where the oat tissue is highly disrupted) appear to be less effective at reducing serum cholesterol, but the reasons are not well understood. Therefore, the mechanisms involved still need further clarification. The purpose of this paper is to review current evidence of the cholesterol-lowering effect of oat in the context of the structure and complexity of the oat matrix. The possibility of a synergistic action and interaction between the oat constituents promoting hypocholesterolaemia is also discussed. A review of the literature suggested that for a similar dose of β-glucan, (1) liquid oat-based foods seem to give more consistent, but moderate reductions in cholesterol than semi-solid or solid foods where the results are more variable; (2) the quantity of β-glucan and the molecular weight at expected consumption levels (∼3 g day

12 Review Phagocyte NADPH oxidase, oxidative stress and lipids: Anti- or pro ageing? 2018

Baciou, Laura / Masoud, Rawand / Souabni, Hager / Serfaty, Xavier / Karimi, Gilda / Bizouarn, Tania / Houée Levin, Chantal. ·Laboratoire de Chimie Physique, Université Paris Sud, UMR 8000, CNRS, 91405, Orsay Cedex, France. · Laboratoire de Chimie Physique, Université Paris Sud, UMR 8000, CNRS, 91405, Orsay Cedex, France. Electronic address: Chantal.houee@u-psud.fr. ·Mech Ageing Dev · Pubmed #29103982.

ABSTRACT: The role of NADPH oxidase in ageing is debated because of the dual roles of free radicals, toxic though necessary. In this paper we summarize some results about two aspects linked to the regulation of the activity of phagocyte NADPH oxidase (Nox2), encountered frequently in elderly people: inflammation and hypercholesterolemia. In the presence of a high amount of reactive oxygen species (ROS) created by itself or by any other source, the enzyme activity is mostly lowered. Oxidation of the membrane and/or of one of the cytosolic partners could be responsible for this loss of activity. However using a cell free system, we had also shown that a low amount of ROS could activate this enzyme. Similarly, cholesterol has a similar dual role, either activating or inhibiting. In in vitro cell free system with neutrophil membranes from healthy donors, the addition, as well as the removal of cholesterol, diminishes the Nox2 activity. The activity of Nox2 is lowered in neutrophils of untreated hypercholesterolemic patients. Finally oxysterols (25-hydroxy-cholesterol or 5α, 6α - epoxy-cholesterol) do not induce effects different from that of non-oxidized cholesterol. These findings are in agreement with the Janus role of NADPH oxidase, the main source of non-mitochondrial ROS.

13 Review The Oxygen Paradox, the French Paradox, and age-related diseases. 2017

Davies, Joanna M S / Cillard, Josiane / Friguet, Bertrand / Cadenas, Enrique / Cadet, Jean / Cayce, Rachael / Fishmann, Andrew / Liao, David / Bulteau, Anne-Laure / Derbré, Frédéric / Rébillard, Amélie / Burstein, Steven / Hirsch, Etienne / Kloner, Robert A / Jakowec, Michael / Petzinger, Giselle / Sauce, Delphine / Sennlaub, Florian / Limon, Isabelle / Ursini, Fulvio / Maiorino, Matilde / Economides, Christina / Pike, Christian J / Cohen, Pinchas / Salvayre, Anne Negre / Halliday, Matthew R / Lundquist, Adam J / Jakowec, Nicolaus A / Mechta-Grigoriou, Fatima / Mericskay, Mathias / Mariani, Jean / Li, Zhenlin / Huang, David / Grant, Ellsworth / Forman, Henry J / Finch, Caleb E / Sun, Patrick Y / Pomatto, Laura C D / Agbulut, Onnik / Warburton, David / Neri, Christian / Rouis, Mustapha / Cillard, Pierre / Capeau, Jacqueline / Rosenbaum, Jean / Davies, Kelvin J A. ·The Medical Group, Internal Medicine, Rheumatology & Osteoporosis, Dermatology, Pulmonology, Ophthalmology, and Cardiology; the Hospital of the Good Samaritan, Los Angeles, CA, 90017, USA. · Leonard Davis School of Gerontology of the Ethel Percy Andrus Gerontology Center, University of Southern California, Los Angeles, CA, 90089-0191, USA. · Lab de Biologie Cellulaire et Végétale, Faculté de Pharmacie, Université de Rennes, 35043, Rennes Cedex, France. · Institut de Biologie Paris-Seine (IBPS), UMR CNRS 8256, Biological Adaptation and Ageing, Sorbonne Universités, UPMC Univ Paris 06, 75005, Paris, France. · INSERM ERL U1164, 75005, Paris, France. · School of Pharmacy, University of Southern California, Los Angeles, CA, 90089-9121, USA. · Department of Biochemistry & Molecular Medicine, Keck School of Medicine of USC, University of Southern California, Los Angeles, CA, 90033, USA. · Département de Médecine nucléaire et Radiobiologie, Faculté de médecine et des sciences de la santé, Université de Sherbrooke, Sherbrooke, Québec, J1H 5N4, Canada. · Institut de Génomique Fonctionnelle de Lyon,ENS de Lyon, CNRS, 69364, Lyon Cedex 07, France. · Laboratory for Movement, Sport and Health Sciences-EA 1274, M2S, Université de Rennes 2-ENS, Bruz, 35170, Rennes, France. · INSERM UMR 1127-CNRS UMR 7225, Institut du cerveau et de la moelle épinière-ICM Thérapeutique Expérimentale de la Maladie de Parkinson, Université Pierre et Marie Curie, 75651, Paris Cedex 13, France. · Huntington Medical Research Institutes, Pasadena, CA, 91105, USA. · Department of Neurology, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA. · Chronic infections and Immune ageing, INSERM U1135, Hopital Pitie-Salpetriere, Pierre et Marie Curie University, 75013, Paris, France. · INSERM Equipe 14 Institut de la Vision, 75012, Paris, France. · Department of Molecular Medicine, University of Padova, 35121, Padova, Italy. · Los Angeles Cardiology Associates, Hospital of the Good Samaritan, Los Angeles, CA, 90017, USA. · Division of Neurobiology, Department of Biological Sciences of the Dornsife College of Letters, Arts, and Sciences, University of Southern California, Los Angeles, CA, 90089-0191, USA. · Keck School of Medicine of USC, University of Southern California, Los Angeles, CA, 90033, USA. · Lipid peroxidation, Signalling and Vascular Diseases INSERM U1048, 31432, Toulouse Cedex 4, France. · Stress and Cancer Laboratory, Institut Curie-Inserm U830, 75248, Paris Cedex 05, France. · Laboratoire de Signalisation et Physiopathologie Cardiovasculaire-Inserm UMR-S 1180, Faculté de Pharmacie, Université Paris-Sud, 92296 Châtenay-Malabry, Paris, France. · Department of Radiation Oncology, Hospital of the Good Samaritan, Los Angeles, CA, 90017, USA. · Department of Oncology & Hematology, Hospital of the Good Samaritan, Los Angeles, CA, 90017, USA. · Division of Molecular & Computational Biology, Department of Biological Sciences of the Dornsife College of Letters, Arts, and Sciences, University of Southern California, Los Angeles, CA, 90089-0191, USA. · Children's Hospital of Los Angeles, Developmental Biology, Regenerative Medicine and Stem Cell Therapeutics program and the Center for Environmental Impact on Global Health Across the Lifespan at The Saban Research Institute, Los Angeles, CA, 90027, USA. · Department of Pediatrics, Keck School of Medicine of USC, University of Southern California, Los Angeles, CA, 90033, USA. · DR Saint-Antoine UMR_S938, UPMC, Inserm Faculté de Médecine, Université Pierre et Marie Curie, 75012, Paris, France. · Scientific Service of the Embassy of France in the USA, Consulate General of France in Los Angeles, Los Angeles, CA, 90025, USA. · Leonard Davis School of Gerontology of the Ethel Percy Andrus Gerontology Center, University of Southern California, Los Angeles, CA, 90089-0191, USA. kelvin@usc.edu. · Department of Biochemistry & Molecular Medicine, Keck School of Medicine of USC, University of Southern California, Los Angeles, CA, 90033, USA. kelvin@usc.edu. · Division of Molecular & Computational Biology, Department of Biological Sciences of the Dornsife College of Letters, Arts, and Sciences, University of Southern California, Los Angeles, CA, 90089-0191, USA. kelvin@usc.edu. ·Geroscience · Pubmed #29270905.

ABSTRACT: A paradox is a seemingly absurd or impossible concept, proposition, or theory that is often difficult to understand or explain, sometimes apparently self-contradictory, and yet ultimately correct or true. How is it possible, for example, that oxygen "a toxic environmental poison" could be also indispensable for life (Beckman and Ames Physiol Rev 78(2):547-81, 1998; Stadtman and Berlett Chem Res Toxicol 10(5):485-94, 1997)?: the so-called Oxygen Paradox (Davies and Ursini 1995; Davies Biochem Soc Symp 61:1-31, 1995). How can French people apparently disregard the rule that high dietary intakes of cholesterol and saturated fats (e.g., cheese and paté) will result in an early death from cardiovascular diseases (Renaud and de Lorgeril Lancet 339(8808):1523-6, 1992; Catalgol et al. Front Pharmacol 3:141, 2012; Eisenberg et al. Nat Med 22(12):1428-1438, 2016)?: the so-called, French Paradox. Doubtless, the truth is not a duality and epistemological bias probably generates apparently self-contradictory conclusions. Perhaps nowhere in biology are there so many apparently contradictory views, and even experimental results, affecting human physiology and pathology as in the fields of free radicals and oxidative stress, antioxidants, foods and drinks, and dietary recommendations; this is particularly true when issues such as disease-susceptibility or avoidance, "healthspan," "lifespan," and ageing are involved. Consider, for example, the apparently paradoxical observation that treatment with low doses of a substance that is toxic at high concentrations may actually induce transient adaptations that protect against a subsequent exposure to the same (or similar) toxin. This particular paradox is now mechanistically explained as "Adaptive Homeostasis" (Davies Mol Asp Med 49:1-7, 2016; Pomatto et al. 2017a; Lomeli et al. Clin Sci (Lond) 131(21):2573-2599, 2017; Pomatto and Davies 2017); the non-damaging process by which an apparent toxicant can activate biological signal transduction pathways to increase expression of protective genes, by mechanisms that are completely different from those by which the same agent induces toxicity at high concentrations. In this review, we explore the influences and effects of paradoxes such as the Oxygen Paradox and the French Paradox on the etiology, progression, and outcomes of many of the major human age-related diseases, as well as the basic biological phenomenon of ageing itself.

14 Review PCSK9 Mutations in Familial Hypercholesterolemia: from a Groundbreaking Discovery to Anti-PCSK9 Therapies. 2017

El Khoury, Petra / Elbitar, Sandy / Ghaleb, Youmna / Khalil, Yara Abou / Varret, Mathilde / Boileau, Catherine / Abifadel, Marianne. ·LVTS, INSERM U1148, Hôpital Xavier-Bichat, Paris Cedex 18, France. · Laboratory of Biochemistry and Molecular Therapeutics, Faculty of Pharmacy, Pôle Technologie Santé, Saint Joseph University, Beirut, Lebanon. · Faculté de Médecine Paris 7, Université Denis Diderot, Paris, France. · LVTS, INSERM U1148, Hôpital Xavier-Bichat, Paris Cedex 18, France. catherine.boileau@inserm.fr. · Faculté de Médecine Paris 7, Université Denis Diderot, Paris, France. catherine.boileau@inserm.fr. · Département de Génétique, AP-HP, CHU Xavier Bichat, Paris, France. catherine.boileau@inserm.fr. ·Curr Atheroscler Rep · Pubmed #29038906.

ABSTRACT: PURPOSE OF REVIEW: In 2003, Abifadel et al. (Nat. Genet. 34:154-156, 2003) identified PCSK9, encoding proprotein convertase subtilisin/kexin type 9, as the third causal gene for autosomal dominant hypercholesterolemia. This review focuses on the main steps from this major breakthrough in familial hypercholesterolemia (FH) to the latest clinical trials with the anti-PCSK9 antibodies. RECENT FINDINGS: The year 2015 was remarkable in cardiovascular disease through the field of cholesterol. Nearly 30 years after the discovery of statins, a new class of effective lipid-lowering drugs has emerged: the anti-PCSK9 antibodies. The discovery of the first gain-of-function mutations of PCSK9 in FH rapidly became the center of interest of researchers worldwide. Preclinical and clinical studies launched by pharmaceutical companies led to the first three anti-PCSK9 antibodies, two of which (evolocumab and alirocumab) reduce LDL cholesterol levels by 50-60% and received FDA and European Medicines Agency approvals in 2015 on top of statin therapy. Recently, results of the Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk (FOURIER) trial, the outcome trial of evolocumab over 2.2 years, showed a reduction of 15-20% in the risk of major cardiovascular outcomes in high-risk patients receiving statin therapy. Results of ODYSSEY OUTCOMES trial, evaluating the effect of alirocumab in 18,000 patients with established CVD are also eagerly awaited in 2018. The evolution of research on PCSK9, starting from the discovery of the first set of mutations in PCSK9 in FH in 2003, is an amazing example of successful translational research. It shows how rigorous and powered genetic analyses can lead to the discovery of a new class of lipid-lowering drugs that give hope in fighting high cholesterol levels and their cardiovascular complications.

15 Review A nutraceutical approach (Armolipid Plus) to reduce total and LDL cholesterol in individuals with mild to moderate dyslipidemia: Review of the clinical evidence. 2017

Barrios, Vivencio / Escobar, Carlos / Cicero, Arrigo Francesco Giuseppe / Burke, David / Fasching, Peter / Banach, Maciej / Bruckert, Eric. ·Department of Cardiology, Hospital Ramon y Cajal, Madrid, Spain. Electronic address: vivenciobarrios@gmail.com. · Department of Cardiology, Hospital La Paz, Madrid, Spain. · Diseases Research Center, Medicine & Surgery Department, Alma Mater Studiorum Atherosclerosis and Metabolic University of Bologna, Bologna, Italy. · Beacon Heart Centre, Beacon Hospital, Dublin, Ireland. · 5th Medical Department, Wilhelminenspital, Vienna, Austria. · Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Lodz, Poland. · Department of Endocrinology and Cardiovascular Disease Prevention, Hôpital Pitié-Salpêtrière, Paris, France. ·Atheroscler Suppl · Pubmed #27998714.

ABSTRACT: Compelling evidence supports the effectiveness of the reduction of total and LDL cholesterol (TC and LDL-C) in primarily preventing cardiovascular events, within the framework of life-long prevention programs mainly consisting in lifestyle changes. Pharmacological treatment should be introduced when lifestyle changes, including use of nutraceuticals, have failed. ESC/EAS guidelines list a number of nutraceutical compounds and functional foods which have been individually studied in randomized, controlled clinical trials (RCTs). To date only a proprietary formulation of three naturally occurring substances with putative complementary lipid-lowering properties - red yeast rice, policosanol and berberine - combined with folic acid, astaxanthin, and coenzyme Q10 (Armolipid Plus

16 Review The Proprotein Convertases in Hypercholesterolemia and Cardiovascular Diseases: Emphasis on Proprotein Convertase Subtilisin/Kexin 9. 2017

Seidah, Nabil G / Abifadel, Marianne / Prost, Stefan / Boileau, Catherine / Prat, Annik. ·Laboratory of Biochemical Neuroendocrinology, Institut de Recherches Cliniques de Montréal, affiliated to Université de Montréal, QC, Canada (N.G.S., A.P.); LVTS, INSERM U1148, Hôpital Xavier-Bichat, Paris, France (M.A., C.B.); Laboratory of Biochemistry and Molecular Therapeutics, Faculty of Pharmacy, Pôle Technologie-Santé, Saint-Joseph University, Beirut, Lebanon (M.A.); Department of Integrative Biology, Center for Theoretical Evolutionary Genomics, University of California Berkeley, Berkeley, California (S.P.); Department of Biology, Stanford University, Stanford, California (S.P.); and Département de Génétique, AP-HP, CHU Xavier Bichat, and Université Paris Diderot, Paris, France (C.B.) seidahn@ircm.qc.ca. · Laboratory of Biochemical Neuroendocrinology, Institut de Recherches Cliniques de Montréal, affiliated to Université de Montréal, QC, Canada (N.G.S., A.P.); LVTS, INSERM U1148, Hôpital Xavier-Bichat, Paris, France (M.A., C.B.); Laboratory of Biochemistry and Molecular Therapeutics, Faculty of Pharmacy, Pôle Technologie-Santé, Saint-Joseph University, Beirut, Lebanon (M.A.); Department of Integrative Biology, Center for Theoretical Evolutionary Genomics, University of California Berkeley, Berkeley, California (S.P.); Department of Biology, Stanford University, Stanford, California (S.P.); and Département de Génétique, AP-HP, CHU Xavier Bichat, and Université Paris Diderot, Paris, France (C.B.). ·Pharmacol Rev · Pubmed #27920219.

ABSTRACT: The secretory proprotein convertase (PC) family comprises nine members, as follows: PC1/3, PC2, furin, PC4, PC5/6, paired basic amino acid cleaving enzyme 4, PC7, subtilisin kexin isozyme 1/site 1 protease (SKI-1/S1P), and PC subtilisin/kexin type 9 (PCSK9). The first seven PCs cleave their substrates at single/paired basic residues and exhibit specific and often essential functions during development and/or in adulthood. The essential SKI-1/S1P cleaves membrane-bound transcription factors at nonbasic residues. In contrast, PCSK9 cleaves itself once, and the secreted inactive protease drags the low-density lipoprotein receptors (LDLR) and very LDLR (VLDLR) to endosomal/lysosomal degradation. Inhibitory PCSK9 monoclonal antibodies are now prescribed to treat hypercholesterolemia. This review focuses on the implication of PCs in cardiovascular functions and diseases, with a major emphasis on PCSK9. We present a phylogeny of the PCs and the analysis of PCSK9 haplotypes in modern and archaic human species. The absence of PCSK9 in mice led to the discovery of a sex- and tissue-specific subcellular distribution of the LDLR and VLDLR. PCSK9 inhibition may have other applications because it reduces inflammation and sepsis in a LDLR-dependent manner. Our present understanding of the cellular mechanism(s) that enables PCSK9 to induce the degradation of receptors is reviewed, as well as the consequences of its key natural mutations. The PCSK9 ongoing clinical trials are reviewed. Finally, how the other PCs may impact cardiovascular disease and the metabolic syndrome, and become relevant targets, is discussed.

17 Review Statin intolerance - a question of definition. 2017

Algharably, Engi Abdel-Hady / Filler, Iris / Rosenfeld, Stephanie / Grabowski, Katja / Kreutz, Reinhold. ·a Institut für Klinische Pharmakologie und Toxikologie , Charité - Universitätsmedizin Berlin , Berlin , Germany. · b Department of Clinical Pharmacy, Faculty of Pharmacy , Ain Shams University , Cairo , Egypt. · c Sanofi-Aventis Deutschland GmbH , Evidence Based Medicine , Berlin , Germany. ·Expert Opin Drug Saf · Pubmed #27645111.

ABSTRACT: INTRODUCTION: Statin therapy is the backbone of pharmacologic therapy for low-density lipoproteins cholesterol lowering and plays a pivotal role in cardiovascular disease prevention. Statin intolerance is understood as the inability to continue using a statin to reduce individual cardiovascular risk sufficiently, due to the development of symptoms or laboratory abnormalities attributable to the initiation or dose escalation of a statin. Muscle symptoms are the most common side effects observed. Areas covered: The main aim of this article is to present a review on published definitions of statin intolerance. In addition, a brief review on clinical aspects and risk factors of statin intolerance is provided and features for a common definition for statin intolerance are suggested. Expert opinion: A definition of statin intolerance by major drug regulatory agencies is not available. In clinical studies, different definitions are chosen and results are not comparable; different medical associations do not agree on one common definition. There is an unmet need to establish a common definition of statin intolerance to ensure an appropriate clinical use of this important drug class. Further work is required to develop a consensus definition on statin intolerance that could have significant positive impact on both research and clinical management.

18 Review PCSK9 Inhibition With Monoclonal Antibodies: Modern Management of Hypercholesterolemia. 2017

Ito, Matthew K / Santos, Raul D. ·Sanofi US, Bridgewater, NJ, USA. · Oregon State University/Oregon Health and Science University, College of Pharmacy, Portland, OR, USA (during initial development of this article). · Lipid Clinic, Heart Institute (InCor), University of Sao Paulo Medical School Hospital, and Preventive Medicine Center and Cardiology Program, Hospital Israelita Albert Einstein, Sao Paulo, Brazil. ·J Clin Pharmacol · Pubmed #27195910.

ABSTRACT: Current guidelines for hypercholesterolemia treatment emphasize lifestyle modification and lipid-modifying therapy to reduce the risk for cardiovascular disease. Statins are the primary class of agents used for the treatment of hypercholesterolemia. Although statins are effective for many patients, they fail to achieve optimal reduction in lipids for some patients, including those who have or are at high risk for cardiovascular disease. The PCSK9 gene was identified in the past decade as a potential therapeutic target for the management of patients with hypercholesterolemia. Pharmacologic interventions to decrease PCSK9 levels are in development, with the most promising approach using monoclonal antibodies that bind to PCSK9 in the plasma. Two monoclonal antibodies, alirocumab and evolocumab, have recently been approved for the treatment of hypercholesterolemia, and a third one, bococizumab, is in phase 3 clinical development. All 3 agents achieve significant reductions in levels of low-density lipoprotein cholesterol, as well as reductions in non-high-density lipoprotein cholesterol, apolipoprotein B, and lipoprotein(a). Long-term outcome trials are under way to determine the sustained efficacy, safety, and tolerability of PCSK9 inhibitors and whether this novel class of agents decreases the risk for major cardiovascular events in patients on lipid-modifying therapy. Available data suggest that PCSK9 inhibitors provide a robust reduction in atherogenic cholesterol levels with a good safety profile, especially for patients who fail to obtain an optimal clinical response to statin therapy, those who are statin intolerant or have contraindications to statin therapy, and those with familial hypercholesterolemia.

19 Review Management of cholestatic pruritus in children with Alagille syndrome: Case report and literature review. 2016

Ben Ameur, S / Chabchoub, I / Telmoudi, J / Belfitouri, Y / Rebah, O / Lacaille, F / Aloulou, H / Mehrzi, A / Hachicha, M. ·Pediatric department, Hedi Chaker Hospital, El ain street km 0,5, 3029 Sfax, Tunisia; Faculty of medicine, university of Sfax, Tunisia. Electronic address: benameursalma@gmail.com. · Pediatric department, Hedi Chaker Hospital, El ain street km 0,5, 3029 Sfax, Tunisia. · Pediatric department, La Marsa Hospital, Tunis, Tunisia. · Hepatogastroenterology-nutrition unit, Hôpital Necker-Enfants-Malades, 149, rue de Sèvres, 75015 Paris, France. ·Arch Pediatr · Pubmed #28492167.

ABSTRACT: Alagille syndrome causes intractable pruritus and disfiguring xanthomas because of retained bile acids and cholesterol. Drug therapy in addition to surgical intervention may be effective in many patients in reducing serum bile acids, cholesterol levels, pruritus, and skin xanthomas. In this report, we describe a child with Alagille syndrome who presented with severe pruritus and xanthomas as a consequence of severe hypercholesterolemia and discuss the treatment modalities.

20 Review Laboratory Medicine in the Clinical Decision Support for Treatment of Hypercholesterolemia: Pharmacogenetics of Statins. 2016

Ruaño, Gualberto / Seip, Richard / Windemuth, Andreas / Wu, Alan H B / Thompson, Paul D. ·Genomas Inc., 67 Jefferson Street, Hartford, CT 06106, USA. Electronic address: g.ruano@genomas.net. · Sanofi Genzyme, 500 Kendall Street, Cambridge, MA 02142, USA. · Cyclica Inc., 10 Jonathan Street, Belmont, MA 02478, USA. · Department of Laboratory Medicine, San Francisco General Hosptial, 1001 Potrero Avenue, San Francisco, CA 94110, USA. · Division of Cardiology, Hartford Hospital, 80 Seymour Street, Hartford, CT 06106, USA. ·Clin Lab Med · Pubmed #27514463.

ABSTRACT: Statin responsiveness is an area of great research interest given the success of the drug class in the treatment of hypercholesterolemia and in primary and secondary prevention of cardiovascular disease. Interrogation of the patient's genome for gene variants will eventually guide anti-hyperlipidemic intervention. In this review, we discuss methodological approaches to discover genetic markers predictive of class-wide and drug-specific statin efficacy and safety. Notable pharmacogenetic findings are summarized from hypothesis-free genome wide and hypothesis-led candidate gene association studies. Physiogenomic models and clinical decision support systems will be required for DNA-guided statin therapy to reach practical use in medicine.

21 Review Cardiovascular Disease Risk Associated With Familial Hypercholesterolemia: A Systematic Review of the Literature. 2016

Wong, Bruce / Kruse, Gregory / Kutikova, Lucie / Ray, Kausik K / Mata, Pedro / Bruckert, Eric. ·Centre for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address: brucejowong@gmail.com. · The Wharton School of Business, University of Pennsylvania, Philadelphia, Pennsylvania. · Amgen (Europe) GmbH, Zug, Switzerland. · Imperial College London, London, United Kingdom. · Fundación Hipercoesterolaemia Familiar, Madrid, Spain. · Hôpital Pitié Salpêtrière, Paris, France. ·Clin Ther · Pubmed #27261205.

ABSTRACT: PURPOSE: The goal of this study was to determine cardiovascular disease (CVD) risk associated with familial hypercholesterolemia (FH). METHODS: A systematic review of the published literature was conducted. All publications describing FH risk from PubMed ("cardiovascular disease risk + familial hypercholesterolaemia," 2004-2015), Internet and Medline search of FH registries, and associated references were screened for FH-related CVD risk in titles, abstracts, and study methods. CVD risk expressed as rates, odds, or ratios of mortality and morbidity were extracted. Each article was reviewed for bias by 2 reviewers within 17 items in 7 categories; a modified Newcastle-Ottawa assessment scale was used for nonrandomized studies. FINDINGS: The complete literature search identified 712 potential publications: 549 from PubMed (Medline), 150 from registries, and 13 from references. Fourteen articles met the inclusion criteria: 8 from registries in the United Kingdom, the Netherlands, Norway, and Spain; 5 from single hospitals or families in Japan, Denmark, the Netherlands, and the United Kingdom; and a population survey in Denmark. Across studies, attrition bias was low in 22 (80%) of 28 items. Risk of selection bias was high in 35 (63%) of 56 items. Selection bias risk was due to low representativeness and lack of a non-FH comparator group within the same study; detection bias risk was due to variable definitions of CVD outcomes/measurement; and performance bias risk was due to long-term, intensive treatment, the most common limitations for registries. Studies from single hospitals and families lacked generalizability. In contrast, the Danish study revealed a low bias in each of the 4 selection bias criteria and 2 attrition risk criteria. Fatal and nonfatal CVD events were collected in the study. Comparing patients with FH versus non-FH patients, the odds ratios for coronary artery disease were 10.3 (95% CI, 7.8-13.8) and 13.2 (95% CI, 10.0-17.4) in subjects treated and not treated with lipid-lowering therapy, respectively. These ratios fall within the ranges of ratios reported in other studies but are generally higher than the ratios from registries and clinics, in which intensive specialized management is available. IMPLICATIONS: There is a lack of available data describing CVD risk in patients with FH, and many of the existing studies have biases in their design that could affect their risk estimates. A Danish study had the highest quality based on a predefined quality check list, providing the most credible estimates of the increase in CVD risk in patients with FH. The CVD risk due to FH is high and represents unmet medical need for patients with FH. Further research is warranted to validate the magnitude of risk.

22 Review The year in cardiology 2015: prevention. 2016

Chapman, M John / Blankenberg, Stefan / Landmesser, Ulf. ·National Institute for Health and Medical Research (INSERM), Dyslipidemia and Atherosclerosis Research, Pitié-Salpêtrière University Hospital, Paris FR-75651, France University of Pierre and Marie Curie, Paris, France john.chapman@upmc.fr. · Clinic for Cardiology, University Heart Center Hamburg, German Center for Cardiovascular Research (DZHK), Hamburg, Germany. · Department of Cardiology, Charité Universitätsmedizin Berlin (CBF), Berlin, Germany German Center for Cardiovascular Research (DZHK), Berlin Institute of Health (BIH), Berlin, Germany. ·Eur Heart J · Pubmed #26726043.

ABSTRACT: -- No abstract --

23 Review Recent Patents on Hypocholesterolemic Therapeutic Strategies: An Update. 2015

Potiron, Aline / Gérard, Philippe / Le Roy, Tiphaine / Lesnik, Philippe / Maguin, Emmanuelle / Rhimi, Moez. ·INRA, UMR1319 MICALIS, Jouy-en-Josas, France, AgroParisTech, UMR MICALIS, Jouy-en- Josas, France. moez.rhimi@jouy.inra.fr. ·Recent Adv DNA Gene Seq · Pubmed #26675942.

ABSTRACT: Worldwide, the cardiovascular diseases constitute a major cause of death with an ever growing incidence. Many medical approaches were developed against this physiopathology and patented; however up to now, no efficient treatment exists. Future developments are not only focusing on the identification of new therapeutic strategies against the cardiovascular diseases but also on a better understanding of the determinants of these multifactorial diseases. In this report, we reviewed the most recent patents that have been reported in this field of research.

24 Review Prevalence, Treatment, and Control of Hypercholesterolemia in High Cardiovascular Risk Patients: Evidences from a Systematic Literature Review in Spain. 2015

de la Sierra, Alex / Pintó, Xavier / Guijarro, Carlos / Miranda, José López / Callejo, Daniel / Cuervo, Jesús / Subirà, Rudi / Rubio, Marta. ·Department of Internal Medicine, University Hospital Mutua Terrassa, Barcelona, Spain. adelasierra@mutuaterrassa.cat. · Lipid Unit, Internal Medicine Service, University Hospital of Bellvitge, Barcelona, Spain. · Internal Medicine Service, University Hospital Alcorcón Foundation, Madrid, Spain. · Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofıa University Hospital, University of Cordoba and CIBER Fisiopatologia Obesidad y Nutricion, Instituto de Salud Carlos III, Cordoba, Spain. · Reina Sofia University Hospital, IMIBIC/Fundacion para la Investigacion Biomedica de Cordoba, Cordoba, Spain. · BAP Health Outcomes Research, Oviedo, Spain. · Health Economics and Outcomes Research, Sanofi Iberia, Barcelona, Spain. ·Adv Ther · Pubmed #26499178.

ABSTRACT: INTRODUCTION: Cardiovascular diseases (CVDs) represent a major Public Health burden. High serum cholesterol levels have been linked to major CV risk. The objectives of this study were to review the epidemiology of hypercholesterolemia in high risk CV patients from Spain, by assessing its prevalence, the proportion of diagnosed patients undergoing pharmacological treatment and the degree of attained lipid control. METHODS: A systematic literature review was carried out using Medline and two Spanish databases. Manuscripts containing information on hypercholesterolemia in several high CV risk groups [diabetes mellitus (DM), Systematic COronary Risk Evaluation (SCORE) risk >5, or documented CVD], published between January 2010 and October 2014, were included. RESULTS: Of the 1947 published references initially retrieved, a full-text review was done on 264 manuscripts and 120 were finally included. Prevalence of hypercholesterolemia ranged from 50 to 84% in diabetics, 30-60% in patients with DM or elevated SCORE risk, 64-74% with coronary heart disease, 40-70% in stroke patients, and 60-80% in those with peripheral artery disease. Despite the finding that most of them were on pharmacological treatment, acceptable control of serum lipids was very variable, ranging from 15% to 65%. Among those with heterozygous familial hypercholesterolemia, 95-100% received treatment but less than 50% achieved their therapeutic goals. CONCLUSIONS: An elevated prevalence of hypercholesterolemia can be found in targeted groups at high CV risk. Although most patients are receiving pharmacological treatment, rates of lipid control continue to be low, both in primary and secondary prevention.

25 Review Recommendations for the management of patients with homozygous familial hypercholesterolaemia: overview of a new European Atherosclerosis Society consensus statement. 2014

Bruckert, Eric. ·Institute of Cardiometabolism and Nutrition, Hôpital Pitié-Salpêtrière, Paris, France. Electronic address: eric.bruckert@psl.aphp.fr. ·Atheroscler Suppl · Pubmed #25257074.

ABSTRACT: Although homozygous familial hypercholesterolaemia (HoFH) is rare, patients with this disease have a poor prognosis, even when they receive the best available treatment, including pharmacotherapy and apheresis. The current therapeutic gap emphasizes the potential impact of new and developmental treatment options, which include lomitapide, mipomersen, anti-PCSK9 monoclonal antibodies and CETP inhibitors. It is imperative that patients with HoFH receive the most appropriate treatment as early as possible and clinical guidance is needed to provide clinicians with the information they require to expedite diagnosis and initiate effective treatment. Until now, however, guidance on the management of (HoFH) has generally been included as part of broader guidelines on dyslipidemia, FH or low-density lipoprotein (LDL)-apheresis and even in guidelines specifically on FH, HoFH has been under-represented. A consensus statement on recommendations for the management of HoFH has recently been published by a working group of the European Atherosclerosis Society. An outline of the content of the statement is presented in the current paper.

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