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1. Obicetrapib on top of maximally tolerated lipid‐modifying therapies in participants with or at high risk for atherosclerotic cardiovascular disease: rationale and designs of BROADWAY and BROOKLYN

Author

Nicholls, Stephen J., Nelson, Adam J., Ditmarsch, Marc, Kastelein, John J.P., Ballantyne, Christie M., Ray, Kausik K., Navar, Ann Marie, Nissen, Steven E., Golberg, Anne C., Brunham, Liam R., Curcio, Danielle, Wuerdeman, Erin, Neild, Annie, Kling, Douglas, Hsieh, Andrew, Dicklin, Mary R., Ference, Brian A., Laufs, Ulrich, Banach, Maciej, Mehran, Roxana, Catapano, Alberico L., and Davidson, Michael H.

Published
2024
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2. World Heart Federation Cholesterol Roadmap 2022

Author

Ray, Kausik K, Ference, Brian A, Séverin, Tania, Blom, Dirk, Nicholls, Stephen J, Shiba, Mariko H, Almahmeed, Wael, Alonso, Rodrigo, Daccord, Magdalena, Ezhov, Marat, Olmo, Rosa Fernández, Jankowski, Piotr, Lanas, Fernando, Mehta, Roopa, Puri, Raman, Wong, Nathan D, Wood, David, Zhao, Dong, Gidding, Samuel S, Virani, Salim S, Lloyd-Jones, Donald, Pinto, Fausto, Perel, Pablo, and Santos, Raul D

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Heart Disease, Health Services, Patient Safety, Prevention, Atherosclerosis, Cardiovascular, Clinical Research, Heart Disease - Coronary Heart Disease, Good Health and Well Being, Humans, Cholesterol, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Dyslipidemias, Lipoproteins, Apolipoproteins B, Cardiovascular Diseases, cholesterol, low-density lipoprotein cholesterol prevention, ASCVD, lipid lowering therapy, familial hypercholesterolaemia, Cardiorespiratory Medicine and Haematology, Cardiovascular medicine and haematology
Abstract

BackgroundAtherosclerotic cardiovascular diseases (ASCVD) including myocardial infarction, stroke and peripheral arterial disease continue to be major causes of premature death, disability and healthcare expenditure globally. Preventing the accumulation of cholesterol-containing atherogenic lipoproteins in the vessel wall is central to any healthcare strategy to prevent ASCVD. Advances in current concepts about reducing cumulative exposure to apolipoprotein B (apo B) cholesterol-containing lipoproteins and the emergence of novel therapies provide new opportunities to better prevent ASCVD. The present update of the World Heart Federation Cholesterol Roadmap provides a conceptual framework for the development of national policies and health systems approaches, so that potential roadblocks to cholesterol management and thus ASCVD prevention can be overcome.MethodsThrough a review of published guidelines and research papers since 2017, and consultation with a committee composed of experts in clinical management of dyslipidaemias and health systems research in low-and-middle income countries (LMICs), this Roadmap identifies (1) key principles to effective ASCVD prevention (2) gaps in implementation of these interventions (knowledge-practice gaps); (3) health system roadblocks to treatment of elevated cholesterol in LMICs; and (4) potential strategies for overcoming these.ResultsReducing the future burden of ASCVD will require diverse approaches throughout the life-course. These include: a greater focus on primordial prevention; availability of affordable cholesterol testing; availability of universal cholesterol screening for inherited dyslipidaemias; risk stratification moving beyond 10-year risk to look at lifetime risk with adequate risk estimators; wider availability of affordable cholesterol-lowering therapies which should include statins as essential medications globally; use of adequate doses of potent statin regimens; and combination therapies with ezetimibe or other therapies in order to attain and maintain robust reductions in LDL-C in those at highest risk. Continuing efforts are needed on health literacy for both the public and healthcare providers, utilising multi-disciplinary teams in healthcare and applications that quantify both ASCVD risk and benefits of treatment as well as increased adherence to therapies.ConclusionsThe adverse effects of LDL-cholesterol and apo B containing lipoprotein exposure are cumulative and result in ASCVD. These are preventable by implementation of different strategies, aimed at efficiently tackling atherosclerosis at different stages throughout the human life-course. Preventive strategies should therefore be updated to implement health policy, lifestyle changes and when needed pharmacotherapies earlier with investment in, and a shift in focus towards, early preventive strategies that preserve cardiovascular health rather than treat the consequences of ASCVD.

Published
2022

3. Frequent questions and responses on the 2022 lipoprotein(a) consensus statement of the European Atherosclerosis Society

Author

Kronenberg, Florian, Mora, Samia, Stroes, Erik S.G., Ference, Brian A., Arsenault, Benoit J., Berglund, Lars, Dweck, Marc R., Koschinsky, Marlys L., Lambert, Gilles, Mach, François, McNeal, Catherine J., Moriarty, Patrick M., Natarajan, Pradeep, Nordestgaard, Børge G., Parhofer, Klaus G., Virani, Salim S., von Eckardstein, Arnold, Watts, Gerald F., Stock, Jane K., Ray, Kausik K., Tokgözoğlu, Lale S., and Catapano, Alberico L.

Published
2023
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5. Neural network-based integration of polygenic and clinical information: development and validation of a prediction model for 10-year risk of major adverse cardiac events in the UK Biobank cohort

Author

Steinfeldt, Jakob, Buergel, Thore, Loock, Lukas, Kittner, Paul, Ruyoga, Greg, zu Belzen, Julius Upmeier, Sasse, Simon, Strangalies, Henrik, Christmann, Lara, Hollmann, Noah, Wolf, Benedict, Ference, Brian, Deanfield, John, Landmesser, Ulf, and Eils, Roland

Published
2022
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9. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel

Author

Ference, Brian A, Ginsberg, Henry N, Graham, Ian, Ray, Kausik K, Packard, Chris J, Bruckert, Eric, Hegele, Robert A, Krauss, Ronald M, Raal, Frederick J, Schunkert, Heribert, Watts, Gerald F, Borén, Jan, Fazio, Sergio, Horton, Jay D, Masana, Luis, Nicholls, Stephen J, Nordestgaard, Børge G, van de Sluis, Bart, Taskinen, Marja-Riitta, Tokgözoğlu, Lale, Landmesser, Ulf, Laufs, Ulrich, Wiklund, Olov, Stock, Jane K, Chapman, M John, and Catapano, Alberico L

Subjects
Cardiovascular, Atherosclerosis, Clinical Trials and Supportive Activities, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Anticholesteremic Agents, Cholesterol, HDL, Cholesterol, LDL, Consensus, Epidemiologic Methods, Ezetimibe, Genetic Predisposition to Disease, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hyperlipidemias, Lipoproteins, LDL, PCSK9 Inhibitors, Cardiovascular disease, Causality, Clinical trials, Low-density lipoprotein, Mendelian randomization, PCSK9, Recommendations, Statin, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology
Abstract

AimsTo appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD).Methods and resultsWe assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects.ConclusionConsistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.

Published
2017

11. Cardiovascular Effects of Exposure to Cigarette Smoke and Electronic Cigarettes Clinical Perspectives From the Prevention of Cardiovascular Disease Section Leadership Council and Early Career Councils of the American College of Cardiology

Author

Morris, Pamela B, Ference, Brian A, Jahangir, Eiman, Feldman, Dmitriy N, Ryan, John J, Bahrami, Hossein, El-Chami, Mikhael F, Bhakta, Shyam, Winchester, David E, Al-Mallah, Mouaz H, Shields, Monica Sanchez, Deedwania, Prakash, Mehta, Laxmi S, Phan, Binh An P, and Benowitz, Neal L

Subjects
atherogenesis, genetic and epigenetic effects, smoke-free legislation, thrombosis, tobacco cessation, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology
Published
2015

12. 2019 ESC/EAS guidelines for the management of dyslipidaemias: Lipid modification to reduce cardiovascular risk

Author

Mach, François, Baigent, Colin, Catapano, Alberico L., Koskinas, Konstantinos C., Casula, Manuela, Badimon, Lina, Chapman, M. John, De Backer, Guy G., Delgado, Victoria, Ference, Brian A., Graham, Ian M., Halliday, Alison, Landmesser, Ulf, Mihaylova, Borislava, Pedersen, Terje R., Riccardi, Gabriele, Richter, Dimitrios J., Sabatine, Marc S., Taskinen, Marja-Riitta, Tokgozoglu, Lale, Wiklund, Olov, Windecker, Stephan, Aboyans, Victor, Collet, Jean-Philippe, Dean, Veronica, Fitzsimons, Donna, Gale, Chris P., Grobbee, Diederick, Halvorsen, Sigrun, Hindricks, Gerhard, Iung, Bernard, Jüni, Peter, Katus, Hugo A., Leclercq, Christophe, Lettino, Maddalena, Lewis, Basil S., Merkely, Bela, Mueller, Christian, Petersen, Steffen, Petronio, Anna Sonia, Roffi, Marco, Shlyakhto, Evgeny, Simpson, Iain A., Sousa-Uva, Miguel, Touyz, Rhian M., Nibouche, Djamaleddine, Zelveian, Parounak H., Siostrzonek, Peter, Najafov, Ruslan, van de Borne, Philippe, Pojskic, Belma, Postadzhiyan, Arman, Kypris, Lambros, Špinar, Jindřich, Larsen, Mogens Lytken, Eldin, Hesham Salah, Viigimaa, Margus, Strandberg, Timo E., Ferrières, Jean, Agladze, Rusudan, Laufs, Ulrich, Rallidis, Loukianos, Bajnok, László, Gudjónsson, Thorbjörn, Maher, Vincent, Henkin, Yaakov, Gulizia, Michele Massimo, Mussagaliyeva, Aisulu, Bajraktari, Gani, Kerimkulova, Alina, Latkovskis, Gustavs, Hamoui, Omar, Slapikas, Rimvydas, Visser, Laurent, Dingli, Philip, Ivanov, Victoria, Boskovic, Aneta, Nazzi, Mbarek, Visseren, Frank, Mitevska, Irena, Retterstøl, Kjetil, Jankowski, Piotr, Fontes-Carvalho, Ricardo, Gaita, Dan, Ezhov, Marat, Foscoli, Marina, Giga, Vojislav, Pella, Daniel, Fras, Zlatko, Perez de Isla, Leopoldo, Hagström, Emil, Lehmann, Roger, Abid, Leila, Ozdogan, Oner, Mitchenko, Olena, and Patel, Riyaz S.

Published
2019
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15. Exploring apolipoprotein C-III: pathophysiological and pharmacological relevance.

Author

Packard, Chris J, Pirillo, Angela, Tsimikas, Sotirios, Ference, Brian A, and Catapano, Alberico L

Subjects
APOLIPOPROTEIN C, LIPOPROTEIN lipase, BLOOD lipids, CARDIOVASCULAR diseases, SMALL interfering RNA, LIPOPROTEINS, FILAGGRIN, LDL cholesterol
Abstract

The availability of pharmacological approaches able to effectively reduce circulating LDL cholesterol (LDL-C) has led to a substantial reduction in the risk of atherosclerosis-related cardiovascular disease (CVD). However, a residual cardiovascular (CV) risk persists in treated individuals with optimal levels of LDL-C. Additional risk factors beyond LDL-C are involved, and among these, elevated levels of triglycerides (TGs) and TG-rich lipoproteins are causally associated with an increased CV risk. Apolipoprotein C-III (apoC-III) is a key regulator of TG metabolism and hence circulating levels through several mechanisms including the inhibition of lipoprotein lipase activity and alterations in the affinity of apoC-III-containing lipoproteins for both the hepatic receptors involved in their removal and extracellular matrix in the arterial wall. Genetic studies have clarified the role of apoC-III in humans, establishing a causal link with CVD and showing that loss-of-function mutations in the APOC3 gene are associated with reduced TG levels and reduced risk of coronary heart disease. Currently available hypolipidaemic drugs can reduce TG levels, although to a limited extent. Substantial reductions in TG levels can be obtained with new drugs that target specifically apoC-III; these include two antisense oligonucleotides, one small interfering RNA and an antibody. [ABSTRACT FROM AUTHOR]

Published
2023
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19. From the EAS:* frequent questions and responses on the 2022 lipoprotein(a) consensus statement of the European Atherosclerosis Society

Author

Kronenberg, Florian, primary, Mora, Samia, additional, Stroes, Erik S.G., additional, Ference, Brian A., additional, Arsenault, Benoit J., additional, Berglund, Lars, additional, Dweck, Marc R., additional, Koschinsky, Marlys L., additional, Lambert, Gilles, additional, Mach, François, additional, McNeal, Catherine J., additional, Moriarty, Patrick M., additional, Natarajan, Pradeep, additional, Nordestgaard, Børge G., additional, Parhofer, Klaus G., additional, Virani, Salim S., additional, von Eckardstein, Arnold, additional, Watts, Gerald F., additional, Stock, Jane K., additional, Ray, Kausik K., additional, Tokgözoğlu, Lale S., additional, and Catapano, Alberico L., additional

Published
2023
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20. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement

Author

Kronenberg, Florian, Mora, Samia, Stroes, Erik S G, Ference, Brian A, Arsenault, Benoit J, Berglund, Lars, Dweck, Marc R, Koschinsky, Marlys, Lambert, Gilles, Mach, François, McNeal, Catherine J, Moriarty, Patrick M, Natarajan, Pradeep, Nordestgaard, Børge G, Parhofer, Klaus G, Virani, Salim S, von Eckardstein, Arnold, Watts, Gerald F, Stock, Jane K, Ray, Kausik K, Tokgözoğlu, Lale S, Catapano, Alberico L, University of Zurich, Experimental Vascular Medicine, Vascular Medicine, and ACS - Atherosclerosis & ischemic syndromes

Subjects
Adult, Consensus, Aortic stenosis, Testing, Calcinosis, 610 Medicine & health, Aortic Valve Stenosis, Cholesterol, LDL, Cardiovascular risk, Atherosclerosis, 2705 Cardiology and Cardiovascular Medicine, Model of care, Treatment, Cardiovascular Diseases, Risk Factors, Clinical guidance, 540 Chemistry, Humans, Cardiology and Cardiovascular Medicine, 10038 Institute of Clinical Chemistry, Lipoprotein(a)
Abstract

This 2022 European Atherosclerosis Society lipoprotein(a) [Lp(a)] consensus statement updates evidence for the role of Lp(a) in atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis, provides clinical guidance for testing and treating elevated Lp(a) levels, and considers its inclusion in global risk estimation. Epidemiologic and genetic studies involving hundreds of thousands of individuals strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes in different ethnicities; elevated Lp(a) is a risk factor even at very low levels of low-density lipoprotein cholesterol. High Lp(a) is associated with both microcalcification and macrocalcification of the aortic valve. Current findings do not support Lp(a) as a risk factor for venous thrombotic events and impaired fibrinolysis. Very low Lp(a) levels may associate with increased risk of diabetes mellitus meriting further study. Lp(a) has pro-inflammatory and pro-atherosclerotic properties, which may partly relate to the oxidized phospholipids carried by Lp(a). This panel recommends testing Lp(a) concentration at least once in adults; cascade testing has potential value in familial hypercholesterolaemia, or with family or personal history of (very) high Lp(a) or premature ASCVD. Without specific Lp(a)-lowering therapies, early intensive risk factor management is recommended, targeted according to global cardiovascular risk and Lp(a) level. Lipoprotein apheresis is an option for very high Lp(a) with progressive cardiovascular disease despite optimal management of risk factors. In conclusion, this statement reinforces evidence for Lp(a) as a causal risk factor for cardiovascular outcomes. Trials of specific Lp(a)-lowering treatments are critical to confirm clinical benefit for cardiovascular disease and aortic valve stenosis.

Published
2022

25. The time is now: Achieving FH paediatric screening across Europe - The Prague Declaration

Author

Bedlington, Nicole, Abifadel, Marianne, Beger, Birgit, Bourbon, Mafalda, Bueno, Héctor, Ceska, Richard, Cillíková, Kristýna, Cimická, Zdenka, Daccord, Magdalena, Beaufort, Carine de, Dharmayat, Kanika I., Ference, Brian A., Freiberger, Tomáš, Geanta, Marius, Gidding, Samuel S., Grošelj, Urh, Halle, Martin, Johnson, Neil, Novakovic, Tanja, Májek, Ondrej, Pallidis, Athanasios, Peretti, Noel, Pinto, Fausto J., Ray, Kausik Kosh, Rees, Bleddyn, Reeve, John, Reiner, Željko, Santos, Raul D., Schunkert, Heribert, Šikonja, Jaka, Sokolovic, Milka, Tokgözoglu, Lale, Vrablík, Michal, Wiegman, Albert, and Gutiérrez-Ibarluzea, Iñaki

Subjects
Declaration, FH, Doenças Cardio e Cérebro-vasculares, children, prevention, cardiovascular disease, EU best practice, Cardiovascular Disease, declaration, implementation, Children, Cardiovascular Health, Prevention, CVD, CVH, EU, Europe, cardiovascular health, familial hypercholesterolaemia, health systems, public health, screening, EU Best Practice, ddc: 610, Implementation, Screening, Public Health, Health Systems, Familial Hypercholesterolaemia
Abstract

Familial hypercholesterolaemia (FH) is the most common inherited metabolic disorder characterized by high cholesterol and if left untreated leads to premature cardiovascular disease, such as heart attacks. Treatment that begins early in life, particularly in childhood, is highly efficacious in preventing cardiovascular disease and cost-effective, thus early detection of FH is crucial. However, in Europe, less than 10% of people living with FH are diagnosed and even less receive life-saving treatment. The Prague Declaration is a call to action for national and European Union policymakers and decision-makers and a result of the Czech EU Presidency meeting on FH Paediatric Screening (early detection of inherited high cholesterol) at the Czech Senate in Prague on 6th September 2022. It builds on a considerable body of evidence which was discussed at the Technical Meeting under the auspices of the Slovenian EU Presidency in October 2021. The Prague meeting addressed the outstanding barriers to the systematic implementation of FH paediatric screening across Europe. In this article, we present the key points from the Prague meeting and concrete actions needed to move forward.

Published
2022

30. Association of Apolipoprotein B–Containing Lipoproteins and Risk of Myocardial Infarction in Individuals With and Without Atherosclerosis

Author

Marston, Nicholas A., primary, Giugliano, Robert P., additional, Melloni, Giorgio E. M., additional, Park, Jeong-Gun, additional, Morrill, Valerie, additional, Blazing, Michael A., additional, Ference, Brian, additional, Stein, Evan, additional, Stroes, Erik S., additional, Braunwald, Eugene, additional, Ellinor, Patrick T., additional, Lubitz, Steven A., additional, Ruff, Christian T., additional, and Sabatine, Marc S., additional

Published
2022
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32. Asian Pacific Society of Cardiology Consensus Recommendations on Dyslipidaemia

Author

Koh, Natalie, primary, Ference, Brian A, additional, Nicholls, Stephen J, additional, Navar, Ann Marie, additional, Chew, Derek P, additional, Kostner, Karam, additional, He, Ben, additional, Tse, Hung Fat, additional, Dalal, Jamshed, additional, Santoso, Anwar, additional, Ako, Junya, additional, Tada, Hayato, additional, Park, Jin Joo, additional, Ong, Mei Lin, additional, Lim, Eric, additional, Subramaniam, Tavin, additional, Li, Yi-Heng, additional, Phrommintikul, Arintaya, additional, Iyengar, SS, additional, Ray, Saumitra, additional, Park, Kyung Woo, additional, Tan, Hong Chang, additional, Chunhamaneewat, Narathip, additional, Yeo, Khung Keong, additional, and Tan, Jack Wei Chieh, additional

Published
2021
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35. Population genomic screening of young adults for familial hypercholesterolaemia: a cost-effectiveness analysis

Author

Marquina, Clara, primary, Lacaze, Paul, additional, Tiller, Jane, additional, Riaz, Moeen, additional, Sturm, Amy C, additional, Nelson, Mark R, additional, Ference, Brian A, additional, Pang, Jing, additional, Watts, Gerald F, additional, Nicholls, Stephen J, additional, Zoungas, Sophia, additional, Liew, Danny, additional, McNeil, John, additional, and Ademi, Zanfina, additional

Published
2021
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36. Triglyceride-rich lipoproteins and their remnants: metabolic insights, role in atherosclerotic cardiovascular disease, and emerging therapeutic strategies—a consensus statement from the European Atherosclerosis Society

Author

Ginsberg, Henry N, primary, Packard, Chris J, additional, Chapman, M John, additional, Borén, Jan, additional, Aguilar-Salinas, Carlos A, additional, Averna, Maurizio, additional, Ference, Brian A, additional, Gaudet, Daniel, additional, Hegele, Robert A, additional, Kersten, Sander, additional, Lewis, Gary F, additional, Lichtenstein, Alice H, additional, Moulin, Philippe, additional, Nordestgaard, Børge G, additional, Remaley, Alan T, additional, Staels, Bart, additional, Stroes, Erik S G, additional, Taskinen, Marja-Riitta, additional, Tokgözoğlu, Lale S, additional, Tybjaerg-Hansen, Anne, additional, Stock, Jane K, additional, and Catapano, Alberico L, additional

Published
2021
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38. New Way to "SCORE" Risk: Updates on the ESC Scoring System and Incorporation into ESC Cardiovascular Prevention Guidelines.

Author

Graham, Ian M., Di Angelantonio, Emanuele, Huculeci, Radu, on behalf of the European Society of Cardiology's Cardiovascular Risk Collaboration (CRC), De Bacquer, Dirk, Ference, Brian, Halle, Martin, McEvoy, John, Timmis, Adam, Vardas, Panos, and Visseren, Frank

Abstract

Purpose of Review: Prior European Society of Cardiology (ESC) guidelines endorsed the SCORE 10-year cardiovascular disease (CVD) risk calculator to inform the total risk approach to CVD prevention, including the use of preventive interventions like lipid lowering therapies. However, SCORE was released in 2003, did not allow for estimation of fatal and non-fatal CVD events, and was limited to adults aged 40 to 70 years. The ESC's Cardiovascular Risk Collaboration (CRC) was tasked with updating SCORE (SCORE2) and with extending the upper age range of adults eligible for risk estimation (SCORE2-OP). This review summarises these two deliverables. Recent Findings: Published in 2021, these updated risk scores allow for estimation of 10 year total (fatal + non-fatal) risks of a first atherosclerotic cardiovascular event in adults (SCORE2) and older persons (SCORE2-OP), calibrated for use in four European risk regions. The models account for competing risk of non-CVD death. These were extensively validated with excellent calibration and C-statistics ranging from 0.67 to 0.81. Summary: SCORE2 and SCORE2-OP have informed the 2021 ESC Guidelines on cardiovascular disease prevention in clinical practice. In addition to endorsing these two updated risk calculators, these guidelines have, for the first time, recommended the use of age-related risk categories. This change was motivated to prevent overreliance on age when making CVD prevention decisions. [ABSTRACT FROM AUTHOR]

Published
2022
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39. Population genomic screening of young adults for familial hypercholesterolaemia: a cost-effectiveness analysis.

Author

Marquina, Clara, Lacaze, Paul, Tiller, Jane, Riaz, Moeen, Sturm, Amy C, Nelson, Mark R, Ference, Brian A, Pang, Jing, Watts, Gerald F, Nicholls, Stephen J, Zoungas, Sophia, Liew, Danny, McNeil, John, and Ademi, Zanfina

Subjects
YOUNG adults, MEDICAL screening, FAMILIAL hypercholesterolemia, GENETIC testing, QUALITY-adjusted life years, COST effectiveness, MEDICAL care costs
Abstract

Aims The aim of this study was to assess the impact and cost-effectiveness of offering population genomic screening to all young adults in Australia to detect heterozygous familial hypercholesterolaemia (FH). Methods and results We designed a decision analytic Markov model to compare the current standard of care for heterozygous FH diagnosis in Australia (opportunistic cholesterol screening and genetic cascade testing) with the alternate strategy of population genomic screening of adults aged 18–40 years to detect pathogenic variants in the LDLR/APOB/PCSK9 genes. We used a validated cost-adaptation method to adapt findings to eight high-income countries. The model captured coronary heart disease (CHD) morbidity/mortality over a lifetime horizon, from healthcare and societal perspectives. Risk of CHD, treatment effects, prevalence, and healthcare costs were estimated from published studies. Outcomes included quality-adjusted life years (QALYs), costs and incremental cost-effectiveness ratio (ICER), discounted 5% annually. Sensitivity analyses were undertaken to explore the impact of key input parameters on the robustness of the model. Over the lifetime of the population (4 167 768 men; 4 129 961 women), the model estimated a gain of 33 488years of life lived and 51 790 QALYs due to CHD prevention. Population genomic screening for FH would be cost-effective from a healthcare perspective if the per-test cost was ≤AU$250, yielding an ICER of

Published
2022
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43. LDL-cholesterol lowering and clinical outcomes in hypercholesterolemic subjects with and without a familial hypercholesterolemia phenotype: Analysis from the secondary prevention 4S trial

Author

Vallejo Vaz, Antonio Javier, Packard, Chris J., Ference, Brian A., Santos, Raúl D., Kastelein, John J. P., Stein, Evan A., Ray, Kausik K., and Universidad de Sevilla. Departamento de Medicina

Subjects
Familial hypercholesterolemia, LDL cholesterol, Statins, Cardiovascular disease prevention, Coronary artery disease
Abstract

Background and aims: Trial evidence for the benefits of cholesterol-lowering is limited for familial hypercho lesterolemia (FH) patients, since they have not been the focus of large outcome trials. We assess statin use in coronary artery disease (CAD) subjects with low-density lipoprotein cholesterol (LDL-C) ≥4.9 mmol/L with or without an FH phenotype. Methods: The 4S trial randomized hypercholesterolemic CAD patients to simvastatin or placebo. We first strat ified participants into baseline LDL-C

Published
2021

49. Corrigendum to “2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk” [Atherosclerosis 290 (2019) 140–205]

Author

Mach, Francois, Baigent, Colin, Catapano, Alberico L., Koskinas, Konstantinos C., Casula, Manuela, Badimon, Lina, Chapman, M. John, De Backer, Guy G., Delgado, Victoria, Ference, Brian A., Graham, Ian M., Halliday, Alison, Landmesser, Ulf, Mihaylova, Borislava, Pedersen, Terje R., Riccardi, Gabriele, Richter, Dimitrios J., Sabatine, Marc S., Taskinen, Marja-Riitta, Tokgozoglu, Lale, Wiklund, Olov, Nibouche, Djamaleddine, Zelveian, Parounak H., Siostrzonek, Peter, Najafov, Ruslan, van de Borne, Philippe, Pojskic, Belma, Postadzhiyan, Arman, Kypris, Lambros, Špinar, Jindřich, Larsen, Mogens Lytken, Eldin, Hesham Salah, Viigimaa, Margus, Strandberg, Timo E., Ferrieres, Jean, Agladze, Rusudan, Laufs, Ulrich, Rallidis, Loukianos, Bajnok, Laszlo, Gudjonsson, Thorbjorn, Maher, Vincent, Henkin, Yaakov, Gulizia, Michele Massimo, Mussagaliyeva, Aisulu, Bajraktari, Gani, Kerimkulova, Alina, Latkovskis, Gustavs, Hamoui, Omar, Slapikas, Rimvydas, Visser, Laurent, Dingli, Philip, Ivanov, Victoria, Boskovic, Aneta, Nazzi, Mbarek, Visseren, Frank, Mitevska, Irena, Retterstol, Kjetil, Jankowski, Piotr, Fontes-Carvalho, Ricardo, Gaita, Dan, Ezhov, Marat, Foscoli, Marina, Giga, Vojislav, Pella, Daniel, Fras, Zlatko, Perez de Isla, Leopoldo, Hagstrom, Emil, Lehmann, Roger, Abid, Leila, Ozdogan, Oner, Mitchenko, Olena, Patel, Riyaz S., Windecker, Stephan, Aboyans, Victor, Collet, Jean-Philippe, Dean, Veronica, Fitzsimons, Donna, Gale, Chris P., Grobbee, Diederick, Halvorsen, Sigrun, Hindricks, Gerhard, Iung, Bernard, Juni, Peter, Katus, Hugo A., Leclercq, Christophe, Lettino, Maddalena, Lewis, Basil S., Merkely, Bela, Mueller, Christian, Petersen, Steffen, Petronio, Anna Sonia, Roffi, Marco, Shlyakhto, Evgeny, Simpson, Iain A., Sousa-Uva, Miguel, and Touyz, Rhian M.

Published
2020
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50. Erratum to “2019 ESC/EAS guidelines for the management of dyslipidemias: Lipid modification to reduce cardiovascular risk” [Atherosclerosis 290 (2019) 140–205]

Author

Mach, Francois, Baigent, Colin, Catapano, Alberico L., Koskinas, Konstantinos C., Casula, Manuela, Badimon, Lina, Chapman, M. John, De Backer, Guy G., Delgado, Victoria, Ference, Brian A., Graham, Ian M., Halliday, Alison, Landmesser, Ulf, Mihaylova, Borislava, Pedersen, Terje R., Riccardi, Gabriele, Richter, Dimitrios J., Sabatine, Marc S., Taskinen, Marja-Riitta, Tokgozoglu, Lale, Wiklund, Olov, Nibouche, Djamaleddine, Zelveian, Parounak H., Siostrzonek, Peter, Najafov, Ruslan, van de Borne, Philippe, Pojskic, Belma, Postadzhiyan, Arman, Kypris, Lambros, Špinar, Jindřich, Larsen, Mogens Lytken, Eldin, Hesham Salah, Viigimaa, Margus, Strandberg, Timo E., Ferrieres, Jean, Agladze, Rusudan, Laufs, Ulrich, Rallidis, Loukianos, Bajnok, Laszlo, Gudjonsson, Thorbjorn, Maher, Vincent, Henkin, Yaakov, Gulizia, Michele Massimo, Mussagaliyeva, Aisulu, Bajraktari, Gani, Kerimkulova, Alina, Latkovskis, Gustavs, Hamoui, Omar, Slapikas, Rimvydas, Visser, Laurent, Dingli, Philip, Ivanov, Victoria, Boskovic, Aneta, Nazzi, Mbarek, Visseren, Frank, Mitevska, Irena, Retterstol, Kjetil, Jankowski, Piotr, Fontes-Carvalho, Ricardo, Gaita, Dan, Ezhov, Marat, Foscoli, Marina, Giga, Vojislav, Pella, Daniel, Fras, Zlatko, de Isla, Leopoldo Perez, Hagstrom, Emil, Lehmann, Roger, Abid, Leila, Ozdogan, Oner, Mitchenko, Olena, Patel, Riyaz S., Windecker, Stephan, Aboyans, Victor, Collet, Jean-Philippe, Dean, Veronica, Fitzsimons, Donna, Gale, Chris P., Grobbee, Diederick, Halvorsen, Sigrun, Hindricks, Gerhard, Iung, Bernard, Juni, Peter, Katus, Hugo A., Leclercq, Christophe, Lettino, Maddalena, Lewis, Basil S., Merkely, Bela, Mueller, Christian, Petersen, Steffen, Petronio, Anna Sonia, Roffi, Marco, Shlyakhto, Evgeny, Simpson, Iain A., Sousa-Uva, Miguel, and Touyz, Rhian M.

Published
2020
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