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1. 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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2. Adverse effects of statin therapy: perception vs. the evidence – focus on glucose homeostasis, cognitive, renal and hepatic function, haemorrhagic stroke and cataract

Author

Mach, François, Ray, Kausik K, Wiklund, Olov, Corsini, Alberto, Catapano, Alberico L, Bruckert, Eric, De Backer, Guy, Hegele, Robert A, Hovingh, G Kees, Jacobson, Terry A, Krauss, Ronald M, Laufs, Ulrich, Leiter, Lawrence A, März, Winfried, Nordestgaard, Børge G, Raal, Frederick J, Roden, Michael, Santos, Raul D, Stein, Evan A, Stroes, Erik S, Thompson, Paul D, Tokgözoğlu, Lale, Vladutiu, Georgirene D, Gencer, Baris, Stock, Jane K, Ginsberg, Henry N, and Chapman, M John

Subjects
Aging, Brain Disorders, Prevention, Patient Safety, Liver Disease, Clinical Trials and Supportive Activities, Digestive Diseases, Stroke, Clinical Research, Evaluation of treatments and therapeutic interventions, Aetiology, 2.1 Biological and endogenous factors, 6.1 Pharmaceuticals, Cataract, Cerebral Hemorrhage, Chemical and Drug Induced Liver Injury, Cognition Disorders, Glucose, Homeostasis, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Kidney Diseases, European Atherosclerosis Society Consensus Panel, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology
Abstract

AimsTo objectively appraise evidence for possible adverse effects of long-term statin therapy on glucose homeostasis, cognitive, renal and hepatic function, and risk for haemorrhagic stroke or cataract.Methods and resultsA literature search covering 2000-2017 was performed. The Panel critically appraised the data and agreed by consensus on the categorization of reported adverse effects. Randomized controlled trials (RCTs) and genetic studies show that statin therapy is associated with a modest increase in the risk of new-onset diabetes mellitus (about one per thousand patient-years), generally defined by laboratory findings (glycated haemoglobin ≥6.5); this risk is significantly higher in the metabolic syndrome or prediabetes. Statin treatment does not adversely affect cognitive function, even at very low levels of low-density lipoprotein cholesterol and is not associated with clinically significant deterioration of renal function, or development of cataract. Transient increases in liver enzymes occur in 0.5-2% of patients taking statins but are not clinically relevant; idiosyncratic liver injury due to statins is very rare and causality difficult to prove. The evidence base does not support an increased risk of haemorrhagic stroke in individuals without cerebrovascular disease; a small increase in risk was suggested by the Stroke Prevention by Aggressive Reduction of Cholesterol Levels study in subjects with prior stroke but has not been confirmed in the substantive evidence base of RCTs, cohort studies and case-control studies.ConclusionLong-term statin treatment is remarkably safe with a low risk of clinically relevant adverse effects as defined above; statin-associated muscle symptoms were discussed in a previous Consensus Statement. Importantly, the established cardiovascular benefits of statin therapy far outweigh the risk of adverse effects.

Published
2018

4. 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

5. Rare dyslipidaemias, from phenotype to genotype to management: a European Atherosclerosis Society task force consensus statement

Author

Hegele, Robert A, Borén, Jan, Ginsberg, Henry N, Arca, Marcello, Averna, Maurizio, Binder, Christoph J, Calabresi, Laura, Chapman, M John, Cuchel, Marina, von Eckardstein, Arnold, Frikke-Schmidt, Ruth, Gaudet, Daniel, Hovingh, G Kees, Kronenberg, Florian, Lütjohann, Dieter, Parhofer, Klaus G, Raal, Frederick J, Ray, Kausik K, Remaley, Alan T, Stock, Jane K, Stroes, Erik S, Tokgözoğlu, Lale, and Catapano, Alberico L

Published
2020
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7. Residual vascular risk in diabetes – Will the SPPARM alpha concept hold the key?

Author

Fruchart, Jean-Charles, Santos, Raul D., Yamashita, Shizuya, Aikawa, Masanori, Libby, Peter, Plutzky, Jorge, Pradhan, Aruna, Ridker, Paul, Aguilar-Salinas, Carlos, Al Rasadi, Khalid, Amarenco, Pierre, Barter, Philip J., Ceska, Richard, Corsini, Alberto, Ruscica, Massimiliano, Després, Jean-Pierre, Duriez, Patrick, Eckel, Robert H., Ezhov, Marat V., Farnier, Michel, Ginsberg, Henry N., Hermans, Michel P., Ishibashi, Shun, Karpe, Fredrik, Kodama, Tatsuhiko, Koenig, Wolfgang, Krempf, Michel, Lim, Soo, Lorenzatti, Alberto J., McPherson, Ruth, Nuñez-Cortes, Jesus Millan, Nordestgaard, Børge G., Ogawa, Hisao, Packard, Chris J., Ponte-Negretti, Carlos I., Reiner, Željko, Sadikot, Shaukat, Shimano, Hitoshi, Sritara, Piyamitr, Stock, Jane K., Su, Ta-Chen, Susekov, Andrey V., Tartar, André, Taskinen, Marja-Riitta, Tenenbaum, Alexander, Tokgözoğlu, Lale S., Tomlinson, Brian, Tybjærg-Hansen, Anne, Valensi, Paul, Vrablík, Michal, Wahli, Walter, Watts, Gerald F., Yokote, Koutaro, and Zambon, Alberto

Published
2019
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8. Women, lipids, and atherosclerotic cardiovascular disease: a call to action from the European Atherosclerosis Society

Author

Roeters van Lennep, Jeanine E, primary, Tokgözoğlu, Lale S, additional, Badimon, Lina, additional, Dumanski, Sandra M, additional, Gulati, Martha, additional, Hess, Connie N, additional, Holven, Kirsten B, additional, Kavousi, Maryam, additional, Kayıkçıoğlu, Meral, additional, Lutgens, Esther, additional, Michos, Erin D, additional, Prescott, Eva, additional, Stock, Jane K, additional, Tybjaerg-Hansen, Anne, additional, Wermer, Marieke J H, additional, and Benn, Marianne, additional

Published
2023
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9. 2023 Update on European Atherosclerosis Society Consensus Statement on Homozygous Familial Hypercholesterolaemia: new treatments and clinical guidance

Author

Cuchel, Marina, primary, Raal, Frederick J, additional, Hegele, Robert A, additional, Al-Rasadi, Khalid, additional, Arca, Marcello, additional, Averna, Maurizio, additional, Bruckert, Eric, additional, Freiberger, Tomas, additional, Gaudet, Daniel, additional, Harada-Shiba, Mariko, additional, Hudgins, Lisa C, additional, Kayikcioglu, Meral, additional, Masana, Luis, additional, Parhofer, Klaus G, additional, Roeters van Lennep, Jeanine E, additional, Santos, Raul D, additional, Stroes, Erik S G, additional, Watts, Gerald F, additional, Wiegman, Albert, additional, Stock, Jane K, additional, Tokgözoğlu, Lale S, additional, Catapano, Alberico L, additional, and Ray, Kausik K, additional

Published
2023
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10. 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

11. 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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12. Women, lipids, and atherosclerotic cardiovascular disease:a call to action from the European Atherosclerosis Society

Author

Roeters Van Lennep, Jeanine E., Tokgözoǧlu, Lale S., Badimon, Lina, Dumanski, Sandra M., Gulati, Martha, Hess, Connie N., Holven, Kirsten B., Kavousi, Maryam, Kaylkçloǧlu, Meral, Lutgens, Esther, Michos, Erin D., Prescott, Eva, Stock, Jane K., Tybjaerg-Hansen, Anne, Wermer, Marieke J.H., Benn, Marianne, Roeters Van Lennep, Jeanine E., Tokgözoǧlu, Lale S., Badimon, Lina, Dumanski, Sandra M., Gulati, Martha, Hess, Connie N., Holven, Kirsten B., Kavousi, Maryam, Kaylkçloǧlu, Meral, Lutgens, Esther, Michos, Erin D., Prescott, Eva, Stock, Jane K., Tybjaerg-Hansen, Anne, Wermer, Marieke J.H., and Benn, Marianne

Abstract

Cardiovascular disease is the leading cause of death in women and men globally, with most due to atherosclerotic cardiovascular disease (ASCVD). Despite progress during the last 30 years, ASCVD mortality is now increasing, with the fastest relative increase in middle-aged women. Missed or delayed diagnosis and undertreatment do not fully explain this burden of disease. Sex-specific factors, such as hypertensive disorders of pregnancy, premature menopause (especially primary ovarian insufficiency), and polycystic ovary syndrome are also relevant, with good evidence that these are associated with greater cardiovascular risk. This position statement from the European Atherosclerosis Society focuses on these factors, as well as sex-specific effects on lipids, including lipoprotein(a), over the life course in women which impact ASCVD risk. Women are also disproportionately impacted (in relative terms) by diabetes, chronic kidney disease, and auto-immune inflammatory disease. All these effects are compounded by sociocultural components related to gender. This panel stresses the need to identify and treat modifiable cardiovascular risk factors earlier in women, especially for those at risk due to sex-specific conditions, to reduce the unacceptably high burden of ASCVD in women.

Published
2023

13. 2023 Update on European Atherosclerosis Society Consensus Statement on Homozygous Familial Hypercholesterolaemia:New treatments and clinical guidance

Author

Cuchel, Marina, Raal, Frederick J., Hegele, Robert A., Al-Rasadi, Khalid, Arca, Marcello, Averna, Maurizio, Bruckert, Eric, Freiberger, Tomas, Gaudet, Daniel, Harada-Shiba, Mariko, Hudgins, Lisa C., Kayikcioglu, Meral, Masana, Luis, Parhofer, Klaus G., Roeters Van Lennep, Jeanine E., Santos, Raul D., Stroes, Erik S.G., Watts, Gerald F., Wiegman, Albert, Stock, Jane K., Tokgözoǧlu, Lale S., Catapano, Alberico L., Ray, Kausik K., Cuchel, Marina, Raal, Frederick J., Hegele, Robert A., Al-Rasadi, Khalid, Arca, Marcello, Averna, Maurizio, Bruckert, Eric, Freiberger, Tomas, Gaudet, Daniel, Harada-Shiba, Mariko, Hudgins, Lisa C., Kayikcioglu, Meral, Masana, Luis, Parhofer, Klaus G., Roeters Van Lennep, Jeanine E., Santos, Raul D., Stroes, Erik S.G., Watts, Gerald F., Wiegman, Albert, Stock, Jane K., Tokgözoǧlu, Lale S., Catapano, Alberico L., and Ray, Kausik K.

Abstract

This 2023 statement updates clinical guidance for homozygous familial hypercholesterolaemia (HoFH), explains the genetic complexity, and provides pragmatic recommendations to address inequities in HoFH care worldwide. Key strengths include updated criteria for the clinical diagnosis of HoFH and the recommendation to prioritize phenotypic features over genotype. Thus, a low-density lipoprotein cholesterol (LDL-C) >10 mmol/L (>400 mg/dL) is suggestive of HoFH and warrants further evaluation. The statement also provides state-of-the art discussion and guidance to clinicians for interpreting the results of genetic testing and for family planning and pregnancy. Therapeutic decisions are based on the LDL-C level. Combination LDL-C-lowering therapy - both pharmacologic intervention and lipoprotein apheresis (LA) - is foundational. Addition of novel, efficacious therapies (i.e. inhibitors of proprotein convertase subtilisin/kexin type 9, followed by evinacumab and/or lomitapide) offers potential to attain LDL-C goal or reduce the need for LA. To improve HoFH care around the world, the statement recommends the creation of national screening programmes, education to improve awareness, and management guidelines that account for the local realities of care, including access to specialist centres, treatments, and cost. This updated statement provides guidance that is crucial to early diagnosis, better care, and improved cardiovascular health for patients with HoFH worldwide.

Published
2023

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

Author

Kronenberg, Florian; https://orcid.org/0000-0003-2229-1120, Mora, Samia; https://orcid.org/0000-0001-6283-0980, Stroes, Erik S G; https://orcid.org/0000-0001-9555-6260, Ference, Brian A, Arsenault, Benoit J; https://orcid.org/0000-0003-2240-8456, Berglund, Lars, Dweck, Marc R; https://orcid.org/0000-0001-9847-5917, Koschinsky, Marlys L, Lambert, Gilles; https://orcid.org/0000-0001-5632-0685, Mach, François; https://orcid.org/0000-0003-3178-9131, McNeal, Catherine J; https://orcid.org/0000-0003-0655-2052, Moriarty, Patrick M, Natarajan, Pradeep; https://orcid.org/0000-0001-8402-7435, Nordestgaard, Børge G; https://orcid.org/0000-0002-1954-7220, Parhofer, Klaus G; https://orcid.org/0000-0001-9873-0412, Virani, Salim S; https://orcid.org/0000-0001-9541-6954, von Eckardstein, Arnold; https://orcid.org/0000-0002-1666-2266, Watts, Gerald F, Stock, Jane K, Ray, Kausik K, Tokgözoğlu, Lale S, Catapano, Alberico L; https://orcid.org/0000-0002-7593-2094, Kronenberg, Florian; https://orcid.org/0000-0003-2229-1120, Mora, Samia; https://orcid.org/0000-0001-6283-0980, Stroes, Erik S G; https://orcid.org/0000-0001-9555-6260, Ference, Brian A, Arsenault, Benoit J; https://orcid.org/0000-0003-2240-8456, Berglund, Lars, Dweck, Marc R; https://orcid.org/0000-0001-9847-5917, Koschinsky, Marlys L, Lambert, Gilles; https://orcid.org/0000-0001-5632-0685, Mach, François; https://orcid.org/0000-0003-3178-9131, McNeal, Catherine J; https://orcid.org/0000-0003-0655-2052, Moriarty, Patrick M, Natarajan, Pradeep; https://orcid.org/0000-0001-8402-7435, Nordestgaard, Børge G; https://orcid.org/0000-0002-1954-7220, Parhofer, Klaus G; https://orcid.org/0000-0001-9873-0412, Virani, Salim S; https://orcid.org/0000-0001-9541-6954, von Eckardstein, Arnold; https://orcid.org/0000-0002-1666-2266, Watts, Gerald F, Stock, Jane K, Ray, Kausik K, Tokgözoğlu, Lale S, and Catapano, Alberico L; https://orcid.org/0000-0002-7593-2094

Published
2023

15. The selective peroxisome proliferator-activated receptor alpha modulator (SPPARMα) paradigm: conceptual framework and therapeutic potential: A consensus statement from the International Atherosclerosis Society (IAS) and the Residual Risk Reduction Initiative (R3i) Foundation

Author

Fruchart, Jean-Charles, Santos, Raul D., Aguilar-Salinas, Carlos, Aikawa, Masanori, Al Rasadi, Khalid, Amarenco, Pierre, Barter, Philip J., Ceska, Richard, Corsini, Alberto, Després, Jean-Pierre, Duriez, Patrick, Eckel, Robert H., Ezhov, Marat V., Farnier, Michel, Ginsberg, Henry N., Hermans, Michel P., Ishibashi, Shun, Karpe, Fredrik, Kodama, Tatsuhiko, Koenig, Wolfgang, Krempf, Michel, Lim, Soo, Lorenzatti, Alberto J., McPherson, Ruth, Nuñez-Cortes, Jesus Millan, Nordestgaard, Børge G., Ogawa, Hisao, Packard, Chris J., Plutzky, Jorge, Ponte-Negretti, Carlos I., Pradhan, Aruna, Ray, Kausik K., Reiner, Željko, Ridker, Paul M., Ruscica, Massimiliano, Sadikot, Shaukat, Shimano, Hitoshi, Sritara, Piyamitr, Stock, Jane K., Su, Ta-Chen, Susekov, Andrey V., Tartar, André, Taskinen, Marja-Riitta, Tenenbaum, Alexander, Tokgözoğlu, Lale S., Tomlinson, Brian, Tybjærg-Hansen, Anne, Valensi, Paul, Vrablík, Michal, Wahli, Walter, Watts, Gerald F., Yamashita, Shizuya, Yokote, Koutaro, Zambon, Alberto, and Libby, Peter

Published
2019
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16. Women, lipids, and atherosclerotic cardiovascular disease: a call to action from the European Atherosclerosis Society.

Author

Lennep, Jeanine E Roeters van, Tokgözoğlu, Lale S, Badimon, Lina, Dumanski, Sandra M, Gulati, Martha, Hess, Connie N, Holven, Kirsten B, Kavousi, Maryam, Kayıkçıoğlu, Meral, Lutgens, Esther, Michos, Erin D, Prescott, Eva, Stock, Jane K, Tybjaerg-Hansen, Anne, Wermer, Marieke J H, and Benn, Marianne

Subjects
PREMATURE menopause, CARDIOVASCULAR diseases, POLYCYSTIC ovary syndrome, CARDIOVASCULAR diseases risk factors, MIDDLE-aged women, ATHEROSCLEROSIS
Abstract

Cardiovascular disease is the leading cause of death in women and men globally, with most due to atherosclerotic cardiovascular disease (ASCVD). Despite progress during the last 30 years, ASCVD mortality is now increasing, with the fastest relative increase in middle-aged women. Missed or delayed diagnosis and undertreatment do not fully explain this burden of disease. Sex-specific factors, such as hypertensive disorders of pregnancy, premature menopause (especially primary ovarian insufficiency), and polycystic ovary syndrome are also relevant, with good evidence that these are associated with greater cardiovascular risk. This position statement from the European Atherosclerosis Society focuses on these factors, as well as sex-specific effects on lipids, including lipoprotein(a), over the life course in women which impact ASCVD risk. Women are also disproportionately impacted (in relative terms) by diabetes, chronic kidney disease, and auto-immune inflammatory disease. All these effects are compounded by sociocultural components related to gender. This panel stresses the need to identify and treat modifiable cardiovascular risk factors earlier in women, especially for those at risk due to sex-specific conditions, to reduce the unacceptably high burden of ASCVD in women. [ABSTRACT FROM AUTHOR]

Published
2023
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17. 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., 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., and Catapano, Alberico L.

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

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

Author

Kronenberg, Florian; https://orcid.org/0000-0003-2229-1120, Mora, Samia; https://orcid.org/0000-0001-6283-0980, Stroes, Erik S G; https://orcid.org/0000-0001-9555-6260, Ference, Brian A, Arsenault, Benoit J; https://orcid.org/0000-0003-2240-8456, Berglund, Lars, Dweck, Marc R; https://orcid.org/0000-0001-9847-5917, Koschinsky, Marlys; https://orcid.org/0000-0002-2643-2288, Lambert, Gilles; https://orcid.org/0000-0001-5632-0685, Mach, François; https://orcid.org/0000-0003-3178-9131, McNeal, Catherine J; https://orcid.org/0000-0003-0655-2052, Moriarty, Patrick M, Natarajan, Pradeep; https://orcid.org/0000-0001-8402-7435, Nordestgaard, Børge G; https://orcid.org/0000-0002-1954-7220, Parhofer, Klaus G; https://orcid.org/0000-0001-9873-0412, Virani, Salim S; https://orcid.org/0000-0001-9541-6954, von Eckardstein, Arnold; https://orcid.org/0000-0002-1666-2266, Watts, Gerald F, Stock, Jane K, Ray, Kausik K, Tokgözoğlu, Lale S, Catapano, Alberico L; https://orcid.org/0000-0002-7593-2094, Kronenberg, Florian; https://orcid.org/0000-0003-2229-1120, Mora, Samia; https://orcid.org/0000-0001-6283-0980, Stroes, Erik S G; https://orcid.org/0000-0001-9555-6260, Ference, Brian A, Arsenault, Benoit J; https://orcid.org/0000-0003-2240-8456, Berglund, Lars, Dweck, Marc R; https://orcid.org/0000-0001-9847-5917, Koschinsky, Marlys; https://orcid.org/0000-0002-2643-2288, Lambert, Gilles; https://orcid.org/0000-0001-5632-0685, Mach, François; https://orcid.org/0000-0003-3178-9131, McNeal, Catherine J; https://orcid.org/0000-0003-0655-2052, Moriarty, Patrick M, Natarajan, Pradeep; https://orcid.org/0000-0001-8402-7435, Nordestgaard, Børge G; https://orcid.org/0000-0002-1954-7220, Parhofer, Klaus G; https://orcid.org/0000-0001-9873-0412, Virani, Salim S; https://orcid.org/0000-0001-9541-6954, von Eckardstein, Arnold; https://orcid.org/0000-0002-1666-2266, Watts, Gerald F, Stock, Jane K, Ray, Kausik K, Tokgözoğlu, Lale S, and Catapano, Alberico L; https://orcid.org/0000-0002-7593-2094

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

24. Practical guidance for combination lipid-modifying therapy in high- and very-high-risk patients: A statement from a European Atherosclerosis Society Task Force

Author

Averna, Maurizio, Banach, Maciej, Bruckert, Eric, Drexel, Heinz, Farnier, Michel, Gaita, Dan, Magni, Paolo, März, Winfried, Masana, Luis, Mello e Silva, Alberto, Reiner, Zeljko, Ros, Emilio, Vrablik, Michal, Zambon, Alberto, Zamorano, Jose L., Stock, Jane K., Tokgözoğlu, Lale S., and Catapano, Alberico L.

Published
2021
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25. 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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28. 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, Packard, Chris J, Chapman, M John, Borén, Jan, Aguilar-Salinas, Carlos A, Averna, Maurizio, Ference, Brian A., Gaudet, Daniel, Hegele, Robert A, Kersten, Sander, Lewis, Gary F., Lichtenstein, Alice H., Moulin, Philippe, Nordestgaard, Børge G., Remaley, Alan T, Staels, Bart, Stroes, Erik S. G., Taskinen, Marja-Riitta, Tokgözoğlu, Lale S, Tybjaerg-Hansen, Anne, Stock, Jane K., Catapano, Alberico L, Ginsberg, Henry N, Packard, Chris J, Chapman, M John, Borén, Jan, Aguilar-Salinas, Carlos A, Averna, Maurizio, Ference, Brian A., Gaudet, Daniel, Hegele, Robert A, Kersten, Sander, Lewis, Gary F., Lichtenstein, Alice H., Moulin, Philippe, Nordestgaard, Børge G., Remaley, Alan T, Staels, Bart, Stroes, Erik S. G., Taskinen, Marja-Riitta, Tokgözoğlu, Lale S, Tybjaerg-Hansen, Anne, Stock, Jane K., and Catapano, Alberico L

Abstract

Recent advances in human genetics, together with a large body of epidemiologic, preclinical, and clinical trial results, provide strong support for a causal association between triglycerides (TG), TG-rich lipoproteins (TRL), and TRL remnants, and increased risk of myocardial infarction, ischaemic stroke, and aortic valve stenosis. These data also indicate that TRL and their remnants may contribute significantly to residual cardiovascular risk in patients on optimized low-density lipoprotein (LDL)-lowering therapy. This statement critically appraises current understanding of the structure, function, and metabolism of TRL, and their pathophysiological role in atherosclerotic cardiovascular disease (ASCVD). Key points are (i) a working definition of normo- and hypertriglyceridaemic states and their relation to risk of ASCVD, (ii) a conceptual framework for the generation of remnants due to dysregulation of TRL production, lipolysis, and remodelling, as well as clearance of remnant lipoproteins from the circulation, (iii) the pleiotropic proatherogenic actions of TRL and remnants at the arterial wall, (iv) challenges in defining, quantitating, and assessing the atherogenic properties of remnant particles, and (v) exploration of the relative atherogenicity of TRL and remnants compared to LDL. Assessment of these issues provides a foundation for evaluating approaches to effectively reduce levels of TRL and remnants by targeting either production, lipolysis, or hepatic clearance, or a combination of these mechanisms. This consensus statement updates current understanding in an integrated manner, thereby providing a platform for new therapeutic paradigms targeting TRL and their remnants, with the aim of reducing the risk of ASCVD.

Published
2021

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

Abstract

Recent advances in human genetics, together with a large body of epidemiologic, preclinical, and clinical trial results, provide strong support for a causal association between triglycerides (TG), TG-rich lipoproteins (TRL), and TRL remnants, and increased risk of myocardial infarction, ischaemic stroke, and aortic valve stenosis. These data also indicate that TRL and their remnants may contribute significantly to residual cardiovascular risk in patients on optimized low-density lipoprotein (LDL)-lowering therapy. This statement critically appraises current understanding of the structure, function, and metabolism of TRL, and their pathophysiological role in atherosclerotic cardiovascular disease (ASCVD). Key points are (i) a working definition of normo- and hypertriglyceridaemic states and their relation to risk of ASCVD, (ii) a conceptual framework for the generation of remnants due to dysregulation of TRL production, lipolysis, and remodelling, as well as clearance of remnant lipoproteins from the circulation, (iii) the pleiotropic proatherogenic actions of TRL and remnants at the arterial wall, (iv) challenges in defining, quantitating, and assessing the atherogenic properties of remnant particles, and (v) exploration of the relative atherogenicity of TRL and remnants compared to LDL. Assessment of these issues provides a foundation for evaluating approaches to effectively reduce levels of TRL and remnants by targeting either production, lipolysis, or hepatic clearance, or a combination of these mechanisms. This consensus statement updates current understanding in an integrated manner, thereby providing a platform for new therapeutic paradigms targeting TRL and their remnants, with the aim of reducing the risk of ASCVD.

Published
2021

30. Practical guidance for combination lipid-modifying therapy in high- and very-high-risk patients: A statement from a European Atherosclerosis Society Task Force

Author

Universitat Rovira i Virgili, Averna, Maurizio; Banach, Maciej; Bruckert, Eric; Drexel, Heinz; Farnier, Michel; Gaita, Dan; Magni, Paolo; Maerz, Winfried; Masana, Luis; Mello e Silva, Alberto; Reiner, Zeljko; Ros, Emilio; Vrablik, Michal; Zambon, Alberto; Zamorano, Jose L.; Stock, Jane K.; Tokgozoglu, Lale S.; Catapano, Alberico L., Universitat Rovira i Virgili, and Averna, Maurizio; Banach, Maciej; Bruckert, Eric; Drexel, Heinz; Farnier, Michel; Gaita, Dan; Magni, Paolo; Maerz, Winfried; Masana, Luis; Mello e Silva, Alberto; Reiner, Zeljko; Ros, Emilio; Vrablik, Michal; Zambon, Alberto; Zamorano, Jose L.; Stock, Jane K.; Tokgozoglu, Lale S.; Catapano, Alberico L.

Abstract

Background and aims: This European Atherosclerosis Society (EAS) Task Force provides practical guidance for combination therapy for elevated low-density lipoprotein cholesterol (LDL-C) and/or triglycerides (TG) in highrisk and very-high-risk patients. Methods: Evidence-based review. Results: Statin-ezetimibe combination treatment is the first choice for managing elevated LDL-C and should be given upfront in very-high-risk patients with high LDL-C unlikely to reach goal with a statin, and in primary prevention familial hypercholesterolaemia patients. A proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor may be added if LDL-C levels remain high. In high and very-high-risk patients with mild to moderately elevated TG levels (>2.3 and < 5.6 mmol/L [>200 and < 500 mg/dL) on a statin, treatment with either a fibrate or high-dose omega-3 fatty acids (icosapent ethyl) may be considered, weighing the benefit versus risks. Combination with fenofibrate may be considered for both macro- and microvascular benefits in patients with type 2 diabetes mellitus. Conclusions: This guidance aims to improve real-world use of guideline-recommended combination lipid modifying treatment.

Published
2021

32. The Residual Risk Reduction Initiative: A Call to Action to Reduce Residual Vascular Risk in Patients with Dyslipidemia

Author

Fruchart, Jean-Charles, Sacks, Frank, Hermans, Michel P., Assmann, Gerd, Brown, W. Virgil, Ceska, Richard, Chapman, M. John, Dodson, Paul M., Fioretto, Paola, Ginsberg, Henry N., Kadowaki, Takashi, Lablanche, Jean-Marc, Marx, Nikolaus, Plutzky, Jorge, Reiner, Željko, Rosenson, Robert S., Staels, Bart, Stock, Jane K., Sy, Rody, Wanner, Christoph, Zambon, Alberto, and Zimmet, Paul

Published
2008
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36. Rare dyslipidaemias, from phenotype to genotype to management:a European Atherosclerosis Society task force consensus statement

Author

Hegele, Robert A., Borén, Jan, Ginsberg, Henry N., Arca, Marcello, Averna, Maurizio, Binder, Christoph J., Calabresi, Laura, Chapman, M. John, Cuchel, Marina, von Eckardstein, Arnold, Frikke-Schmidt, Ruth, Gaudet, Daniel, Hovingh, G. Kees, Kronenberg, Florian, Lütjohann, Dieter, Parhofer, Klaus G., Raal, Frederick J., Ray, Kausik K., Remaley, Alan T., Stock, Jane K., Stroes, Erik S., Tokgözoğlu, Lale, Catapano, Alberico L., Hegele, Robert A., Borén, Jan, Ginsberg, Henry N., Arca, Marcello, Averna, Maurizio, Binder, Christoph J., Calabresi, Laura, Chapman, M. John, Cuchel, Marina, von Eckardstein, Arnold, Frikke-Schmidt, Ruth, Gaudet, Daniel, Hovingh, G. Kees, Kronenberg, Florian, Lütjohann, Dieter, Parhofer, Klaus G., Raal, Frederick J., Ray, Kausik K., Remaley, Alan T., Stock, Jane K., Stroes, Erik S., Tokgözoğlu, Lale, and Catapano, Alberico L.

Abstract

Genome sequencing and gene-based therapies appear poised to advance the management of rare lipoprotein disorders and associated dyslipidaemias. However, in practice, underdiagnosis and undertreatment of these disorders are common, in large part due to interindividual variability in the genetic causes and phenotypic presentation of these conditions. To address these challenges, the European Atherosclerosis Society formed a task force to provide practical clinical guidance focusing on patients with extreme concentrations (either low or high) of plasma low-density lipoprotein cholesterol, triglycerides, or high-density lipoprotein cholesterol. The task force also recognises the scarcity of quality information regarding the prevalence and outcomes of these conditions. Collaborative registries are needed to improve health policy for the care of patients with rare dyslipidaemias.

Published
2020

43. The selective peroxisome proliferator-activated receptor alpha modulator (SPPARMα) paradigm: conceptual framework and therapeutic potential

Author

Fruchart, Jean-Charles, Santos, Raul D., Aguilar-Salinas, Carlos, Aikawa, Masanori, Al Rasadi, Khalid, Amarenco, Pierre, Barter, Philip J., Ceska, Richard, Corsini, Alberto, Després, Jean-Pierre, Duriez, Patrick, Eckel, Robert H., Ezhov, Marat V., Farnier, Michel, Ginsberg, Henry N., Hermans, Michel P., Ishibashi, Shun, Karpe, Fredrik, Kodama, Tatsuhiko, Koenig, Wolfgang, Krempf, Michel, Lim, Soo, Lorenzatti, Alberto J., McPherson, Ruth, Nuñez-Cortes, Jesus Millan, Nordestgaard, Børge G., Ogawa, Hisao, Packard, Chris J., Plutzky, Jorge, Ponte-Negretti, Carlos I., Pradhan, Aruna, Ray, Kausik K., Reiner, Željko, Ridker, Paul M., Ruscica, Massimiliano, Sadikot, Shaukat, Shimano, Hitoshi, Sritara, Piyamitr, Stock, Jane K., Su, Ta-Chen, Susekov, Andrey V., Tartar, André, Taskinen, Marja-Riitta, Tenenbaum, Alexander, Tokgözoğlu, Lale S., Tomlinson, Brian, Tybjærg-Hansen, Anne, Valensi, Paul, Vrablík, Michal, Wahli, Walter, Watts, Gerald F., Yamashita, Shizuya, Yokote, Koutaro, Zambon, Alberto, and Libby, Peter

Subjects
ddc
Published
2018

44. The selective peroxisome proliferator-activated receptor alpha modulator (SPPARMα) paradigm:conceptual framework and therapeutic potential : A consensus statement from the International Atherosclerosis Society (IAS) and the Residual Risk Reduction Initiative (R3i) Foundation

Author

Fruchart, Jean-Charles, Santos, Raul D, Aguilar-Salinas, Carlos, Aikawa, Masanori, Al Rasadi, Khalid, Amarenco, Pierre, Barter, Philip J, Ceska, Richard, Corsini, Alberto, Després, Jean-Pierre, Duriez, Patrick, Eckel, Robert H, Ezhov, Marat V, Farnier, Michel, Ginsberg, Henry N, Hermans, Michel P, Ishibashi, Shun, Karpe, Fredrik, Kodama, Tatsuhiko, Koenig, Wolfgang, Krempf, Michel, Lim, Soo, Lorenzatti, Alberto J, McPherson, Ruth, Nuñez-Cortes, Jesus Millan, Nordestgaard, Børge G, Ogawa, Hisao, Packard, Chris J, Plutzky, Jorge, Ponte-Negretti, Carlos I, Pradhan, Aruna, Ray, Kausik K, Reiner, Željko, Ridker, Paul M, Ruscica, Massimiliano, Sadikot, Shaukat, Shimano, Hitoshi, Sritara, Piyamitr, Stock, Jane K, Su, Ta-Chen, Susekov, Andrey V, Tartar, André, Taskinen, Marja-Riitta, Tenenbaum, Alexander, Tokgözoğlu, Lale S, Tomlinson, Brian, Tybjærg-Hansen, Anne, Valensi, Paul, Vrablík, Michal, Wahli, Walter, Watts, Gerald F, Yamashita, Shizuya, Yokote, Koutaro, Zambon, Alberto, Libby, Peter, Fruchart, Jean-Charles, Santos, Raul D, Aguilar-Salinas, Carlos, Aikawa, Masanori, Al Rasadi, Khalid, Amarenco, Pierre, Barter, Philip J, Ceska, Richard, Corsini, Alberto, Després, Jean-Pierre, Duriez, Patrick, Eckel, Robert H, Ezhov, Marat V, Farnier, Michel, Ginsberg, Henry N, Hermans, Michel P, Ishibashi, Shun, Karpe, Fredrik, Kodama, Tatsuhiko, Koenig, Wolfgang, Krempf, Michel, Lim, Soo, Lorenzatti, Alberto J, McPherson, Ruth, Nuñez-Cortes, Jesus Millan, Nordestgaard, Børge G, Ogawa, Hisao, Packard, Chris J, Plutzky, Jorge, Ponte-Negretti, Carlos I, Pradhan, Aruna, Ray, Kausik K, Reiner, Željko, Ridker, Paul M, Ruscica, Massimiliano, Sadikot, Shaukat, Shimano, Hitoshi, Sritara, Piyamitr, Stock, Jane K, Su, Ta-Chen, Susekov, Andrey V, Tartar, André, Taskinen, Marja-Riitta, Tenenbaum, Alexander, Tokgözoğlu, Lale S, Tomlinson, Brian, Tybjærg-Hansen, Anne, Valensi, Paul, Vrablík, Michal, Wahli, Walter, Watts, Gerald F, Yamashita, Shizuya, Yokote, Koutaro, Zambon, Alberto, and Libby, Peter

Abstract

In the era of precision medicine, treatments that target specific modifiable characteristics of high-risk patients have the potential to lower further the residual risk of atherosclerotic cardiovascular events. Correction of atherogenic dyslipidemia, however, remains a major unmet clinical need. Elevated plasma triglycerides, with or without low levels of high-density lipoprotein cholesterol (HDL-C), offer a key modifiable component of this common dyslipidemia, especially in insulin resistant conditions such as type 2 diabetes mellitus. The development of selective peroxisome proliferator-activated receptor alpha modulators (SPPARMα) offers an approach to address this treatment gap. This Joint Consensus Panel appraised evidence for the first SPPARMα agonist and concluded that this agent represents a novel therapeutic class, distinct from fibrates, based on pharmacological activity, and, importantly, a safe hepatic and renal profile. The ongoing PROMINENT cardiovascular outcomes trial is testing in 10,000 patients with type 2 diabetes mellitus, elevated triglycerides, and low levels of HDL-C whether treatment with this SPPARMα agonist safely reduces residual cardiovascular risk.

Published
2019

48. 2017 Update of ESC/EAS Task Force on practical clinical guidance for proprotein convertase subtilisin/kexin type 9 inhibition in patients with atherosclerotic cardiovascular disease or in familial hypercholesterolaemia

Author

Landmesser, Ulf, Chapman, M. John, Stock, Jane K, Amarenco, Pierre, Belch, Jill J F, Borén, Jan, Farnier, Michel, Ference, Brian A, Gielen, Stephan, Graham, Ian, Grobbee, Diederick E, Hovingh, G. Kees, Lüscher, Thomas Felix, Piepoli, Massimo F., Ray, Kausik K., Stroes, Erik S G, Wiklund, Olov, Windecker, Stephan, Zamorano, Jose Luis, Pinto, Fausto, Tokgözoglu, Lale, Bax, Jeroen J., Catapano, Alberico L., Landmesser, Ulf, Chapman, M. John, Stock, Jane K, Amarenco, Pierre, Belch, Jill J F, Borén, Jan, Farnier, Michel, Ference, Brian A, Gielen, Stephan, Graham, Ian, Grobbee, Diederick E, Hovingh, G. Kees, Lüscher, Thomas Felix, Piepoli, Massimo F., Ray, Kausik K., Stroes, Erik S G, Wiklund, Olov, Windecker, Stephan, Zamorano, Jose Luis, Pinto, Fausto, Tokgözoglu, Lale, Bax, Jeroen J., and Catapano, Alberico L.

Published
2018

49. 2017 Update of ESC/EAS Task Force on practical clinical guidance for proprotein convertase subtilisin/kexin type 9 inhibition in patients with atherosclerotic cardiovascular disease or in familial hypercholesterolaemia

Author

Cardiovasculaire Epi Team 9, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, Landmesser, Ulf, Chapman, M. John, Stock, Jane K, Amarenco, Pierre, Belch, Jill J F, Borén, Jan, Farnier, Michel, Ference, Brian A, Gielen, Stephan, Graham, Ian, Grobbee, Diederick E, Hovingh, G. Kees, Lüscher, Thomas Felix, Piepoli, Massimo F., Ray, Kausik K., Stroes, Erik S G, Wiklund, Olov, Windecker, Stephan, Zamorano, Jose Luis, Pinto, Fausto, Tokgözoglu, Lale, Bax, Jeroen J., Catapano, Alberico L., Cardiovasculaire Epi Team 9, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, Landmesser, Ulf, Chapman, M. John, Stock, Jane K, Amarenco, Pierre, Belch, Jill J F, Borén, Jan, Farnier, Michel, Ference, Brian A, Gielen, Stephan, Graham, Ian, Grobbee, Diederick E, Hovingh, G. Kees, Lüscher, Thomas Felix, Piepoli, Massimo F., Ray, Kausik K., Stroes, Erik S G, Wiklund, Olov, Windecker, Stephan, Zamorano, Jose Luis, Pinto, Fausto, Tokgözoglu, Lale, Bax, Jeroen J., and Catapano, Alberico L.

Published
2018

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