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1. Lipoprotein(a) in children and adolescents with genetically confirmed familial hypercholesterolemia followed up at a specialized lipid clinic

Author

Anja K. Johansen, Martin P. Bogsrud, Magne Thoresen, Jacob J. Christensen, Ingunn Narverud, Gisle Langslet, Tone Svilaas, Kjetil Retterstøl, and Kirsten B. Holven

Subjects
Familial hypercholesterolemia, lipoprotein(a), Children, Cardiovascular disease, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Background and aim: Many children with an FH mutation also exhibit elevated lipoprotein(a) levels, which is an independent risk factor for atherosclerotic cardiovascular disease. Studies have reported higher levels of lipoprotein(a) in adult and middle-aged women than men. There is limited knowledge on the concentration and change of lipoprotein(a) levels in children with genetic FH, and therefore we investigated sex-differences in lipoprotein(a) level and change in lipoprotein(a) in girls and boys with genetically confirmed FH. Methods: Medical records were reviewed retrospectively in 438 subjects with heterozygous FH that started follow-up below the age of 19 years at the Lipid Clinic, Oslo University Hospital in Norway, and of these we included 386 subjects with at least one Lp(a) measurement. Results: Mean (SD) age at baseline was 13.8 (7.3) years and the age was similar between sexes. Girls had a higher lipoprotein(a) level than boys at baseline: median (25–75 percentile) 223 (108–487) vs. 154 (78–360) mg/L, respectively (p 0.05). Conclusions: We found an increase in Lp(a) levels in children with genetic FH with age, and higher levels in girls than boys, which could impact risk assessment and future ASCVD. Further research is needed to elucidate whether subjects with FH could benefit from lipoprotein(a)-lowering therapies that are under current investigations.

Published
2024
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2. Young women with familial hypercholesterolemia have higher LDL-cholesterol burden than men: Novel data using repeated measurements during 12-years follow-up

Author

Anja K. Johansen, Martin P. Bogsrud, Jacob J. Christensen, Amanda Rundblad, Ingunn Narverud, Stine Ulven, Gisle Langslet, Kjetil Retterstøl, and Kirsten B. Holven

Subjects
Low-density-lipoprotein exposure, Familial hypercholesterolemia, Cholesterol lowering, Sex-differences, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Background and aims: The concentration and the duration of exposure to low-density lipoprotein cholesterol (LDL-C) (LDL-C burden) is an important determinant of risk for cardiovascular disease and thresholds has recently been estimated. Individuals with familial hypercholesterolemia (FH) have increased risk of premature cardiovascular disease. The overall aim of the present study was to describe differences in LDL-C level and LDL-C burden in females and males with FH visiting an outpatient lipid clinic from a young age, using multiple LDL-C measurements during a follow-up time of 12 years. First, we aimed to study if the LDL-C concentration and the LDL-C burden is different between females and males at ages 0–10, 10–20, 20–30 and >30 years. Second, we aimed to estimate the subject-specific LDL-C burden at age 19 and 30 years, and the proportion of female and male patients that reach suggested LDL-C thresholds indicating high risk of ASCVD. Methods: Data was retrospectively collected from medical records of 438 subjects (207 girls and 231 boys) with FH, referred to the Lipid Clinic, Oslo University Hospital below the age of 19 years. The LDL-C burden was estimated based on repeated LDL-C measurements over time. Results: Subjects were followed over a period of mean 12.0 (SD 7.0) years, with median 10 years (7–17; 25–75 percentiles, minimum 2), with median 6 (4–9; 25–75 percentiles, minimum 2) available LDL-C measurements, starting at mean age 11 (SD 3.9) years. There was a difference in both LDL-C and LDL-C burden between sexes at different ages. On average, males had lower LDL-C over time, although this difference was less pronounced with age and males also had lower estimated LDL-C burden over time, and this difference was further exacerbated with age. Conclusion: Our study shows that young women with FH have a higher LDL-C burden than their male counterparts, potentially explaining the increased excess CVD risk seen among these. It underscores the importance of careful-follow up and early treatment initiation both prior to and after pregnancies in order to limit statin-free periods.

Published
2023
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3. Maternal prenatal cholesterol levels predict offspring weight trajectories during childhood in the Norwegian Mother, Father and Child Cohort Study

Author

Linn K. L. Øyri, Jacob J. Christensen, Sylvain Sebert, Magne Thoresen, Trond M. Michelsen, Stine M. Ulven, Hilde K. Brekke, Kjetil Retterstøl, Anne Lise Brantsæter, Per Magnus, Martin P. Bogsrud, and Kirsten B. Holven

Subjects
MoBa, MBRN, Cholesterol, Weight trajectories, Parental negative control study, Medicine
Abstract

Abstract Background Numerous intrauterine factors may affect the offspring’s growth during childhood. We aimed to explore if maternal and paternal prenatal lipid, apolipoprotein (apo)B and apoA1 levels are associated with offspring weight, length, and body mass index from 6 weeks to eight years of age. This has previously been studied to a limited extent. Methods This parental negative control study is based on the Norwegian Mother, Father and Child Cohort Study and uses data from the Medical Birth Registry of Norway. We included 713 mothers and fathers with or without self-reported hypercholesterolemia and their offspring. Seven parental metabolites were measured by nuclear magnetic resonance spectroscopy, and offspring weight and length were measured at 12 time points. Data were analyzed by linear spline mixed models, and the results are presented as the interaction between parental metabolite levels and offspring spline (age). Results Higher maternal total cholesterol (TC) level was associated with a larger increase in offspring body weight up to 8 years of age (0.03 ≤ P interaction ≤ 0.04). Paternal TC level was not associated with change in offspring body weight (0.17 ≤ P interaction ≤ 0.25). Higher maternal high-density lipoprotein cholesterol (HDL-C) and apoA1 levels were associated with a lower increase in offspring body weight up to 8 years of age (0.001 ≤ P interaction ≤ 0.005). Higher paternal HDL-C and apoA1 levels were associated with a lower increase in offspring body weight up to 5 years of age but a larger increase in offspring body weight from 5 to 8 years of age (0.01 ≤ P interaction ≤ 0.03). Parental metabolites were not associated with change in offspring height or body mass index up to 8 years of age (0.07 ≤ P interaction ≤ 0.99). Conclusions Maternal compared to paternal TC, HDL-C, and apoA1 levels were more strongly and consistently associated with offspring body weight during childhood, supporting a direct intrauterine effect.

Published
2023
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4. Differential effects of bariatric surgery and lifestyle interventions on plasma levels of Lp(a) and fatty acids

Author

Kirsten A. Berk, Heidi Borgeraas, Ingunn Narverud, Monique T. Mulder, Linn K. L. Øyri, Adrie J. M. Verhoeven, Milada Cvancarova Småstuen, Martin P. Bogsrud, Torbjørn Omland, Jens Kristoffer Hertel, Espen Gjevestad, Njord Nordstrand, Kirsten B. Holven, and Jøran Hjelmesæth

Subjects
Lp(a), Fatty acids, Obesity, Bariatric surgery, Lifestyle intervention, Nutritional diseases. Deficiency diseases, RC620-627
Abstract

Abstract Background Limited evidence suggests that surgical and non-surgical obesity treatment differentially influence plasma Lipoprotein (a) [Lp(a)] levels. Further, a novel association between plasma arachidonic acid and Lp(a) has recently been shown, suggesting that fatty acids are a possible target to influence Lp(a). Here, the effects of bariatric surgery and lifestyle interventions on plasma levels of Lp(a) were compared, and it was examined whether the effects were mediated by changes in plasma fatty acid (FA) levels. Methods The study includes two independent trials of patients with overweight or obesity. Trial 1: Two-armed intervention study including 82 patients who underwent a 7-week low energy diet (LED), followed by Roux-en-Y gastric bypass and 52-week follow-up (surgery-group), and 77 patients who underwent a 59-week energy restricted diet- and exercise-program (lifestyle-group). Trial 2: A clinical study including 134 patients who underwent a 20-week very-LED/LED (lifestyle-cohort). Results In the surgery-group, Lp(a) levels [median (interquartile range)] tended to increase in the pre-surgical LED-phase [17(7–68)-21(7–81)nmol/L, P = 0.05], but decreased by 48% after surgery [21(7–81)—11(7–56)nmol/L, P

Published
2022
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5. Novel associations between parental and newborn cord blood metabolic profiles in the Norwegian Mother, Father and Child Cohort Study

Author

Linn K. L. Øyri, Martin P. Bogsrud, Jacob J. Christensen, Stine M. Ulven, Anne Lise Brantsæter, Kjetil Retterstøl, Hilde K. Brekke, Trond M. Michelsen, Tore Henriksen, Jeanine E. Roeters van Lennep, Per Magnus, Marit B. Veierød, and Kirsten B. Holven

Subjects
MoBa, the Norwegian Mother, Father and Child Cohort Study, MBRN, Medical Birth Registry of Norway, Cholesterol, Metabolic profiling, Cord blood, Sex differences, Medicine
Abstract

Abstract Background More than one third of Norwegian women and men between 20 and 40 years of age have elevated cholesterol concentration. Parental metabolic health around conception or during pregnancy may affect the offspring’s cardiovascular disease risk. Lipids are important for fetal development, but the determinants of cord blood lipids have scarcely been studied. We therefore aimed to describe the associations between maternal and paternal peri-pregnancy lipid and metabolic profile and newborn cord blood lipid and metabolic profile. Methods This study is based on 710 mother–father–newborn trios from the Norwegian Mother, Father and Child Cohort Study (MoBa) and uses data from the Medical Birth Registry of Norway (MBRN). The sample included in this study consisted of parents with and without self-reported hypercholesterolemia the last 6 months before pregnancy and their partners and newborns. Sixty-four cord blood metabolites detected by nuclear magnetic resonance spectroscopy were analyzed by linear mixed model analyses. The false discovery rate procedure was used to correct for multiple testing. Results Among mothers with hypercholesterolemia, maternal and newborn plasma high-density lipoprotein cholesterol, apolipoprotein A1, linoleic acid, docosahexaenoic acid, alanine, glutamine, isoleucine, leucine, valine, creatinine, and particle concentration of medium high-density lipoprotein were significantly positively associated (0.001 ≤ q ≤ 0.09). Among mothers without hypercholesterolemia, maternal and newborn linoleic acid, valine, tyrosine, citrate, creatinine, high-density lipoprotein size, and particle concentration of small high-density lipoprotein were significantly positively associated (0.02 ≤ q ≤ 0.08). Among fathers with hypercholesterolemia, paternal and newborn ratio of apolipoprotein B to apolipoprotein A1 were significantly positively associated (q = 0.04). Among fathers without hypercholesterolemia, no significant associations were found between paternal and newborn metabolites. Sex differences were found for many cord blood lipids. Conclusions Maternal and paternal metabolites and newborn sex were associated with several cord blood metabolites. This may potentially affect the offspring’s long-term cardiovascular disease risk.

Published
2021
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6. Thirty percent of children and young adults with familial hypercholesterolemia treated with statins have adherence issues

Author

Gisle Langslet, Anja K. Johansen, Martin P. Bogsrud, Ingunn Narverud, Hilde Risstad, Kjetil Retterstøl, and Kirsten B. Holven

Subjects
Familial hypercholesterolemia, Young adults, Children, Statins, Adherence, Diseases of the circulatory (Cardiovascular) system, RC666-701, Public aspects of medicine, RA1-1270
Abstract

Objective: To assess adherence to lipid lowering therapy (LLT), reasons for poor adherence, and achievement of LDL-C treatment goals in children and young adults with familial hypercholesterolemia (FH). Methods: Retrospective review of the medical records of 438 children that started follow-up at the Lipid Clinic, Oslo University hospital, between 1990 and 2010, and followed-up to the end of July 2019. Based on information on adherence to the LLT at the latest visit, patients were assigned to “good adherence” or “poor adherence” groups. Reasons for poor adherence were categorized as: “lack of motivation”, “ran out of drugs”, or “side effects”. Results: Three hundred and seventy-one patients were included. Mean (SD) age and follow-up time at the latest visit was 24.0 (7.1) and 12.9 (6.7) years; 260 patients (70%, 95% CI: 65–74%) had “good adherence” and 111 (30%, 95% CI: 25–35%) had “poor adherence”. “Lack of motivation” was the most common reason for poor adherence (n = 85, 23%). In patients with good adherence, compared to patients with poor adherence, age at latest visit (24.6 versus 22.0 years; p = 0.001), years of follow-up (13.5 versus 11.4 years; p = 0.003), and number of visits (8.1 versus 6.5 visits; p

Published
2021
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7. Gender differences in nutrition literacy levels among university students and employees: a descriptive study

Author

Karianne Svendsen, Liv E. Torheim, Vibeke Fjelberg, Anita Sorprud, Ingunn Narverud, Kjetil Retterstøl, Martin P. Bogsrud, Kirsten B. Holven, Mari C. W. Myhrstad, and Vibeke H. Telle-Hansen

Subjects
Socioeconomic status, Education, Nutrition literacy, Public health, University, Nutrition. Foods and food supply, TX341-641, Medicine
Abstract

The impact of nutrition information on public health is partly determined by the population's level of nutrition literacy (NL), which involves functional NL (such as knowledge of dietary guidelines) and critical NL (such as the ability to distinguish between evidence-based nutrition information and alternative facts). The aim of this cross-sectional study was to describe aspects of functional and critical NL and predictors of NL scores among university students and employees. We recruited at different university campuses, 414 students and 112 employees, of which 80 % were females and 69 % were in the ages of 18–30 years. In total, 82 % reported knowledge about where to find information on nutrition issues, and 70 % were familiar with Norwegian dietary guidelines. Being female, having higher age, being highly physically active and studying or working within health sciences were significant predictors of higher levels of functional nutrition knowledge. Significantly more women than men found it difficult to judge if media information on nutritional issues could be trusted (69 v. 54 %) and found it hard to distinguish between scientific and non-scientific information about diet (60 v. 42 %). Our findings indicate that for a sample of university students and employees, affiliation with health sciences, being female, having a higher age and being physically active were associated with higher functional NL. Women did, however, seem to have lower levels of some aspects of critical NL, e.g. how to critically judge nutrition information. A more thorough assessment of NL in university students and employees should therefore be conducted.

Published
2021
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8. Data on circulating leukocyte subpopulations and inflammatory proteins in children with familial hypercholesterolemia and healthy children

Author

Jacob J. Christensen, Liv Osnes, Bente Halvorsen, Kjetil Retterstøl, Martin P. Bogsrud, Cecilie Wium, Arne Svilaas, Ingunn Narverud, Stine M. Ulven, Pål Aukrust, and Kirsten B. Holven

Subjects
Computer applications to medicine. Medical informatics, R858-859.7, Science (General), Q1-390
Abstract

The data in this relies on a previous publication: “Altered leukocyte distribution under hypercholesterolemia: a cross-sectional study in children with familial hypercholesterolemia” (Christensen et al. 2016) [1]. In the present paper, whole blood leukocyte distribution and plasma inflammatory proteins were measured for association with cholesterol concentration and CRP in children with familial hypercholesterolemia (FH) and healthy children.

Published
2017
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9. Postprandial changes in gene expression of cholesterol influx and efflux mediators after intake of SFA compared with n-6 PUFA in subjects with and without familial hypercholesterolaemia: secondary outcomes of a randomised controlled trial

Author

Linn K. L. Øyri, Ingunn Narverud, Martin P. Bogsrud, Patrik Hansson, Lena Leder, Marte G. Byfuglien, Marit B. Veierød, Magne Thoresen, Stine M. Ulven, and Kirsten B. Holven

Subjects
Familial hypercholesterolaemia, Fat quality, Gene expression, LDL receptor, Postprandial responses, Nutrition. Foods and food supply, TX341-641, Medicine
Abstract

The long-term cholesterol-lowering effect of replacing intake of SFA with PUFA is well established, but has not been fully explained mechanistically. We examined the postprandial response of meals with different fat quality on expression of lipid genes in peripheral blood mononuclear cells (PBMC) in subjects with and without familial hypercholesterolaemia (FH). Thirteen subjects with FH (who had discontinued lipid-lowering treatment ≥4 weeks prior to both test days) and fourteen normolipidaemic controls were included in a randomised controlled double-blind crossover study with two meals, each with 60 g of fat either mainly SFA (about 40% energy) or n-6 PUFA (about 40% energy). PBMC were isolated in fasting, and 4 and 6 h postprandial blood samples. Expression of thirty-three lipid genes was analysed by reverse transcription quantitative PCR. A linear mixed model was used to assess postprandial effects between meals and groups. There was a significant interaction between meal and group for MSR1 (P = 0·03), where intake of SFA compared with n-6 PUFA induced a larger reduction in gene expression in controls only (P = 0·01). Intake of SFA compared with n-6 PUFA induced larger reductions in gene expression levels of LDLR and FADS1/2, smaller increases of INSIG1 and FASN, and larger increases of ABCA1 and ABCG1 (P = 0·01 for all, no group interaction). Intake of SFA compared with n-6 PUFA induced changes in gene expression of cholesterol influx and efflux mediators in PBMC including lower LDLR and higher ABCA1/G1, potentially explaining the long-term cholesterol-raising effect of a high SFA intake.

Published
2019
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11. Timing of cardioverter-defibrillator implantation in patients with cardiac laminopathies—External validation of the LMNA-risk ventricular tachyarrhythmia calculator

Author

Christine Rootwelt-Norberg, Alex Hørby Christensen, Eystein T. Skjølsvik, Monica Chivulescu, Christoffer R. Vissing, Henning Bundgaard, Eivind W. Aabel, Martin P. Bogsrud, Nina E. Hasselberg, Øyvind H. Lie, and Kristina H. Haugaa

Subjects
Lamin A/C, LMNA cardiomyopathy, Laminopathy, Physiology (medical), Primary preventive ICD, LMNA-risk VTA calculator, Cardiology and Cardiovascular Medicine, Ventricular tachyarrhythmia
Abstract

Background: LMNA genotype-positive patients have high risk of experiencing life-threatening ventricular tachyarrhythmias (VTAs). The LMNA-risk VTA calculator published in 2019 has not been externally validated. Objective: The purpose of this study was to validate the LMNA-risk VTA calculator. Methods: We included LMNA genotype-positive patients without previous VTAs from 2 large Scandinavian centers. Patients underwent electrocardiography, 24-hour Holter monitoring, and echocardiographic examinations at baseline and repeatedly during follow-up. Validation of the LMNA-risk VTA calculator was performed using Harrell's C-statistic derived from multivariable Cox regression analysis. Results: We included 118 patients (age 37 years [IQR 27–49 years]; 39 [33%] probands; 65 [55%] women; 100 [85%] with non-missense LMNA variants). Twenty-three patients (19%) experienced VTA during 6.1 years (interquartile range 3.0–9.1 years) follow-up, resulting in 3.0% (95% confidence interval 2.0%–4.5%) yearly incidence rate. Atrioventricular block and reduced left ventricular ejection fraction were independent predictors of VTAs, while nonsustained ventricular tachycardia, male sex, and non-missense LMNA variants were not. The LMNA-risk VTA calculator showed 83% sensitivity and 26% specificity for identifying patients with VTAs during the coming 5 years, and a Harrell's C-statistic of 0.85, when applying ≥7% predicted 5-year VTA risk as threshold. The sensitivity increased to 100% when reevaluating risk at the time of last consultation before VTA. The calculator overestimated arrhythmic risk in patients with mild and moderate phenotype, particularly in men. Conclusion: Validation of the LMNA-risk VTA calculator showed high sensitivity for subsequent VTAs, but overestimated arrhythmic risk when using ≥7% predicted 5-year risk as threshold. Frequent reevaluation of risk was necessary to maintain the sensitivity of the model.

Published
2023

12. Left Ventricular Dysfunction in Arrhythmogenic Cardiomyopathy: Association With Exercise Exposure, Genetic Basis, and Prognosis

Author

Øyvind H. Lie, Monica Chivulescu, Christine Rootwelt‐Norberg, Margareth Ribe, Martin Prøven Bogsrud, Erik Lyseggen, Jan Otto Beitnes, Vibeke Almaas, and Kristina H. Haugaa

Subjects
arrhythmogenic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, left ventricular dysfunction, ventricular arrhythmia, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Background Arrhythmogenic cardiomyopathy (AC) is characterized by biventricular dysfunction, exercise intolerance, and high risk of ventricular tachyarrhythmias and sudden death. Predisposing factors for left ventricular (LV) disease manifestation and its prognostic implication in AC are poorly described. We aimed to assess the associations of exercise exposure and genotype with LV dysfunction in AC, and to explore the impact of LV disease progression on adverse arrhythmic outcome. Methods and Results We included 168 patients with AC (50% probands, 45% women, 40±16 years old) with 715 echocardiographic exams (4.1±1.7 exams/patient, follow‐up 7.6 [interquartile range (IQR), 5.4–10.9] years) and complete exercise and genetic data in a longitudinal study. LV function by global longitudinal strain was −18.8% [IQR, −19.2% to −18.3%] at presentation and was worse in patients with greater exercise exposure (global longitudinal strain worsening, 0.09% [IQR, 0.01%–0.17%] per 5 MET‐hours/week, P=0.02). LV function by global longitudinal strain worsened, with 0.08% [IQR, 0.05%–0.12%] per year; (P

Published
2021
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13. Evaluation of lipoprotein(a) in the prevention and management of atherosclerotic cardiovascular disease: A survey among the Lipid Clinics Network

Author

Catapano, Alberico L, Tokgözoğlu, Lale, Banach, Maciej, Gazzotti, Marta, Olmastroni, Elena, Casula, Manuela, Ray, Kausik K, the Lipid Clinics Network, Alaa ABDELRAZIK (University Hospital of North Midland, United Kingdom), Alberto MELLO E SILVA (Sociedade Portuguesa de Aterosclerose, Portugal), Alexander VONBANK (VIVIT Institute, Austria), Alexandros, D TSELEPIS (Dept of Chemistry, Atherothrombosis Research Center, University of Ioannina, Greece), Alper SONMEZ (Department of Endocrinology and Metabolism, Ankara Guven Hospital, Turkey), Angelina PASSARO (Department of Translational Medicine, University of Ferrara &amp, Center for the Study and Treatment of Metabolic Diseases, Atherosclerosis, and Clinical Nutrition, University Hospital of Ferrara Arcispedale Sant’Anna, Italy), Anja VOGT (Medizinische Klinik und Poliklinik IV, Klinikum der Universit¨at München, Germany), Ann MERTENS (Clinical and Experimental Endocrinology, Leuven, Ku, Leuven, Belgium), Ann VERHAEGEN (Antwerp University Hospital, Belgium), Arman, S POSTADZHIYAN (Medical University of Sofia, Saint Anna University Hospital, Departement of Cardiology, Bulgaria), BAHADIR KIRILMAZ (Canakkale Onsekiz Mart University, Medical Faculty Cardiology Dept, Baris GUNGOR (University of Health Sciences Dr. Siyami Ersek Hospital, Turkey), Berit S HEDEGAARD (Aalborg University, Denmark), Bertrand CARIOU (Nantes Universit´e, Chu, Nantes, Cnrs, Inserm, l’institut du thorax, Nantes, France), Britta OTTE (Universit¨atsklinikum Münster, Lipidambulanz, Germany), Bu˘gra ¨OZKAN (Mersin University, Turkey), of cardiology, Christ BERGE (Dept., Unversity Hopsital, Haukeland., Norway), F EBENBICHLER (Department for Internal Medicine I, Christoph, Medical University Innsbruck, Austria), Christoph J BINDER (Medical University of Vienna, Austria), Christoph OLIVIER (Department of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Faculty of Medicine, University of Freiburg, Conrad AZZOPARDI (Mater Dei Hospital, Malta), Cristina SOLER (Lipid Unit, Hospital de Sta Caterina, Spain), Dan GAITA (Universitatea de Medicina si Farmacie Victor Babes din Timisoara &amp, Clinica de Cardiologie, Institutul de Boli Cardiovasculare Timisoara, Romania), Daniel WEGHUBER (Department of Pediatrics, Paracelsus Medical University, Dilek URAL (Koç University School of Medicine Department of Cardiology, Turkey), Diogo CRUZ (Hospital de Cascais - Dr. Jos´e de Almeida, Portugal), Dragos VINEREANU (University of Medicine and Pharmacy, University and Emergency Hospital, Bucharest, Romania), Elena D PENCU (Grand Hˆopital de Charleroi GHDC, Belgium), Emil HAGSTR¨OM (Dept of medical sciences, Uppsala, University, Sweden), Erik B SCHMIDT (Aalborg University, Denmark), Erik, S STROES (Dept of vascular medicine, Amsterdamumc, The, Netherlands), Evangelos LIBEROPOULOS (1st Department of Propedeutic Medicine, School of Medicine, National and Kapodistrian University of Athens, General Hospital of Athens Laiko, Fabian DEMEURE (CHU UCL Namur - Site Godinne, Belgium), Fabio FIMIANI (Azienda Ospedaliera di Rilievo Nazionale AORN Dei Colli, Monaldi', 'V., Unit of Inherited and Rare Cardiovascular Diseases, Italy, ), Fabio PELLEGATTA (Center for the Study of Atherosclerosis. Bassini Hospital. Cinisello Balsamo, Italy), Fahri BAYRAM (Erciyes University, Turkey), Finn L HENRIKSEN (Department of Cardiology Odense University Hospital, Denmark), Florian H¨OLLERL (1st Medical Department, Landstrasse, Clinic, Vienna Health Association, Francesco CIPOLLONE (Clinica Medica Institute of, Department of Medicine and Aging Sciences, d’Annunzio' University, 'G., Francisco ARAÚJO (Hospital Lusíadas, Portugal), Franck BOCCARA (Sorbonne Universit´e, Groupe de Recherche Clinique number 22, C2MV—Complications Cardiovasculaires et M´etaboliques chez les Patients Vivant avec le Virus de l’Immunod´eficience Humaine, Institut National de la Sant´e et de la Recherche M´edicale Unit´e Mixte de Recherche, S 938, Centre de Recherche Saint-Antoine, Institut Hospital Universitaire de Cardiom ´etabolisme et Nutrition Cardiologie, Hˆopital Saint Antoine Assistance Publique–Hˆopitaux de Paris, Paris, France), François PAILLARD (Cardiologie et Centre Clinico-Biologique des Lipides et Ath´eroscl´erose, Chu, Rennes, France), Imre University Teaching Hospital, Gabor SIMONYI (DBC St., Metabolic, Center, Lipid, Center, Hungary), Gabriella IANNUZZO (Department of Clinical Medicine and Surgery. University of Naples Federico II, Italy), Giuseppe MANDRAFFINO (Department of Clinical and Experimental Medicine, - Lipid Center, University of Messina, Graham BAYLY (Dept Clinical Biochemistry, University Hospitals Bristol, United, Kingdom), Gustavs LATKOVSKIS (Institute of Cardiology and Regenerative Medicine, University of Latvia &amp, Latvian Center of Cardiology, Pauls Stradins Clinical University Hospital &amp, University of Latvia, Latvia), Gy¨orgy PARAGH (Division of Metabolic Disorders, Department of Internal Medicine, University of Debrecen, Debrecen, Hungary), Hana ROSOLOVA (Charles University Prague Medical Hospital in Pilsen, Czech Republic), Handrean SORAN (Central Manchester University Hospital NHS Foundation Trust, United Kingdom), Helle KANSTRUP (Department of cardiology, Aarhus University hospital, Denmark), Hermann TOPLAK (Department of Medicine, Division of Endocrinology and Diabetology, Medical University Graz, Hülya ÇIÇEKÇIO ˘GLU (ankara bilkent city hospital, Turkey), Inanc ARTAC (Department of Cardiology, Kafkas University Hospital, Ioanna GOUNI-BERTHOLD (Center for Endocrinology, Diabetes and Preventive Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Irfan, V DUZEN (Gaziantep University, Cardiology, Department, Isabel M PALMA (CHUPORTO - Centro Hospitalar Universit ´ario do Porto, Portugal), Istvan REIBER (Szent Gyorgy University Teaching Hospital of Fejer County, Hungary), Iveta DZIVITE-KRISANE (Children’s University Hospital, Latvia), Jeanine, E ROETERS VAN LENNEP (Department of Internal medicine, Erasmus MC University Medical Center, Jean-Luc, J BALLIGAND (Institut de Recherche Exp´erimentale et Clinique, Universite catholique de Louvain, Bruxelles), Joao C PORTO (CHUC, Portugal), Jo˜ao, S DUARTE (Hospital Egas Moniz, Lisboa, Portugal), Johan DE SUTTER (AZ Maria Middelares Hospital Gent, Belgium), Jos´e L´OPEZ-MIRANDA (Lipid and Arteriosclerosis Unit. Department of Internal Medicine. Hospital Universitario Reina Sofia. IMIBIC. University of Cordoba. CiberOBN, Spain), Jose M MOSTAZA (Hospital La Paz-Carlos III, Spain), Jurgita PLISIENE (Lithuanian University of Health sciences, Lithuania), Kadir, U MERT (Eskis ¸ehir Osmangazi University, Department of Cardiology, Kirsten, B HOLVEN (Department of Nutrition, University of Oslo and National Advisory unit on FH, Oslo University Hospital, Kjetil RETTERSTØL (The Lipid Clinic, Oslo University Hospital and Department of Nutrition, University of Oslo, Kristian, K THOMSEN (University Hospital of South Denmark, Esbjerg, Denmark), Lale TOKGOZOGLU (Hacettepe University, Turkey), Laszlo BAJNOK (1st Department of Medicine, Medical, School, University of Pecs, Lia E BANG (Copenhagen University Hospital, Denmark), Liliana GRIGORE (IRCCS Multimedica, Italy), Lluís MASANA (Hospital Universitari Sant Joan. Universitat Rovira i Virgili. CIBERDEM. Reus, Spain), Loukianos S RALLIDIS (University General Hospital Attikon, Greece), Maciej BANACH (Department of Preventive Cardiology and Lipidology, Medical University of Lodz, Poland), Małgorzata WALU´S-MIARKA (Jagiellonian University Medical College, Of Metabolic Diseases and Diabetology, Dept., Manuel CASTRO CABEZAS (Franciscus Gasthuis &amp, Vlietland Rotterdam, The Netherlands), Marcello ARCA (Sapienza University of Rome, Italy), Margus VIIGIMAA (North Estonia Medical Centre, Tallinn University of Technology, Estonia), Martin, P BOGSRUD (Unit for Cardiac and Cardiovascular Genetics, Matej MLINARIˇC (Department of Endocrinology, Diabetes and Metabolism, University Children’s Hospital, University Medical Centre Ljubljana, Slovenia), Matteo PIRRO (Section of Internal Medicine, Angiology and Arteriosclerosis Diseases, Maurizio AVERNA (Department PROMISE-University of Palermo &amp, Istituto di Biofisica, Consiglio Nazionale delle Ricerche, Palermo, Italy), Meral KAYIKCIOGLU (Ege University Medical School Department of Cardiology, Turkey), Merete HEITMANN (Bispebjerg-Frederiksberg University Hospital, Denmark), Mette MOURIDSEN (Department of Cardiology, Herlev and Gentofte Hospital, University of Copenhagen, Michal VRABLIK (3rd Department of Internal Medicine, General University Hospital and 1st Medical Faculty, Charles, University, Prague, Czech, Republic), Michel FARNIER (PEC2, University of Bourgogne Franche-Comt´e, Laboratory Medicine, Michel R LANGLOIS (Dept., Jan Hospital, AZ St., Belgium), Milad KHEDR (Department of Clinical Biochemistry and Metabolic Medicine, Royal Liverpool University Hospital, Muge ILDIZLI DEMIRBAS (Kartal Kosuyolu Research and Training Hospital, Turkey), Myra TILNEY (Lipid Clinic, Mater Dei Hospital &amp, Dept of Medicine, University of Malta Medical School, Malta), Nadia CITRONI (Internal Medicine, APSS Trento Hospital, Of Internal Medicine, Niels P RIKSEN (Dept., Radboud university medical center, Nikolay M RUNEV (UMHAT Alexandrovska, Bulgaria), Nora KUPSTYTEKRISTAPONE (Hospital of Lithuanian University of Health Sciences Kaunas Clinics, Lithuania), Olena MITCHENKO (NSC, Clinical and Regenerative Medicine of the NAMS of Ukraine, Ukraine), Oliver WEING¨ARTNER (Universit¨atsklinikum Jena, Department of Internal Medicine, I, Oner OZDOGAN (University of Health Sciences, Izmir Faculty of Medicine, Tepecik Training and Research Hospital, Ovidio MU˜NIZGRIJALVO (Hospital Virgen del Rocío, Spain), Ozcan BASARAN (Mugla Sitki Kocman University, Pankaj GUPTA (University Hospitals of Leicester, United Kingdom), Paolo PARINI (Cardio Metabolic Unit, Karolinska, Institutet, and Theme Inflammation and Ageing, Karolinska University Hospital Huddinge, Patrizia SUPPRESSA (Department of Internal Medicine and rare disease Centre, Bari, Italy), Paul DOWNIE (Salisbury NHS Foundation trust, United Kingdom), Pavel JESINA (Metabolic Center General University Hospital, Czech Republic), of Internal Medicine, Pavel KRAML (Dept., Third Faculty of Medicine, Charles University and Kr´alovsk´e Vinohrady University Hospital Prague, Pawel BURCHARDT (Department of Cardiology, Cardiovascular, Unit, Hospital, J. Stru´s., Pozna´n, &amp, Department of Hypertension, Angiology and Internal Medicine, Poznan University of Medical Sciences, Pozna´n, Poland), Pedro VALDIVIELSO (Hospital VIRGEN DE LA VICTORIA, Spain), Pedro VON HAFE (Instituto Cuf, Portugal), Dept, Peter FASCHING (5th Med., Clinic, Ottakring, Philippe MOULIN (Hospices civils de Lyon/INSERM/Universit ´e Lyon1, Hˆopital Louis Pradel, F´ed´eration, D’Endocrinologie, Quit´eria RATO (Sociedade Portuguesa de Aterosclerose, Portugal), Reinhold INNERHOFER (Medical University Vienna, Austria), Renata C´IFKOV´A (Center for Cardiovascular Prevention, Charles University in Prague, First Faculty of Medicine and Thomayer University Hospital, Rene VALERO (Aix Marseille Univ, Aphm, Inserm, Inrae, C2vn, University Hospital La Conception, Department of Nutrition, Metabolic Diseases and Endocrinology, Scicali, Roberto, Robin URB´ANEK (Internal medicine, Obezita-Ormiga, s. r. o., Roma KAVALIAUSKIENE (Klaip˙ eda Seamen’s Hospital, Lituania), Roman CIBULKA (Department of paramedic science, medical diagnostics studies and public health, Faculty of Health Care Studies, University of West Bohemia, Sabina ZAMBON (Department of Medicine, - DIMED, University of Padova, Sergio D’ADDATO (University of Bologna. IRCCS S. Orsola Bologna, Italy), Stanislav ZEMEK (Lipidova ambulance, Czech Republic), Stefano ROMEO (Gothenburg University, Sweden), Stephanie K¨ONEMANN (Department of Internal Medicine, B, University Medicine Greifswald, DZHK (German Centre for Cardiovascular Research), Susanne GREBER-PLATZER (Clinical Division of Pediatric Pulmonology, Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University Vienna, Thomas STULNIG (Clinical Division of Endocrinology and Metabolism, Department of Medicine III, Medical University Vienna &amp, Third Medical Department and Karl Landsteiner Institute for Metabolic Diseases and Nephrology, Clinic, Hietzing, Vienna, Austria), Thomas MUHR (Dept of Cardiology, Link¨oping University Hospital, Tina, Z KHAN (Consultant Cardiologist, Royal Brompton and Harefield Hospitals Part of Guy’s and St Thomas’ NHS Foundation Trust, Tomas FREIBERGER (Centre of Cardiovascular Surgery and Transplantation, Brno &amp, Medical, Faculty, Masaryk, University, Brno, Tom´aˇs ˇS´ALEK (Metabolic Clinic, Tomas Bata Hospital, Zlín, Tomas VASYLIUS (Republican Panevezys hospital, Of Cardiology, Dep., Lithuania), Ulrich LAUFS (Klinik und Poliklinik für Kardiologie, Universit ¨atsklinikum Leipzig, Ulrike SCHATZ (University Hospital Carl Gustav Carus Dresden at the Technical University Dresden, Department of Internal Medicine III, Urh GROSELJ (UMC, - University Children’s Hospital Ljubljana, University of Ljubljana, Victoria MARCO-BENEDI (Hospital Universitario Miguel Servet, Iisa, Cibercv, Vincent MAHER (Advanced Lipid Management and Research ALMAR centre, Tallaght University Hospital, Ireland), Vladimír BLAHA (University Hospital Hradec Kr´alov´e and Charles University, Faculty of Medicine in Hradec Kr´alov´e, 3rd Department of Internal Medicine, - Metabolism and Gerontology, Vladimir SOSKA (Department of Clinical Biochemistry, St. Anne’s University Hospital Brno, 2nd Clinic of Internal Medicine, Masaryk University Brno, Volker JJ SCHETTLER (Centre of Nephrology G¨ottingen, Germany), Wolfgang REINHARDT (SUS Malmoe, Sweden), Xavier PINT´O (Hospital Universitari de Bellvitge-Idibell-UB-CiberObn, Spain), Yoto YOTOV (Second Cardiology Clinic, Marina, University Hospital Sv., Medical University of Varna, Zaneta PETRULIONIENE (Vilnius University Medical Faculty, Vilnius University Hospital Santaros klinikos, Lithuania), ˇZeljko REINER (Department for Metabolic Diseases, University Hospital Center Zagreb, and Croatia, ).

Subjects
Clinicians, Clinical evaluation, Cardiology and Cardiovascular Medicine, Cardiovascular risk, Lipoprotein(a)
Published
2023

15. Use of statins and other lipid-modifying agents across pregnancy: A nationwide drug utilization study in Norway in 2005–2018

Author

Jacob J. Christensen, Martin P. Bogsrud, Kirsten B. Holven, Kjetil Retterstøl, Marit B. Veierød, and Hedvig Nordeng

Subjects
Cardiology and Cardiovascular Medicine
Abstract

Background and aims Statins are becoming more widely used among women of reproductive age; however, nationwide data on statin use across pregnancy is scarce. We therefore aimed to describe the drug utilization patterns for statins and other lipid-modifying agents (LMAs) before, during, and after pregnancy, for all pregnancies in Norway from 2005 to 2018. Methods We linked individual-level data from four nationwide electronic health care registries in Norway and characterized the prescription fills of statins and other LMAs across pregnancy. We also examined trends in pregnancy-related LMA use, and characterized women using statins and other LMAs on parameters of health status and co-morbidity. Results In total, 822,071 pregnancies for 503,723 women were included. The number of statin prescription fills decreased rapidly during the first trimester and returned to pre-pregnancy levels about one year postpartum. Pregnancy-related statin use increased from 2005 (approx. 0.11% of all pregnancies) to 2018 (approx. 0.29% of all pregnancies); however, in total, few statin prescriptions were filled within any trimester of pregnancy (n = 331, 0.04% of all pregnancies). Statin use was more common in women with higher age, higher weight, smoking, and comorbidities such as hypertension and diabetes mellitus; also, statin users often had co-medication pertinent to these conditions. Conclusions Although statins and other LMAs were increasingly being used around the time of pregnancy among women in Norway, drug use was mostly discontinued during the first trimester. Our results suggest that pregnancy-related statin use should be monitored, and that drug safety analyses for maternal and offspring health outcomes are needed.

Published
2022

16. Risk of stroke in genetically verified familial hypercholesterolemia: A prospective matched cohort study

Author

Karianne Svendsen, Thomas Olsen, Kathrine J. Vinknes, Liv J. Mundal, Kirsten B. Holven, Martin P. Bogsrud, Trond P. Leren, Jannicke Igland, and Kjetil Retterstøl

Subjects
Cohort Studies, Hyperlipoproteinemia Type II, Stroke, Hemorrhagic Stroke, Fibrinolytic Agents, Risk Factors, Humans, Cholesterol, LDL, Prospective Studies, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Cardiology and Cardiovascular Medicine, Ischemic Stroke
Abstract

Background and aims Individuals with familial hypercholesterolemia (FH), causing severely elevated LDL-C, are expected to have a higher risk of ischemic stroke. The risk of hemorrhagic stroke and impact of statin use are, however, not known. We aimed to investigate the risk of incident total, ischemic and hemorrhagic stroke in individuals with FH compared to controls, and to explore the association between cumulative statin use and risk of total stroke in FH. Methods This prospective cohort study consists of 4186 individuals with genetically verified FH and 82 180 age and sex matched controls followed from 2008 to 2018 for incident stroke. Daily defined doses (DDD) described cumulative statin exposure: 0–5000 DDD (“low”), 5000–10,000 DDD (“intermediate”), and >10 000 DDD (“high”). Results were presented as hazard ratio (95% CI) derived from Cox proportional hazards models. Results Individuals with FH did not have a higher risk of total stroke (1.16 (0.95–1.43) nor ischemic stroke (1.11 (0.88–1.38). Excess risk of hemorrhagic stroke was observed (1.63 (1.07, 2.48) but attenuated after adjusting for antithrombotic medication (1.25 (0.81, 1.93). Among individuals with FH, there was no association between statin use and total stroke for intermediate vs. low DDD [0.69 (0.32, 1.48)] or for high vs. low DDD [0.83 (0.41, 1.67)]. Conclusions No significant excess risk of incident total and ischemic stroke in FH, and no difference in total stroke risk among the FH population with low, intermediate, and high statin exposure were observed. The observed relationship between FH and hemorrhagic stroke was no longer significant after adjusting for use of anti-thrombotic medication. publishedVersion

Published
2022

17. Children with familial hypercholesterolemia display changes in LDL and HDL function : A cross-sectional study

Author

Ingunn Narverud, Bente Halvorsen, Kjetil Retterstøl, Maija Ruuth, Jacob J. Christensen, Stine Marie Ulven, Petri T. Kovanen, Katariina Öörni, Matti Jauhiainen, Michael N. Oda, Martin P. Bogsrud, Cecilie Wium, Kirsten B. Holven, Martin Heier, Research Programs Unit, University of Helsinki, Medicum, Molecular and Integrative Biosciences Research Programme, and Biosciences

Subjects
Cross-sectional study, Familial hypercholesterolemia, 030204 cardiovascular system & hematology, chemistry.chemical_compound, 0302 clinical medicine, Phospholipid transfer protein, Child, 0303 health sciences, biology, familial hypercholesterolemia, Atherosclerotic cardiovascular disease, Reverse cholesterol transport, PON1, LDL aggregation, metabolomics, 3. Good health, Cardiovascular Diseases, Acyltransferase, Functional status, lipids (amino acids, peptides, and proteins), Cardiology and Cardiovascular Medicine, medicine.medical_specialty, Hyperlipoproteinemia Type II, 03 medical and health sciences, children, Internal medicine, Cholesterylester transfer protein, Internal Medicine, medicine, Humans, 030304 developmental biology, HDL-apoA-I exchange, Apolipoprotein A-I, Cholesterol, business.industry, Cholesterol, HDL, cholesterol, Cholesterol, LDL, Atherosclerosis, medicine.disease, NMR, reverse cholesterol transport, lipoproteins, Cross-Sectional Studies, Endocrinology, chemistry, 3121 General medicine, internal medicine and other clinical medicine, Lecithin—cholesterol acyltransferase, biology.protein, business, Function (biology), ASCVD, Lipoprotein
Abstract

BackgroundThe functional status of lipoprotein particles contributes to atherogenesis. The tendency of plasma LDL particles to aggregate and the ability of HDL particles to induce and mediate reverse cholesterol transport associate with high and low risk for cardiovascular disease in adult patients, respectively. However, it is unknown whether children with familial hypercholesterolemia (FH) display lipoprotein function alterations.HypothesisWe hypothesized that FH children had disrupted lipoprotein function.MethodsWe analyzed LDL aggregation susceptibility and HDL-apoA-I exchange to apoA-I ratio (HAE/apoA-I ratio), and activity of four proteins that regulate lipoprotein metabolism (CETP, LCAT, PLTP and PON1) in plasma samples derived from children with FH (n = 47) and from healthy children (n = 56). Potential biological mechanisms behind any variation in lipoprotein functionalities were explored using an NMR-based metabolomics profiling approach.ResultsLDL aggregation was higher and HAE/apoA-I ratio was lower in FH children than in healthy children. LDL aggregation associated positively with LDL-C and negatively with triglycerides, and HAE/apoA-I ratio associated negatively with LDL-C. Generally, the metabolomic profile for LDL aggregation was a mirror image of that for HAE/apoA-I ratio.ConclusionsFH children displayed increased atherogenicity of LDL and disrupted HDL function. These newly observed functional alterations in LDL and HDL may increase the risk for atherosclerotic cardiovascular disease in FH children.

Published
2021

18. Global perspective of familial hypercholesterolaemia: a cross-sectional study from the EAS Familial Hypercholesterolaemia Studies Collaboration (FHSC)

Author

Jie Lin, Snejana Tisheva, Ishwar C. Verma, Francesco Cipollone, Liam R. Brunham, Florentina Predica, Perla A.C. Gonzalez, Jocelyne Inamo, André R. Miserez, Belma Pojskic, Michel Farnier, Avishay Ellis, Katia Bonomo, Ibrahim Al-Zakwani, Maria Grazia Zenti, Humberto A. Lopez, Khairul Shafiq Ibrahim, Erkin M. Mirrakhimov, Alexey Meshkov, Jose P. de Moura, Muthukkaruppan Annamalai, Raul D. Santos, F. Paillard, Maria Del Ben, Jan Lacko, Miguel T. Rico, Ximena Reyes, Laura E.G. de Leon, Noor Shafina Mohd Nor, Ulrich Julius, Mohammed A. Batais, Dieter Böhm, Ta-Chen Su, Takuya Kobayashi, Magdalena Chmara, Marco Gebauer, Marcos M. Lima-Martínez, Ravshanbek D. Kurbanov, Daisaku Masuda, Amro El-Hadidy, Melanie Schüler, Francisco Fuentes, Florian J. Mayer, Helena Vaverkova, F. Ulrich Beil, Juraj Bujdak, Mario Stoll, Isabelle Ruel, Elena Dorn, Thomas M. Stulnig, Abubaker Elfatih, Rano B. Alieva, Jiri Vesely, Valérie Carreau, Cristina M. Sibaja, Sophie Béliard, Olivier Ziegler, Adriana Branchi, Daniel Schurr, G.B. John Mancini, Tai E. Shyong, Eric L.T. Siang, Mafalda Bourbon, Zerrin Yigit, Meral Kayıkçıoğlu, Jacques Genest, Wei Yu, Michal Vrablík, Shavkat U. Hoshimov, Dan Gaita, Antonio Pipolo, Ashraf H.A. AlQudaimi, Walter Speidl, Gianfranco Parati, Zaliha Ismail, Victoria M. Zubieta, René Valéro, Tomas Salek, Hana Halamkova, Gustavs Latkovskis, Nicole Allendorf-Ostwald, Agnes Perrin, Vladimir Soska, Anastasia Garoufi, Francisco Araujo, Nacu C. Portilla, Thomas Segiet, Charalambos Koumaras, Hila Knobler, Fatih Sivri, Hani Altaradi, Ivan Pećin, Long Jiang, Alexander Dressel, Marlena Woś, Jana Franekova, D. Agapakis, Quitéria Rato, Dirk J. Blom, Marcin A. Bartlomiejczyk, Krzysztof Dyrbuś, Maurizio Averna, Phivos Symeonides, Yung A. Chua, Asim Rana, András Nagy, Juan C.G. Cuellar, Alexander Jäkel, Maya Safarova, Neama Luqman, Amalia-Despoina Koutsogianni, Patrick Tounian, Jose A. Alvarez, Ada Cuevas, Corinna Richter, Sybil Charrieres, Vitaliy Zafiraki, Michalis Doumas, Angela Lux, Thanh Huong Truong, Elaine Chow, José Luis Díaz-Díaz, Jesus R.H. Almada, Sabine Füllgraf-Horst, Gustavo G. Retana, Claudio Borghi, Gianni Biolo, Ivajlo Tzvetkov, Patrícia Pais, Mehmet Akbulut, Kumiko Nagahama, Oner Ozdogan, Frank Leistikow, Jianxun He, Alexander R.M. Lyons, Poranee Ganokroj, Luis E.S. Mendia, Ann-Cathrin Koschker, Gabriela A.G. Ramirez, Dainus Gilis, Karin Balinth, José Ramiro Cruz, Paolo Calabrò, Alberico L. Catapano, Emmanouil Skalidis, Hamida Al-Barwani, Genovefa Kolovou, Carolyn S.P. Lam, Yoto Yotov, Yaacov Henkin, Gabriella Iannuzzo, Aimi Z. Razman, Alma B.M. Rodriguez, Hans Dieplinger, Darlington E. Obaseki, Ursulo J. Herrera, Arcangelo Iannuzzi, Christoph Säly, Elena Olmastroni, Francisco G. Padilla, S.A. Nazli, Ioanna Gouni-Berthold, Miriam Kozárová, Urh Groselj, Igor Shaposhnik, Lorenzo Iughetti, Nawal Rwaili, Cinthia E. Jannes, Andrea Bartuli, Mikhail Voevoda, Marat V. Ezhov, Yanyu Duan, Alper Sonmez, Mustafa Yenercag, Ariane Sultan, Natasza Gilis-Malinowska, Tavintharan Subramaniam, Mohamed Ashraf, Jing Pang, Kota Matsuki, Tao Jiang, Gerald Klose, Eduardo A.R. Rodriguez, Lucie Solcova, Riccardo Sarzani, Mahmoud Traina, Alejandra Vázquez Cárdenas, Gordon A. Francis, Adolat V. Ziyaeva, Ronen Durst, Maciej Banach, Francisco Silva, Heribert Schunkert, Børge G. Nordestgaard, Ziyou Liu, Ahmad Bakhtiar Md Radzi, Hana Rosolova, Andrea Bäßler, Abdulhalim Jamal Kinsara, Noël Peretti, Victor Gurevich, Margarita T. Tamayo, Abdullah Tuncez, Florian Höllerl, Ljubica Stosic, Jianguang Qi, Anja Kirschbaum, Jitendra P.S. Sawhney, Michael Scholl, Kausik K. Ray, Mohamed Bendary, Hapizah Nawawi, Adrienne Tarr, Barbora Nussbaumerova, B.C. Brice, Kurt Huber, Noor Alicezah Mohd Kasim, A. Rahman A. Jamal, Vaclava Palanova, Giacomo Biasucci, Pucong Ye, Eva Cubova, Roopa Mehta, Rüdiger Schweizer, Veronica Zampoleri, Jacek Jóźwiak, Alyaa Al-Khateeb, Jing Hong, Katarina Raslova, Kirsten B. Holven, Tatiana Rozkova, Reinhold Busch, Alexander Klabnik, Konrad Hein, Eloy A.Z. Carrillo, Robin Urbanek, Livia Pisciotta, Fatma Y. Coskun, Jose J.G. Garcia, Valerio Pecchioli, Azra D. Nalbantic, Weerapan Khovidhunkit, Jernej Kovac, Michaela Kadurova, Mohammed Al-Jarallah, Vita Saripo, Christos V. Rizos, Jie Peng, Ang L. Chua, Dorothee Deiss, Nor A.A. Murad, Aneta Stróżyk, See Kwok, Gökhan Alici, Gillian J. Pilcher, John J.P. Kastelein, Dmitry Duplyakov, Calin Lengher, Milena Budikova, C. Azzopardi, Christina Antza, Luis E.V. Arroyo, Khalid Al-Jumaily, Ahmad Al-Sarraf, Carlos A. Aguilar-Salinas, Erkayim Bektasheva, Arta Upena-RozeMicena, Qian Wang, Xumin Wang, Leah Leavit, Radzi Rahmat, Selim Topcu, Željko Reiner, Lorenzo Maroni, Matija Cevc, Elizabeth R. Cooremans, Masatsune Ogura, Tevfik Sabuncu, Ruy D Arjona Villicaña, Andrea Giaccari, Xuesong Fan, Auryan Szalat, Sanjaya Dissanayake, Etienne Khoury, Anja Vogt, Hermann Toplak, Alexis Baass, Isabel Palma, Gaelle Sablon, Dana A. Hay, Ya Yang, Margus Viigimaa, Erik S.G. Stroes, Dror Harats, Konstantin Krychtiuk, Zesen Liu, Aleksandra Parczewska, Yves Cottin, Yichen Qu, Mathilde Di-Fillipo, Agnieszka Konopka, Lamija Pojskic, Guadalupe J. Dominguez, Ahmet Temizhan, Roberto C. Chacon, Ibrahim E. Dural, Qiang Yong, G. Kees Hovingh, Kang Meng, Sandra Kutkiene, Julie Lemale, Reinhold Innerhofer, Alexandros D. Tselepis, Handrean Soran, Wolfgang König, Bassam Atallah, Olena Mitchenko, Jana Cepova, Eduardo M. Rodriguez, Ulrich Laufs, Norhidayah Rosman, Alena Lubasova, V. Durlach, Frederick J. Raal, Elyor Khodzhiboboev, Cristina Pederiva, Hui Yuan, Ashraf Reda, Fahad Alnouri, Konstantinos Tziomalos, Thanh T. Le, Jana Sirotiakova, Régis Hankard, Hector E.A. Cazares, Betsabel Rodriguez, Lenka Pavlickova, Assen Goudev, Julius Katzmann, Diana Boger, Wael Almahmeed, Katarina T. Podkrajsek, Sabina Zambon, Fahri Bayram, Nadia Citroni, Samir Rafla, Vincent Rigalleau, Aleksandr B. Shek, Hani Sabbour, Berenice G. Guzman, Shoshi Shpitzen, Eric Tarantino, Ahmed Bendary, Fedya Nikolov, Jean Bergeron, Stefan Kopf, Iva Rasulic, Gerald F. Watts, Muhammad I.A. Hafidz, Mehmet B. Yilmaz, Kathrin Biolik, Ira A. Haack, Robert A. Hegele, Sonia Dulong, Bartosz Wasąg, Osama Sanad, Susana Correia, Zhenjia Wang, Dana Biedermann, Christel König, Helena Podzimkova, Ihab Daoud, Mohammad Alghamdi, Dražen Perica, László Márk, Iosif Koutagiar, Volkan Dogan, Vladimir Blaha, Chandrashekhar K. Ponde, Katerina Valoskova, Amer A. Jabbar, Azhari Rosman, Sazzli Kasim, Mesut Demir, Ulugbek I. Nizamov, Aldo Ferreira-Hermosillo, Dilek Yesilbursa, Atef Elbahry, Arshad Abdulrasheed, Omer A. Elamin, Vasileios Athyros, Joanna Lewek, Gergely Nagy, Ursula Kassner, Jian Jiao, Klaus G. Parhofer, Charlotte Nzeyimana, Marcin Pajkowski, Stanislav Zemek, Jose J.C. Macías, Cornelius Müller, G. Sfikas, Leopoldo Pérez de Isla, Yulia Ragino, Fahad Al-Zadjali, Abdul Rais Sanusi, Anna Rita Roscini, Jean Ferrières, Selim Jambart, Jean Pierre Rabes, Laura Schreier, Hofit Cohen, Olivier S. Descamps, N. Lalic, Christine Stumpp, Antonio J. Vallejo-Vaz, Jutta Christmann, Manuela Casula, Mariko Harada-Shiba, Olga Lunegova, Ewa Starostecka, Nicolas D. Oca, Alain Carrié, Achilleas Attilakos, Savas Ozer, Andreea Dumitrescu, Jürgen Merke, Urte Aliosaitiene, Evangelos Liberopoulos, Manuel O. De los Rios Ibarra, Maria J. Virtuoso, Alessandro Lupi, Panagiotis Anagnostis, Ruth Agar, Dorota Ferrieres, George Liamis, José Eduardo Krieger, Mariann Harangi, Fouzia Sadiq, Francois Schiele, Saif Kamal, Mária Audikovszky, Peter Baumgartner, Marta Gazzotti, Daniel Gaudet, Ashanty F. Ortega, Marcin Gruchała, Philippe Moulin, Ljiljana Popovic, Luca Bonanni, E. Kiouri, Mika Hori, Chiara Trenti, Elena Repetti, Carlo Sabbà, Sophie Bernard, Alejandro R. Zazueta, Mirac Vural, Jesus R. Gonzalez, C. Stevens, Francesca Carubbi, Wenhui Wen, Sabri Demircan, Kanika I. Dharmayat, Anne Tybjærg-Hansen, Elizabete Terauda, Claudia Zemmrich, Alphonsus Isara, Fabiola L. Sobrevilla, Anell Hernandez Garcia, Ibrahim Sisic, Justin T. I-Shing, Yvonne Winhofer-Stöckl, Luya Wang, Manfred Mayer, Mohanad Al-ageedi, Judith Wiener, Mohammed Al-Kindi, Anis Safura Ramli, Yan Chen, Denis Angoulvant, Aytekin Oguz, K.H. Wolmarans, Claudio Ferri, Tomáš Freiberger, Lubomira Cermakova, Julieta D.M. Portano, Pierre Henri Ducluzeau, Katerina Vonaskova, Levent H. Can, Mario H.F. Andrade, György Paragh, C. Ebenbichler, Karina J.A. Rivera, Alia Khudari, Elisabeth Steinhagen-Thiessen, Ana C. Alves, Victoria Korneva, Sandra Singh, Georgia Anastasiou, Nur S. Hamzan, Massimo Federici, Lale Tokgozoglu, Hector G. Alcala, Oana Moldovan, Giuseppe Mandraffino, Swarup A.V. Shah, Lukas Burda, Ersel Onrat, Manuel de los Reyes Barrera Bustillo, Mirjana Radovic, Arman Postadzhiyan, Nien-Tzu Chang, Aylin Yildirir, Martin Mäser, Bruno Fink, Svetlana Mosteoru, Ulrike Schatz, Luis A.V. Talavera, Magdalena Dusejovska, Richard Ceska, Faisal A. Al-Allaf, T.F. Ashavaid, Gereon Böll, Sona Machacova, Gonzalo C. Vargas, Antonio Gallo, Elina Pantchechnikova, Lukas Tichy, Gersina Rega-Kaun, Moses Elisaf, Branislav Vohnout, Antonio Bossi, Suad Al-Mukhaini, Natasa Rajkovic, Ursa Sustar, Merih Kutlu, Mohamed Sobhy, Britta Otte, Ana M. Medeiros, Borut Jug, Patrick Couture, Rodrigo Alonso, Wolfgang Seeger, Guzal J. Abdullaeva, Ahmet Celik, Nasreen Al-Sayed, Béla Benczúr, Petra E. Khoury, Rafezah Razali, Ma L.R. Osorio, Ruiying Zhang, Monica M.N. Usme, Humberto Garcia Aguilar, Ceyhun Ceyhan, Antje Spens, Christoph J. Binder, Volker Schrader, Terrance C.S. Jin, Neftali E.A. Villa, Aleksandra Michalska-Grzonkowska, Francesco Purrello, Marshima M. Rosli, Vincent Maher, Dilshad Rasul, Ines Colaço, Ornella Guardamagna, Giuliana Mombelli, Khalid F. AlHabib, Fahmi Alkaf, Marianne Benn, Youmna Ghaleb, Arsenio V. Vazquez, Lakshmi L. Reddy, Salih Kilic, Siti Hamimah Sheikh Abdul Kadir, E. Bilianou, Rossella Marcucci, Sandro Muntoni, Kurt Widhalm, Evangelos A. Zacharis, Kuznetsova T. Yu, Eric Bruckert, Antonia Sonntag, Katerina Rehouskova, Josè Pablo Werba, Leobardo Sauque-Reyna, Myra Tilney, Dov Gavishv, A.M. Fiorenza, Zdenka Krejsova, Hong A. Le, Andrey V. Susekov, Isabel Klein, Mai N.T. Nguyen, Andrejs Erglis, Muge Ildizli, Diane Brisson, Salmi Razali, Winfried März, Ovidio Muñiz-Grijalvo, Justyna Borowiec-Wolna, Ingrid Buganova, Ngoc T. Kim, Yue Wu, István Reiber, Jose C.A. Martinez, Pavel Malina, Sandy Elbitar, Stephan Matthias, Ali F. Abdalsahib, Zlatko Fras, Wilson E Sadoh, Lucas Kleemann, Tayfun Sahin, Martin P. Bogsrud, Fabio Pellegatta, Mohamed A. Shafy, Yuntao Li, Martine Paquette, Zuhier Awan, Arturo Pujia, Xiantao Song, Renata Cifkova, Alexandre C. Pereira, Ioannis Skoumas, Roman Cibulka, Tadej Battelino, Mariusz Gąsior, Ghada Kazamel, Lahore S.U. Shah, Eran Leitersdorf, Niki Katsiki, Daniel Elías-López, Khalid Al-Rasadi, Grete Talviste, Sarka Mala, Rocio M. Alvarado, Pavel Kraml, Gerret Paulsen, Angelina Passaro, Zsolt Karányi, Carine Ayoub, Vera Adamkova, Ivo Petrov, Turky H. Almigbal, Rohana Abdul Ghani, Franck Boccara, Brian W. McCrindle, François Martin, Jamshed J. Dalal, Shitong Cheng, Khalid Al-Waili, Chaoyi Zhang, Ramon M. Prado, Lubica Cibickova, Lubomira Fabryova, Tobias Wiesner, Thuhairah Hasrah Abdul Rahman, Tan J. Le, Marcello Arca, Sabine Scholl-Bürgi, Juan R. Saucedo, Georgijs Nesterovics, Carla V.M. Valencia, Alexander Stadelmann, Vasileios Kotsis, Lina Badimon, Shizuya Yamashita, Jose C.M. Oyervides, Lay K. Teh, Susanne Greber-Platzer, Marianne Abifadel, Ruta Meiere, Wibke Reinhard, Pablo Corral, Nina Schmidt, Alain Pradignac, A. David Marais, Marta Jordanova, Marzena Romanowska-Kocejko, Johannes Scholl, Brian Tomlinson, Laura G.G. Herrera, Loukianos S. Rallidis, Pedro Mata, Sameh Emil, Matej Mlinaric, Emile Ferrari, Suraya Abdul Razak, Alexandra Ershova, Andrie G. Panayiotou, Alinna Y.R. Garcia, Kairat Davletov, Katarina Lalic, Doan L. Do, Krzysztof Chlebus, Ricardo A. Carrera, Daniel I.P. Vazquez, Nikolaos Sakkas, Liyuan Xu, Mays Altaey, Aysa Hacioglu, Alexandro J. Martagon, Marta Żarczyńska-Buchowiecka, Michael Schömig, Jürgen Homberger, Andrea Benso, Bertrand Cariou, Ardon Rubinstein, Omer Gedikli, Emre Durakoglugil, Mei Chong, Bahadir Kirilmaz, Suhaila Abd Muid, Jose M. Salgado, Berenice P. Aparicio, Mutaz Alkhnifsawi, Bruno Vergès, Cécile Yelnik, Goreti Lobarinhas, Zaneta Petrulioniene, Sylvia Asenjo, Aytul B. Yildirim, László Bajnok, Vallejo-Vaz A.J., Stevens C.A.T., Lyons A.R.M., Dharmayat K.I., Freiberger T., Hovingh G.K., Mata P., Raal F.J., Santos R.D., Soran H., Watts G.F., Abifadel M., Aguilar-Salinas C.A., Alhabib K.F., Alkhnifsawi M., Almahmeed W., Alnouri F., Alonso R., Al-Rasadi K., Al-Sarraf A., Al-Sayed N., Araujo F., Ashavaid T.F., Banach M., Beliard S., Benn M., Binder C.J., Bogsrud M.P., Bourbon M., Chlebus K., Corral P., Davletov K., Descamps O.S., Durst R., Ezhov M., Gaita D., Genest J., Groselj U., Harada-Shiba M., Holven K.B., Kayikcioglu M., Khovidhunkit W., Lalic K., Latkovskis G., Laufs U., Liberopoulos E., Lima-Martinez M.M., Lin J., Maher V., Marais A.D., Marz W., Mirrakhimov E., Miserez A.R., Mitchenko O., Nawawi H., Nordestgaard B.G., Panayiotou A.G., Paragh G., Petrulioniene Z., Pojskic B., Postadzhiyan A., Raslova K., Reda A., Reiner, Sadiq F., Sadoh W.E., Schunkert H., Shek A.B., Stoll M., Stroes E., Su T.-C., Subramaniam T., Susekov A.V., Tilney M., Tomlinson 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Jiao J., Wu Y., Wen W., Xu L., Zhang R., Qu Y., He J., Fan X., Wang Z., Chow E., Pecin I., Perica D., Symeonides P., Vrablik M., Ceska R., Soska V., Tichy L., Adamkova V., Franekova J., Cifkova R., Kraml P., Vonaskova K., Cepova J., Dusejovska M., Pavlickova L., Blaha V., Rosolova H., Nussbaumerova B., Cibulka R., Vaverkova H., Cibickova L., Krejsova Z., Rehouskova K., Malina P., Budikova M., Palanova V., Solcova L., Lubasova A., Podzimkova H., Bujdak J., Vesely J., Jordanova M., Salek T., Urbanek R., Zemek S., Lacko J., Halamkova H., Machacova S., Mala S., Cubova E., Valoskova K., Burda L., Bendary A., Daoud I., Emil S., Elbahry A., Rafla S., Sanad O., Kazamel G., Ashraf M., Sobhy M., El-Hadidy A., Shafy M.A., Kamal S., Bendary M., Talviste G., Angoulvant D., Boccara F., Cariou B., Carreau V., Carrie A., Charrieres S., Cottin Y., Di-Fillipo M., Ducluzeau P.H., Dulong S., Durlach V., Farnier M., Ferrari E., Ferrieres D., Ferrieres J., Gallo A., hankard R., Inamo J., Lemale J., Moulin P., Paillard F., Peretti N., Perrin A., Pradignac A., Rabes J.P., Rigalleau V., Sultan A., Schiele F., Tounian P., Valero R., Verges B., Yelnik C., Ziegler O., Haack I.A., Schmidt N., Dressel A., Klein I., Christmann J., Sonntag A., Stumpp C., Boger D., Biedermann D., Usme M.M.N., Beil F.U., Klose G., Konig C., Gouni-Berthold I., Otte B., Boll G., Kirschbaum A., Merke J., Scholl J., Segiet T., Gebauer M., Predica F., Mayer M., Leistikow F., Fullgraf-Horst S., Muller C., Schuler M., Wiener J., Hein K., Baumgartner P., Kopf S., Busch R., Schomig M., Matthias S., Allendorf-Ostwald N., Fink B., Bohm D., Jakel A., Koschker A.-C., Schweizer R., Vogt A., Parhofer K., Konig W., Reinhard W., Bassler A., Stadelmann A., Schrader V., Katzmann J., Tarr A., Steinhagen-Thiessen E., Kassner U., Paulsen G., Homberger J., Zemmrich C., Seeger W., Biolik K., Deiss D., Richter C., Pantchechnikova E., Dorn E., Schatz U., Julius U., Spens A., Wiesner T., Scholl M., Rizos C.V., Sakkas N., Elisaf M., Skoumas I., Tziomalos K., Rallidis L., Kotsis V., Doumas M., Athyros V., Skalidis E., Kolovou G., Garoufi A., Bilianou E., Koutagiar I., Agapakis D., Kiouri E., Antza C., Katsiki N., Zacharis E., Attilakos A., Sfikas G., Koumaras C., Anagnostis P., Anastasiou G., Liamis G., Koutsogianni A.-D., Karanyi Z., Harangi M., Bajnok L., Audikovszky M., Mark L., Benczur B., Reiber I., Nagy G., Nagy A., Reddy L.L., Shah S.A.V., Ponde C.K., Dalal J.J., Sawhney J.P.S., Verma I.C., Altaey M., Al-Jumaily K., Rasul D., Abdalsahib A.F., Jabbar A.A., Al-ageedi M., Agar R., Cohen H., Ellis A., Gavishv D., Harats D., Henkin Y., Knobler H., Leavit L., Leitersdorf E., Rubinstein A., Schurr D., Shpitzen S., Szalat A., Casula M., Zampoleri V., Gazzotti M., Olmastroni E., Sarzani R., Ferri C., Repetti E., Sabba C., Bossi A.C., Borghi C., Muntoni S., Cipollone F., Purrello F., Pujia A., Passaro A., Marcucci R., Pecchioli V., Pisciotta L., Mandraffino G., Pellegatta F., Mombelli G., Branchi A., Fiorenza A.M., Pederiva 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B., Stoll, M., Stroes, E., Su, T. -C., Subramaniam, T., Susekov, A. V., Tilney, M., Tomlinson, B., Truong, T. H., Tselepis, A. D., Tybjaerg-Hansen, A., Vazquez Cardenas, A., Viigimaa, M., Wang, L., Yamashita, S., Kastelein, J. J. P., Bruckert, E., Vohnout, B., Schreier, L., Pang, J., Ebenbichler, C., Dieplinger, H., Innerhofer, R., Winhofer-Stockl, Y., Greber-Platzer, S., Krychtiuk, K., Speidl, W., Toplak, H., Widhalm, K., Stulnig, T., Huber, K., Hollerl, F., Rega-Kaun, G., Kleemann, L., Maser, M., Scholl-Burgi, S., Saly, C., Mayer, F. J., Sablon, G., Tarantino, E., Nzeyimana, C., Pojskic, L., Sisic, I., Nalbantic, A. D., Jannes, C. E., Pereira, A. C., Krieger, J. E., Petrov, I., Goudev, A., Nikolov, F., Tisheva, S., Yotov, Y., Tzvetkov, I., Baass, A., Bergeron, J., Bernard, S., Brisson, D., Brunham, L. R., Cermakova, L., Couture, P., Francis, G. A., Gaudet, D., Hegele, R. A., Khoury, E., Mancini, G. B. J., Mccrindle, B. W., Paquette, M., Ruel, I., Cuevas, A., Asenjo, S., Wang, X., Meng, K., Song, X., Yong, Q., Jiang, T., Liu, Z., Duan, Y., Hong, J., Ye, P., Chen, Y., Qi, J., Li, Y., Zhang, C., Peng, J., Yang, Y., Yu, W., Wang, Q., Yuan, H., Cheng, S., Jiang, L., Chong, M., Jiao, J., Wu, Y., Wen, W., Xu, L., Zhang, R., Qu, Y., He, J., Fan, X., Wang, Z., Chow, E., Pecin, I., Perica, D., Symeonides, P., Vrablik, M., Ceska, R., Soska, V., Tichy, L., Adamkova, V., Franekova, J., Cifkova, R., Kraml, P., Vonaskova, K., Cepova, J., Dusejovska, M., Pavlickova, L., Blaha, V., Rosolova, H., Nussbaumerova, B., Cibulka, R., Vaverkova, H., Cibickova, L., Krejsova, Z., Rehouskova, K., Malina, P., Budikova, M., Palanova, V., Solcova, L., Lubasova, A., Podzimkova, H., Bujdak, J., Vesely, J., Jordanova, M., Salek, T., Urbanek, R., Zemek, S., Lacko, J., Halamkova, H., Machacova, S., Mala, S., Cubova, E., Valoskova, K., Burda, L., Bendary, A., Daoud, I., Emil, S., Elbahry, A., Rafla, S., Sanad, O., Kazamel, G., Ashraf, M., Sobhy, M., El-Hadidy, A., Shafy, M. A., Kamal, S., Bendary, M., Talviste, G., Angoulvant, D., Boccara, F., Cariou, B., Carreau, V., Carrie, A., Charrieres, S., Cottin, Y., Di-Fillipo, M., Ducluzeau, P. H., Dulong, S., Durlach, V., Farnier, M., Ferrari, E., Ferrieres, D., Ferrieres, J., Gallo, A., Hankard, R., Inamo, J., Lemale, J., Moulin, P., Paillard, F., Peretti, N., Perrin, A., Pradignac, A., Rabes, J. P., Rigalleau, V., Sultan, A., Schiele, F., Tounian, P., Valero, R., Verges, B., Yelnik, C., Ziegler, O., Haack, I. A., Schmidt, N., Dressel, A., Klein, I., Christmann, J., Sonntag, A., Stumpp, C., Boger, D., Biedermann, D., Usme, M. M. N., Beil, F. U., Klose, G., Konig, C., Gouni-Berthold, I., Otte, B., Boll, G., Kirschbaum, A., Merke, J., Scholl, J., Segiet, T., Gebauer, M., Predica, F., Mayer, M., Leistikow, F., Fullgraf-Horst, S., Muller, C., Schuler, M., Wiener, J., Hein, K., Baumgartner, P., Kopf, S., Busch, R., Schomig, M., Matthias, S., Allendorf-Ostwald, N., Fink, B., Bohm, D., Jakel, A., Koschker, A. -C., Schweizer, R., Vogt, A., Parhofer, K., Konig, W., Reinhard, W., Bassler, A., Stadelmann, A., Schrader, V., Katzmann, J., Tarr, A., Steinhagen-Thiessen, E., Kassner, U., Paulsen, G., Homberger, J., Zemmrich, C., Seeger, W., Biolik, K., Deiss, D., Richter, C., Pantchechnikova, E., Dorn, E., Schatz, U., Julius, U., Spens, A., Wiesner, T., Scholl, M., Rizos, C. V., Sakkas, N., Elisaf, M., Skoumas, I., Tziomalos, K., Rallidis, L., Kotsis, V., Doumas, M., Athyros, V., Skalidis, E., Kolovou, G., Garoufi, A., Bilianou, E., Koutagiar, I., Agapakis, D., Kiouri, E., Antza, C., Katsiki, N., Zacharis, E., Attilakos, A., Sfikas, G., Koumaras, C., Anagnostis, P., Anastasiou, G., Liamis, G., Koutsogianni, A. -D., Karanyi, Z., Harangi, M., Bajnok, L., Audikovszky, M., Mark, L., Benczur, B., Reiber, I., Nagy, G., Nagy, A., Reddy, L. L., Shah, S. A. V., Ponde, C. K., Dalal, J. J., Sawhney, J. P. S., Verma, I. C., Altaey, M., Al-Jumaily, K., Rasul, D., Abdalsahib, A. F., Jabbar, A. A., Al-ageedi, M., Agar, R., Cohen, H., Ellis, A., Gavishv, D., Harats, D., Henkin, Y., Knobler, H., Leavit, L., Leitersdorf, E., Rubinstein, A., Schurr, D., Shpitzen, S., Szalat, A., Casula, M., Zampoleri, V., Gazzotti, M., Olmastroni, E., Sarzani, R., Ferri, C., Repetti, E., Sabba, C., Bossi, A. C., Borghi, C., Muntoni, S., Cipollone, F., Purrello, F., Pujia, A., Passaro, A., Marcucci, R., Pecchioli, V., Pisciotta, L., Mandraffino, G., Pellegatta, F., Mombelli, G., Branchi, A., Fiorenza, A. M., Pederiva, C., Werba, J. P., Parati, G., Carubbi, F., Iughetti, L., Iannuzzi, A., Iannuzzo, G., Calabro, P., Averna, M., Biasucci, G., Zambon, S., Roscini, A. R., Trenti, C., Arca, M., Federici, M., Del Ben, M., Bartuli, A., Giaccari, A., Pipolo, A., Citroni, N., Guardamagna, O., Bonomo, K., Benso, A., Biolo, G., Maroni, L., Lupi, A., Bonanni, L., Zenti, M. G., Matsuki, K., Hori, M., Ogura, M., Masuda, D., Kobayashi, T., Nagahama, K., Al-Jarallah, M., Radovic, M., Lunegova, O., Bektasheva, E., Khodzhiboboev, E., Erglis, A., Gilis, D., Nesterovics, G., Saripo, V., Meiere, R., Upena-RozeMicena, A., Terauda, E., Jambart, S., Khoury, P. E., Elbitar, S., Ayoub, C., Ghaleb, Y., Aliosaitiene, U., Kutkiene, S., Kasim, N. A. M., Nor, N. S. M., Ramli, A. S., Razak, S. A., Al-Khateeb, A., Kadir, S. H. S. A., Muid, S. A., Rahman, T. A., Kasim, S. S., Radzi, A. B. M., Ibrahim, K. S., Razali, S., Ismail, Z., Ghani, R. A., Hafidz, M. I. A., Chua, A. L., Rosli, M. M., Annamalai, M., Teh, L. K., Razali, R., Chua, Y. A., Rosman, A., Sanusi, A. R., Murad, N. A. A., Jamal, A. R. A., Nazli, S. A., Razman, A. Z., Rosman, N., Rahmat, R., Hamzan, N. S., Azzopardi, C., Mehta, R., Martagon, A. J., Ramirez, G. A. G., Villa, N. E. A., Vazquez, A. V., Elias-Lopez, D., Retana, G. G., Rodriguez, B., Macias, J. J. C., Zazueta, A. R., Alvarado, R. M., Portano, J. D. M., Lopez, H. A., Sauque-Reyna, L., Herrera, L. G. G., Mendia, L. E. S., Aguilar, H. G., Cooremans, E. R., Aparicio, B. P., Zubieta, V. M., Gonzalez, P. A. C., Ferreira-Hermosillo, A., Portilla, N. C., Dominguez, G. J., Garcia, A. Y. R., Cazares, H. E. A., Gonzalez, J. R., Valencia, C. V. M., Padilla, F. G., Prado, R. M., De los Rios Ibarra, M. O., Villicana, R. D. A., Rivera, K. J. A., Carrera, R. A., Alvarez, J. A., Martinez, J. C. A., de los Reyes Barrera Bustillo, M., Vargas, G. C., Chacon, R. C., Andrade, M. H. F., Ortega, A. F., Alcala, H. G., de Leon, L. E. G., Guzman, B. G., Garcia, J. J. G., Cuellar, J. C. G., Cruz, J. R. G., Garcia, A. H., Almada, J. R. H., Herrera, U. J., Sobrevilla, F. L., Rodriguez, E. M., Sibaja, C. M., Rodriguez, A. B. M., Oyervides, J. C. M., Vazquez, D. I. P., Rodriguez, E. A. R., Osorio, M. L. R., Saucedo, J. R., Tamayo, M. T., Talavera, L. A. V., Arroyo, L. E. V., Carrillo, E. A. Z., Isara, A., Obaseki, D. E., Al-Waili, K., Al-Zadjali, F., Al-Zakwani, I., Al-Kindi, M., Al-Mukhaini, S., Al-Barwani, H., Rana, A., Shah, L. S. U., Starostecka, E., Konopka, A., Lewek, J., Bartlomiejczyk, M., Gasior, M., Dyrbus, K., Jozwiak, J., Gruchala, M., Pajkowski, M., Romanowska-Kocejko, M., Zarczynska-Buchowiecka, M., Chmara, M., Wasag, B., Parczewska, A., Gilis-Malinowska, N., Borowiec-Wolna, J., Strozyk, A., Wos, M., Michalska-Grzonkowska, A., Medeiros, A. M., Alves, A. C., Silva, F., Lobarinhas, G., Palma, I., de Moura, J. P., Rico, M. T., Rato, Q., Pais, P., Correia, S., Moldovan, O., Virtuoso, M. J., Salgado, J. M., Colaco, I., Dumitrescu, A., Lengher, C., Mosteoru, S., Meshkov, A., Ershova, A., Rozkova, T., Korneva, V., Yu, K. T., Zafiraki, V., Voevoda, M., Gurevich, V., Duplyakov, D., Ragino, Y., Safarova, M., Shaposhnik, I., Alkaf, F., Khudari, A., Rwaili, N., Al-Allaf, F., Alghamdi, M., Batais, M. A., Almigbal, T. H., Kinsara, A., Alqudaimi, A. H. A., Awan, Z., Elamin, O. A., Altaradi, H., Rajkovic, N., Popovic, L., Singh, S., Stosic, L., Rasulic, I., Lalic, N. M., Lam, C., Le, T. J., Siang, E. L. T., Dissanayake, S., I-Shing, J. T., Shyong, T. E., Jin, T. C. S., Balinth, K., Buganova, I., Fabryova, L., Kadurova, M., Klabnik, A., Kozarova, M., Sirotiakova, J., Battelino, T., Kovac, J., Mlinaric, M., Sustar, U., Podkrajsek, K. T., Fras, Z., Jug, B., Cevc, M., Pilcher, G. J., Blom, D. J., Wolmarans, K. H., Brice, B. C., Muniz-Grijalvo, O., Diaz-Diaz, J. L., de Isla, L. P., Fuentes, F., Badimon, L., Martin, F., Lux, A., Chang, N. -T., Ganokroj, P., Akbulut, M., Alici, G., Bayram, F., Can, L. H., Celik, A., Ceyhan, C., Coskun, F. Y., Demir, M., Demircan, S., Dogan, V., Durakoglugil, E., Dural, I. E., Gedikli, O., Hacioglu, A., Ildizli, M., Kilic, S., Kirilmaz, B., Kutlu, M., Oguz, A., Ozdogan, O., Onrat, E., Ozer, S., Sabuncu, T., Sahin, T., Sivri, F., Sonmez, A., Temizhan, A., Topcu, S., Tuncez, A., Vural, M., Yenercag, M., Yesilbursa, D., Yigit, Z., Yildirim, A. B., Yildirir, A., Yilmaz, M. B., Atallah, B., Traina, M., Sabbour, H., Hay, D. A., Luqman, N., Elfatih, A., Abdulrasheed, A., Kwok, S., Oca, N. D., Reyes, X., Alieva, R. B., Kurbanov, R. D., Hoshimov, S. U., Nizamov, U. I., Ziyaeva, A. V., Abdullaeva, G. J., Do, D. L., Nguyen, M. N. T., Kim, N. T., Le, T. T., Le, H. A., Tokgozoglu, L., Catapano, A. L., Ray, K. K., and EAS Familial Hypercholesterolaemia Studies Collaboration (FHSC), Borghi C

Subjects
Male, Settore MED/09 - Medicina Interna, Arterial disease, Cross-sectional study, Adult population, Coronary Disease, Disease, Global Health, Medical and Health Sciences, Doenças Cardio e Cérebro-vasculares, Anticholesteremic Agent, Monoclonal, Prevalence, Registries, Familial Hypercholesterolemia, Humanized, Stroke, 11 Medical and Health Sciences, LS2_9, Studies Collaboration, Anticholesteremic Agents, General Medicine, Heart Disease Risk Factor, Middle Aged, FHSC global registry data, Europe, Treatment Outcome, Lower prevalence, Guidance, lipids (amino acids, peptides, and proteins), Female, Proprotein Convertase 9, Familial hypercholesterolaemia, Life Sciences & Biomedicine, Human, Adult, medicine.medical_specialty, Combination therapy, FHSC global registry, heterozygous familial hypercholesterolaemia, Cardiovascular risk factors, Antibodies, Monoclonal, Humanized, Insights, Antibodies, NO, Hyperlipoproteinemia Type II, Clinician, Medicine, General & Internal, Internal medicine, General & Internal Medicine, Health Sciences, medicine, Humans, EAS Familial Hypercholesterolaemia Studies Collaboration (FHSC), Cross-Sectional Studie, Science & Technology, Global Perspective, business.industry, Cholesterol, LDL, medicine.disease, Cross-Sectional Studies, Heart Disease Risk Factors, Hydroxymethylglutaryl-CoA Reductase Inhibitor, Hydroxymethylglutaryl-CoA Reductase Inhibitors, business
Abstract

Background The European Atherosclerosis Society Familial Hypercholesterolaemia Studies Collaboration (FHSC) global registry provides a platform for the global surveillance of familial hypercholesterolaemia through harmonisation and pooling of multinational data. In this study, we aimed to characterise the adult population with heterozygous familial hypercholesterolaemia and described how it is detected and managed globally. Methods Using FHSC global registry data, we did a cross-sectional assessment of adults (aged 18 years or older) with a clinical or genetic diagnosis of probable or definite heterozygous familial hypercholesterolaemia at the time they were entered into the registries. Data were assessed overall and by WHO regions, sex, and index versus non-index cases. Findings Of the 61 612 individuals in the registry, 42 167 adults (21 999 [53.6%] women) from 56 countries were included in the study. Of these, 31 798 (75.4%) were diagnosed with the Dutch Lipid Clinic Network criteria, and 35 490 (84.2%) were from the WHO region of Europe. Median age of participants at entry in the registry was 46.2 years (IQR 34.3-58.0); median age at diagnosis of familial hypercholesterolaemia was 44.4 years (32.5-56.5), with 40.2% of participants younger than 40 years when diagnosed. Prevalence of cardiovascular risk factors increased progressively with age and varied by WHO region. Prevalence of coronary disease was 17.4% (2.1% for stroke and 5.2% for peripheral artery disease), increasing with concentrations of untreated LDL cholesterol, and was about two times lower in women than in men. Among patients receiving lipid-lowering medications, 16 803 (81.1%) were receiving statins and 3691 (21.2%) were on combination therapy, with greater use of more potent lipid-lowering medication in men than in women. Median LDL cholesterol was 5.43 mmol/L (IQR 4.32-6.72) among patients not taking lipid-lowering medications and 4.23 mmol/L (3.20-5.66) among those taking them. Among patients taking lipid-lowering medications, 2.7% had LDL cholesterol lower than 1.8 mmol/L; the use of combination therapy, particularly with three drugs and with proprotein convertase subtilisin-kexin type 9 inhibitors, was associated with a higher proportion and greater odds of having LDL cholesterol lower than 1.8 mmol/L. Compared with index cases, patients who were non-index cases were younger, with lower LDL cholesterol and lower prevalence of cardiovascular risk factors and cardiovascular diseases (all p, Pfizer Independent Grant for Learning Change [16157823]; Amgen; Merck Sharp Dohme; Sanofi-Aventis; Daiichi Sankyo; Regeneron; National Institute for Health Research (NIHR) Imperial Biomedical Research Centre, UK; NIHR; Czech Ministry of Health [NU20-02-00261]; Canadian Institutes of Health Research; Austrian Heart Foundation; Tyrolean Regional Government; Gulf Heart Association, The EAS FHSC is an academic initiative that has received funding from a Pfizer Independent Grant for Learning & Change 2014 (16157823) and from investigator-initiated research grants to the European Atherosclerosis Society-Imperial College London from Amgen, Merck Sharp & Dohme, Sanofi-Aventis, Daiichi Sankyo, and Regeneron. KKR acknowledges support from the National Institute for Health Research (NIHR) Imperial Biomedical Research Centre, UK. KID acknowledges support from a PhD Studentship from NIHR under the Applied Health Research programme for Northwest London, UK (the views expressed in this publication are those of the authors and not necessarily those of the National Health Service, the NIHR, or the Department of Health). TF was supported by a grant from the Czech Ministry of Health (NU20-02-00261). JG receives support from the Canadian Institutes of Health Research. The Austrian Familial Hypercholesterolaemia registry has been supported by funds from the Austrian Heart Foundation and the Tyrolean Regional Government. The Gulf Familial Hypercholesterolaemia registry was done under the auspices of the Gulf Heart Association.

Published
2021

19. Loss of statin treatment years during pregnancy and breastfeeding periods in women with familial hypercholesterolemia

Author

Marianne Klevmoen, Martin P. Bogsrud, Kjetil Retterstøl, Tone Svilaas, Elisabeth K. Vesterbekkmo, Anders Hovland, Christ Berge, J.E. (Jeanine) Roeters van Lennep, Kirsten B. Holven, Marianne Klevmoen, Martin P. Bogsrud, Kjetil Retterstøl, Tone Svilaas, Elisabeth K. Vesterbekkmo, Anders Hovland, Christ Berge, J.E. (Jeanine) Roeters van Lennep, and Kirsten B. Holven

Abstract

Background and aims: Women with heterozygous familial hypercholesterolemia (FH) are recommended t

Published
2021
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20. Abstract 15749: Sex-differences in Coronary Heart Disease Between Individuals With Familial Hypercholesterolemia and Controls in Norway During 1992-2017

Author

Karianne Svendsen, Kirsten B. Holven, Kjetil Retterstøl, Trond P. Leren, Henriette Walaas Krogh, Martin P. Bogsrud, Jannicke Igland, Liv Mundal, and Grethe S. Tell

Subjects
medicine.medical_specialty, business.industry, Physiology (medical), Internal medicine, medicine, Familial hypercholesterolemia, Cardiology and Cardiovascular Medicine, medicine.disease, business, Coronary heart disease
Abstract

Introduction: During the last 30 years, treatment of familial hypercholesterolemia (FH) has been revolutionized, but it is not known if both sexes equally benefit in these advances, and whether this could have affected the sex difference in risk of coronary heart disease (CHD). We aimed to study sex difference in the risk of CHD between men and women with FH compared to non-FH men and women. Methods: We obtained data on CHD hospitalization and death from Norwegian health registries in 4,525 individuals diagnosed with FH between 1992 and 2014 and an age and sex matched control population of 88,892. The sex distribution was about 50/50 between women and men, and the mean age at start of follow-up was 36 years. Results: The cumulative incidence of CHD (FH vs. non-FH controls) in women and men are shown in Figure 1 with a clear increased risk in FH compared to controls. The cumulative incidence starts to increase at a younger age in men compared with women, both in FH and non-FH controls. This corresponds to an age adjusted 2.6-fold higher risk of CHD in men compared with women in both the FH and control population. In the FH population, men aged 20-39 years had a hazard ratio (HR) of 5.3 (95% CI: 2.6-10.9) compared with women, whereas the corresponding HR between women and men in non-FH controls was 3.7 (95% CI: 2.6-5.3). There was no significant interaction between sex and FH status, indicating that the excess risk in men was similar in FH and non-FH controls. Stratified by sex and adjusted for age, we found that both men and women with FH had a 2-fold higher risk of CHD than controls. The highest excess risk was observed in ages 20-30 years with a of HR= 4.5 (95% CI: 2.2-9.2) and a HR of= 5.5 (95%CI: 4.60-9.34) in women and men, respectively. Conclusions: The risk of CHD among individuals with FH was higher in men than in women in all age groups presented, with no differences between the FH sample and the non-FH controls. However, the relative risk in FH compared with controls was similar for both sexes.

Published
2020

21. Hyperlipidemia and cardiovascular disease with focus on familial hypercholesterolemia

Author

Stine Marie Ulven, Martin P. Bogsrud, and Kirsten B. Holven

Subjects
Adult, Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Familial hypercholesterolemia, Disease, 030204 cardiovascular system & hematology, Hyperlipoproteinemia Type II, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Internal medicine, Hyperlipidemia, Genetics, Medicine, Humans, 030212 general & internal medicine, Cholesterol metabolism, Molecular Biology, Focus (computing), Nutrition and Dietetics, business.industry, Cholesterol, Cell Biology, Middle Aged, medicine.disease, chemistry, Cardiovascular Diseases, Cardiology, Female, Cardiology and Cardiovascular Medicine, business
Published
2017

22. Lipidprofil ved lavkarbokosthold hos friske

Author

Kjetil Retterstøl, Martine Zakariassen Espeland, Ane Sørlie Kværner, Monica Baumann, and Martin P. Bogsrud

Subjects
Ldl cholesterol, medicine.medical_specialty, medicine.diagnostic_test, Cholesterol, business.industry, Saturated fat, Weight change, General Medicine, Carbohydrate, Individual risk, chemistry.chemical_compound, Endocrinology, Animal science, chemistry, Internal medicine, medicine, Lipid profile, business, Low carbohydrate
Abstract

BACKGROUND: Many Norwegians have embraced the low-carb trend and choose butter and bacon instead of brown bread and carrots. This entails a dramatic change in the total intake of fat and the intake of saturated fat. We have investigated how a low-carb diet can affect the lipid profile in healthy adults with a normal bodyweight. MATERIAL AND METHOD: Seven healthy female participants with normal bodyweight underwent a four-week trial of a low-carb diet (< 20-25 grams of carbohydrates/day). Daily diet registrations were made during the trial period, and diet data for three randomly selected days were included in the estimates. Blood samples and weight data were collected as fasting values prior to and after the intervention. RESULTS: Standardised diet data were available for six participants. On a low-carb diet, the energy intake from carbohydrates accounted for a median of 3 (spread: 2-5) per cent of the total energy intake. The intake of fat accounted for 71 (67-78) per cent of total energy, while protein accounted for 26 (19-31) of total energy intake. At baseline, the median value of total cholesterol was 4.1 mmol/L (dispersion: 3.3-5.7) and LDL cholesterol was 2.2 (1.8-3.4) mmol/L. The values increased to 5.2 (3.7-8.8) mmol/L and 3.1 (1.9-6.2) mmol/L for total and LDL cholesterol respectively. The absolute changes correspond to a percentage increase in total cholesterol of 33 (14-71)% and in LDL cholesterol of 41 (9-84)%. Median weight change amounted to -1.2 kg (-2.8-0.6). INTERPRETATION: A diet with little carbohydrate and a great deal of protein and fat resulted in a considerably heightened level of total cholesterol and LDL cholesterol in young, healthy women with a normal bodyweight. The findings indicate that a low-carb diet may have a negative impact on individual risk profiles. However, the study is small-scale and the results must be interpreted with caution.

Published
2013

23. Pooling and expanding registries of familial hypercholesterolaemia to assess gaps in care and improve disease management and outcomes: Rationale and design of the global EAS Familial Hypercholesterolaemia Studies Collaboration

Author

Della Cole, Hapizah Md Nawawi, Khalid Al-Rasadi, Børge G. Nordestgaard, Josip Car, Tomáš Freiberger, Asif Akram, Martin P. Bogsrud, Lourdes Ella G. Santos, Jie Lin, Branislav Vohnout, Olivier S. Descamps, Antonio J. Vallejo-Vaz, Frederick J. Raal, Alexandros D. Tselepis, G. Kees Hovingh, Fahad Alnouri, André R. Miserez, Belma Pojskic, Nan Lin, Handrean Soran, Ulrich Laufs, Gerald F. Watts, Olena Mitchenko, Zaneta Petrulioniene, Zlatko Fras, Amirhossein Sahebkar, Gustavs Latkovskis, Sreenivasa Rao Kondapally Seshasai, Pedro Mata, Lennart Nilsson, Abdullah Shehab, Erkin M. Mirrakhimov, Nelson Majano, Shizuya Yamashita, Andrey V. Susekov, Vincent Maher, Lixin Jiang, Dan Gaita, I.M. Gaspar, Alberico L. Catapano, Mariko Harada-Shiba, Brian Tomlinson, Marianne Abifadel, Pablo Corral, A. David Marais, Myra Tilney, Carlos A. Aguilar-Salinas, Maciej Banach, Meral Kayıkçıoğlu, Ronen Durst, J. Genest, Heribert Schunkert, M. Naceur Slimane, Željko Reiner, Winfried März, Marat V. Ezhov, Evangelos Liberopoulos, Ta-Chen Su, Kausik K. Ray, Mario Stoll, Mafalda Bourbon, Richard Ceska, Carolyn S.P. Lam, Hans Dieplinger, Rodrigo Alonso, Can T. Do, György Paragh, John J.P. Kastelein, Raul D. Santos, Eric Bruckert, Elisabeth Widen, Vascular Medicine, Ege Üniversitesi, Pfizer Incorporated, European Atherosclerosis Society, Institute for Molecular Medicine Finland, Elisabeth Ingrid Maria Widen / Principal Investigator, and Genomic Discoveries and Clinical Translation

Subjects
PREDICTION, International Cooperation, Pooling, Information Storage and Retrieval, Disease, 030204 cardiovascular system & hematology, GUIDELINES, Doenças Cardio e Cérebro-vasculares, LDL-Cholesterol, 0302 clinical medicine, Cardiovascular Disease, Medicine, Data Mining, Cardiac and Cardiovascular Systems, 030212 general & internal medicine, Registries, Disease management (health), Cooperative Behavior, GENERAL-POPULATION, RISK, Familial hypercholesterolaemia, Cardiovascular disease, Registry, Kardiologi, CONSENSUS PANEL, Delivery of Health Care, Integrated, General Medicine, Orvostudományok, PREVALENCE, 3. Good health, Treatment Outcome, CARDIOVASCULAR-DISEASE, Research Design, Cardiology and Cardiovascular Medicine, medicine.medical_specialty, Best practice, Klinikai orvostudományok, Access to Information, Hyperlipoproteinemia Type II, 03 medical and health sciences, EUROPEAN ATHEROSCLEROSIS SOCIETY, Internal Medicine, Humans, Organizational Objectives, Bespoke, Study Design, GUIDANCE, business.industry, Public health, Study design, Professional Practice Gaps, Data sharing, Clinical trial, Cardiovascular System & Hematology, 3121 General medicine, internal medicine and other clinical medicine, Family medicine, Familial Hypercholesterolaemia Studies Collaboration, Familial Hypercholesterolaemia, INDIVIDUAL PARTICIPANT DATA, business
Abstract

WOS: 000393031600001, PubMed ID: 27939304, Background: The potential for global collaborations to better inform public health policy regarding major non-hypercholesterolaemia (FH), a common genetic disorder associated with premature cardiovascular disease, is yet to be reliably ascertained using similar approaches. The European Atherosclerosis Society FH Studies Collaboration (EAS FHSC) is a new initiative of international stakeholders which will help establish a global FH registry to generate large-scale, robust data on the burden of FH worldwide. Methods: The EAS FHSC will maximise the potential exploitation of currently available and future FH data (retrospective and prospective) by bringing together regional/national/international data sources with access to individuals with a clinical and/or genetic diagnosis of heterozygous or homozygous FH. A novel bespoke electronic platform and FH Data Warehouse will be developed to allow secure data sharing, validation, cleaning, pooling, harmonisation and analysis irrespective of the source or format. Standard statistical procedures will allow us to investigate cross-sectional associations, patterns of real-world practice, trends over time, and analyse risk and outcomes (e.g. cardiovascular outcomes, all-cause death), accounting for potential confounders and subgroup effects. Conclusions: The EAS FHSC represents an excellent opportunity to integrate individual efforts across the world to tackle the global burden of FH. The information garnered from the registry will help reduce gaps in knowledge, inform best practices, assist in clinical trials design, support clinical guidelines and policies development, and ultimately improve the care of FH patients. (C) 2016 Elsevier Ireland Ltd., Pfizer Independent Grant for Learning Change [16157823]; AmgenAmgen; MSD; Sanofi-AventisSanofi-Aventis; Latvian State Research Programme BIOMEDICINE; Czech RepublicCzech Republic Government [MZ CR AZV 15-28277A, 16-29084A], The present project has received support from a Pfizer Independent Grant for Learning & Change 2014 (No: 16157823) and from investigator initiated unrestricted research grants to the European Atherosclerosis Society from Amgen, MSD, and Sanofi-Aventis. The project in Latvia was supported by the Latvian State Research Programme BIOMEDICINE. The project in Czech Republic was partly supported by grants MZ CR AZV 15-28277A and 16-29084A.

Published
2016

24. 3.2% OF YOUNG SUBJECTS UNDER 45 YEARS WITH ACUTE MYOCARDIAL INFARCTION HAVE GENETICALLY VERIFIED FAMILIAL HYPERCHOLESTEROLEMIA

Author

Trond P. Leren, Dan Atar, Martin P. Bogsrud, Linn Kristin Lie Øyri, Kirsten B. Holven, and Sigrun Halvorsen

Subjects
medicine.medical_specialty, business.industry, First myocardial infarction, Mean age, Early death, Norwegian, Disease, Familial hypercholesterolemia, medicine.disease, language.human_language, Increased risk, Internal medicine, language, medicine, Cardiology, lipids (amino acids, peptides, and proteins), Myocardial infarction, Cardiology and Cardiovascular Medicine, business
Abstract

Patients with familial hypercholesterolemia (FH) have increased total- and LDL-cholesterol levels and thus an increased risk of premature cardiovascular disease (CVD) and early death. Mean age of first myocardial infarction (MI) in Norwegian FH patients was recently shown to be 44 years. The aim of

Published
2018

25. Familial hypercholesterolaemia: A global call to arms

Author

Carolyn S.P. Lam, Evangelos Liberopoulos, Pedro Mata, Ta-Chen Su, John O'Donoghue, Elisabeth Widen, Amirhossein Sahebkar, Gustavs Latkovskis, Khalid Al-Rasadi, Olivier S. Descamps, John J.P. Kastelein, Gerald F. Watts, Tomáš Freiberger, I.M. Gaspar, Hans Dieplinger, Mariko Harada-Shiba, Handrean Soran, Rodrigo Alonso, Alberico L. Catapano, Della Cole, Meral Kayıkçıoğlu, Marianne Abifadel, Maciej Banach, J. Genest, Heribert Schunkert, Pablo Corral, Ronen Durst, Sreenivasa Rao Kondapally Seshasai, Martin P. Bogsrud, Antonio J. Vallejo-Vaz, Lixin Jiang, Frederick J. Raal, Josip Car, Børge G. Nordestgaard, Kausik K. Ray, Lennart Nilsson, Andrey V. Susekov, Ulrich Laufs, Raul D. Santos, Asif Akram, Mario Stoll, Mafalda Bourbon, Eric Bruckert, G. Kees Hovingh, Carlos A. Aguilar-Salinas, Abdulla Shehab, Fahad Alnouri, Pfizer Incorporated, ACS - Amsterdam Cardiovascular Sciences, and Vascular Medicine

Subjects
Pathology, Apolipoprotein B, Disease, 030204 cardiovascular system & hematology, medicine.disease_cause, Global Health, DISEASE, Doenças Cardio e Cérebro-vasculares, 0302 clinical medicine, Hyperlipoproteinemia Type II, Societies, Medical, RISK, 0303 health sciences, Mutation, biology, 3. Good health, PREVALENCE, Europe, lipids (amino acids, peptides, and proteins), Cardiology and Cardiovascular Medicine, Familial hypercholesterolaemia, Life Sciences & Biomedicine, medicine.medical_specialty, Heterozygote, 1102 Cardiovascular Medicine And Haematology, 03 medical and health sciences, Internal medicine, medicine, Humans, 030304 developmental biology, Science & Technology, business.industry, GUIDANCE, PCSK9, Heterozygote advantage, 1103 Clinical Sciences, Endocrinology, Peripheral Vascular Disease, Cardiovascular System & Hematology, Receptors, LDL, RECEPTORES DE LIPOPROTEÍNAS, Relative risk, biology.protein, Cardiovascular System & Cardiology, Familial Hypercholesterolaemia, business, CLINICIAN, Lipoprotein
Abstract

Familial Hypercholesterolaemia (FH) is the commonest autosomal co-dominantly inherited condition affecting man. It is caused by mutation in one of three genes, encoding the low-density lipoprotein (LDL) receptor, or the gene for apolipoprotein B (which is the major protein component of the LDL particle), or in the gene coding for PCSK9 (which is involved in the degradation of the LDL-receptor during its cellular recycling). These mutations result in impaired LDL metabolism, leading to life-long elevations in LDL-cholesterol (LDL-C) and development of premature atherosclerotic cardiovascular disease (ASCVD) [1], [2] and [3]. If left untreated, the relative risk of premature coronary artery disease is significantly higher in heterozygous patients than unaffected individuals, with most untreated homozygotes developing ASCVD before the age of 20 and generally not surviving past 30 years [2], [3], [4] and [5]. Although early detection and treatment with statins and other LDL-C lowering therapies can improve survival, FH remains widely underdiagnosed and undertreated [1], thereby representing a major global public health challenge.

Published
2015

28. Postprandial response after intake of saturated fat compared to polyunsaturated fat in subjects with familial hypercholesterolemia and normolipidemic controls-a randomized controlled trial

Author

Ingunn Narverud, Linn Kristin Lie Øyri, Marit B. Veierød, Lena Leder, Stine Marie Ulven, Magne Thoresen, Kirsten B. Holven, Martin P. Bogsrud, Patrik Hansson, Geir Florholmen, and Marte Gjeitung Byfuglien

Subjects
medicine.medical_specialty, business.industry, Saturated fat, Familial hypercholesterolemia, medicine.disease, law.invention, Polyunsaturated fat, Postprandial, Endocrinology, Randomized controlled trial, law, Internal medicine, medicine, Cardiology and Cardiovascular Medicine, business
Published
2017

29. UGT1A1*28 is associated with decreased systemic exposure of atorvastatin lactone

Author

Monica Hermann, Kjetil Retterstøl, Armin P. Piehler, Camilla Stormo, Marianne K. Kringen, Martin P. Bogsrud, and Anders Åsberg

Subjects
Adult, Male, Glucuronosyltransferase, Genotype, Metabolite, Atorvastatin, Glucuronidation, Pharmacology, chemistry.chemical_compound, Lactones, Pharmacokinetics, Muscular Diseases, Genetics, Medicine, Humans, Pyrroles, Alleles, Whole blood, chemistry.chemical_classification, Polymorphism, Genetic, biology, business.industry, Cholesterol, nutritional and metabolic diseases, General Medicine, Middle Aged, chemistry, Heptanoic Acids, biology.protein, Molecular Medicine, lipids (amino acids, peptides, and proteins), Female, business, Lactone, medicine.drug
Abstract

Atorvastatin is commonly used to reduce cholesterol. Atorvastatin acid is converted to its corresponding lactone form spontaneously or via glucuronidation mediated by uridine diphosphate glucuronosyltransferase (UGT) 1A1 and 1A3. Atorvastatin lactone is pharmacologically inactive, but is suspected to be muscle toxic and cause statin-induced myopathy (SIM). A several fold increase in systemic exposure of atorvastatin lactone has previously been observed in patients with SIM compared with healthy control subjects. In this study we aimed to investigate the association between polymorphisms in the UGT1A gene locus and plasma atorvastatin lactone levels. DNA was extracted from whole blood obtained from a previous pharmacokinetic study of patients carefully diagnosed as having true SIM (n = 13) and healthy control subjects (n = 15). The UGT1A1*28(TA) 7 , UGT1A3*2, UGT1A3*3, and UGT1A3*6 polymorphisms were detected by pyrosequencing. Carriers of the low-expression allele UGT1A1*28(TA) 7 tended to have lower levels of atorvastatin lactone (p

Published
2013

30. Exposure of atorvastatin is unchanged but lactone and acid metabolites are increased several-fold in patients with atorvastatin-induced myopathy

Author

Martin P. Bogsrud, Beata U. Mohebi, Espen Molden, Monica Hermann, Anders Åsberg, Kjetil Retterstøl, and Leiv Ose

Subjects
Adult, Male, Organic anion transporter 1, Side effect, Genotype, Metabolite, Atorvastatin, Organic Anion Transporters, Pharmacology, chemistry.chemical_compound, Lactones, Pharmacokinetics, Cytochrome P-450 Enzyme System, Muscular Diseases, medicine, Cytochrome P-450 CYP3A, Humans, Pharmacology (medical), Pyrroles, cardiovascular diseases, ATP Binding Cassette Transporter, Subfamily B, Member 1, Myopathy, Creatine Kinase, Aged, biology, Liver-Specific Organic Anion Transporter 1, Anticholesteremic Agents, nutritional and metabolic diseases, Middle Aged, chemistry, Liver, Heptanoic Acids, Case-Control Studies, Creatinine, biology.protein, lipids (amino acids, peptides, and proteins), Creatine kinase, Female, medicine.symptom, SLCO1B1, medicine.drug
Abstract

Background The most serious side effect from statin treatment is myopathy, which may proceed to rhabdomyolysis. This is the first study to investigate whether the pharmacokinetics of either atorvastatin or its metabolites, or both, is altered in patients with atorvastatin-related myopathy compared with healthy controls. Methods A 24-hour pharmacokinetic investigation was performed in 14 patients with atorvastatin-related myopathy. Relevant polymorphisms in SLCO1B1 (encoding organic anion transporting polypeptide 1B1), MDR1/ABCB1 (encoding P-glycoprotein), and CYP3A5 (encoding cytochrome P450 3A5) were determined. Data from 15 healthy volunteers were used as controls. Results No statistically significant difference in systemic exposure of atorvastatin was observed between the 2 groups. However, patients with atorvastatin-related myopathy had 2.4-fold and 3.1-fold higher systemic exposures of the metabolites atorvastatin lactone (P < .01) and p-hydroxyatorvastatin (P < .01), respectively, compared with controls. There were no differences in frequencies of SLCO1B1, MDR1, and CYP3A5 polymorphisms between the 2 groups. Conclusions This study disclosed a distinct difference in the pharmacokinetics of atorvastatin metabolites between patients with atorvastatin-related myopathy and healthy control subjects. These results are of importance in the further search for the mechanism of statin-induced myopathy. Clinical Pharmacology & Therapeutics (2006) 79, 532–539; doi: 10.1016/j.clpt.2006.02.014

Published
2005

31. M. Baumann og medarbeidere svarer

Author

Monica Baumann, Ane Sørlie Kværner, Martine Zakariassen Espeland, Martin P. Bogsrud, and Kjetil Retterstøl

Subjects
business.industry, Medicine, General Medicine, business
Published
2013

35. Flavonoids regulate LDLR through different mechanisms tied to their specific structures

Author

Katrine Bjune, Pia Skovholt Halvorsen, Helle Wangensteen, Trond P. Leren, Martin Prøven Bogsrud, and Thea Bismo Strøm

Subjects
polyphenols, antioxidants, structure, lipoproteins, cardiovascular disease, nutrition, Biochemistry, QD415-436
Abstract

Flavonoids, polyphenolic compounds found in plant-based diets, are associated with reduced risk of cardiovascular disease and longevity. These components are reported to reduce plasma levels of low-density lipoprotein (LDL) through an upregulation of the LDL receptor (LDLR), but the mechanism is still largely unknown. In this study, we have systematically screened the effect of 12 flavonoids from six different flavonoid subclasses on the effect on LDLR. This paper provides an in-depth analysis on how these flavonoids affect LDLR regulation and functionality. We found that most but not all of the tested flavonoids increased LDLR mRNA levels. Surprisingly, this increase was attributed to different regulatory mechanisms, such as enhanced LDLR promoter activity, LDLR mRNA stabilization, or LDLR protein stabilization, of which specific effectual parts of the flavonoid molecular structure could be assigned. These types of comparative analysis of various flavonoids enhance clarity and deepen the understanding of how the different structures of flavonoids affect LDLR regulation. Our data offer useful insights that may guide future research in developing therapeutic approaches for cardiovascular health.

Published
2024
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36. Functional characterization of missense variants affecting the extracellular domains of ABCA1 using a fluorescence-based assay

Author

Marianne Teigen, Åsa Schawlann Ølnes, Katrine Bjune, Trond P. Leren, Martin Prøven Bogsrud, and Thea Bismo Strøm

Subjects
HEK293 cells, Tangier disease, cholesterol efflux, BODIPY-cholesterol, HDL, ApoA1, Biochemistry, QD415-436
Abstract

Excess cholesterol originating from nonhepatic tissues is transported within HDL particles to the liver for metabolism and excretion. Cholesterol efflux is initiated by lipid-free or lipid-poor apolipoprotein A1 interacting with the transmembrane protein ABCA1, a key player in cholesterol homeostasis. Defective ABCA1 results in reduced serum levels of HDL cholesterol, deposition of cholesterol in arteries, and an increased risk of early onset CVD. Over 300 genetic variants in ABCA1 have been reported, many of which are associated with reduced HDL cholesterol levels. Only a few of these have been functionally characterized. In this study, we have analyzed 51 previously unclassified missense variants affecting the extracellular domains of ABCA1 using a sensitive, easy, and low-cost fluorescence-based assay. Among these, only 12 variants showed a distinct loss-of-function phenotype, asserting their direct association with severe HDL disorders. These findings emphasize the crucial role of functional characterization of genetic variants in pathogenicity assessment and precision medicine. The functional rescue of ABCA1 loss-of-function variants through proteasomal inhibition or by the use of the chemical chaperone 4-phenylbutyric acid was genotype specific. Genotype-specific responses were also observed for the ability of apolipoprotein A1 to stabilize the different ABCA1 variants. In view of personalized medicine, this could potentially form the basis for novel therapeutic strategies.

Published
2024
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37. The risk of various types of cardiovascular diseases in mutation positive familial hypercholesterolemia; a review

Author

Anders Hovland, Liv J. Mundal, Marit B. Veierød, Kirsten B. Holven, Martin Prøven Bogsrud, Grethe S. Tell, Trond P. Leren, and Kjetil Retterstøl

Subjects
familial hypecholesterolemia, ASCVD, LDL, cholesterol, statin (HMG-CoA reductase inhibitor), aortic valve stenosis, Genetics, QH426-470
Abstract

Familial hypercholesterolemia (FH) is a common, inherited disease characterized by high levels of low-density lipoprotein Cholesterol (LDL-C) from birth. Any diseases associated with increased LDL-C levels including atherosclerotic cardiovascular diseases (ASCVDs) would be expected to be overrepresented among FH patients. There are several clinical scoring systems aiming to diagnose FH, however; most individuals who meet the clinical criteria for a FH diagnosis do not have a mutation causing FH. In this review, we aim to summarize the literature on the risk for the various forms of ASCVD in subjects with a proven FH-mutation (FH+). We searched for studies on FH+ and cardiovascular diseases and also included our and other groups published papers on FH + on a wide range of cardiovascular and other diseases of the heart and vessels. FH + patients are at a markedly increased risk of a broad range of ASCVD. Acute myocardial infarction (AMI) is the most common in absolute numbers, but also aortic valve stenosis is by far associated with the highest excess risk. Per thousand patients, we observed 3.6 incident AMI per year compared to 1.9 incident aortic valve stenosis, however, standardized incidence ratio (SIR) for incident AMI was 2.3 compared to 7.9 for incident aortic valve stenosis. Further, occurrence of ischemic stroke seems not to be associated with increased risk in FH+. Clinicians should be aware of the excess risk of almost all kind of ASCVD in FH+, and the neutral risk of stroke need to be studied further in FH + patients.

Published
2022
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