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6. Obicetrapib as an Adjunct to Stable Statin Therapy in Japanese Subjects: Results from a Randomized Phase 2 Trial

Author

Harada-Shiba, Mariko, primary, Davdison, Michael H., additional, Ditmarsch, Marc, additional, Hsieh, Andrew, additional, Wuerdeman, Erin, additional, Kling, Douglas, additional, Nield, Annie, additional, Dicklin, Mary R., additional, Nakata, Akitaka, additional, Sueyoshi, Atsushi, additional, Kuroyanagi, Satoshi, additional, and Kastelein, John J.P., additional

Published
2024
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7. Effect of Evolocumab on Coronary Plaque Composition

Author

Nicholls, Stephen J., Puri, Rishi, Anderson, Todd, Ballantyne, Christie M., Cho, Leslie, Kastelein, John J.P., Koenig, Wolfgang, Somaratne, Ransi, Kassahun, Helina, Yang, Jingyuan, Wasserman, Scott M., Honda, Satoshi, Shishikura, Daisuke, Scherer, Daniel J., Borgman, Marilyn, Brennan, Danielle M., Wolski, Kathy, and Nissen, Steven E.

Published
2018
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8. CETP and SGLT2 inhibitor combination therapy improves glycemic control

Author

Khomtchouk, Bohdan B., Sun, Patrick, Ditmarsch, Marc, Kastelein, John J.P., and Davidson, Michael H.

Subjects
Article
Abstract

IMPORTANCE: Cholesteryl ester transfer protein (CETP) inhibition has been associated with decreased risk of new-onset diabetes in past clinical trials exploring their efficacy in cardiovascular disease and can potentially be repurposed to treat metabolic disease. Notably, as an oral drug it can potentially be used to supplement existing oral drugs such as sodium-glucose cotransporter 2 (SGLT2) inhibitors before patients are required to take injectable drugs such as insulin. OBJECTIVE: To identify whether CETP inhibitors could be used as an oral add-on to SGLT2 inhibition to improve glycemic control. DESIGN, SETTING, AND PARTICIPANTS: 2×2 factorial Mendelian Randomization (MR) is performed on the general population of UK Biobank participants with European ancestry. EXPOSURES: Previously constructed genetic scores for CETP and SGLT2 function are combined in a 2×2 factorial framework to characterize the associations between joint CETP and SGLT2 inhibition compared to either alone. MAIN OUTCOMES AND MEASURES: Glycated hemoglobin and type-2 diabetes incidence. RESULTS: Data on 233,765 UK Biobank participants suggests that individuals with genetic inhibition of both CETP and SGLT2 have significantly lower glycated hemoglobin levels (mmol/mol) than control (Effect size: −0.136; 95% CI: −0.190 to −0.081; p-value: 1.09E-06), SGLT2 inhibition alone (Effect size: −0.082; 95% CI: −0.140 to −0.024; p-value: 0.00558), and CETP inhibition alone (Effect size: −0.08479; 95% CI: −0.136 to −0.033; p-value: 0.00118). Furthermore, joint CETP and SGLT2 inhibition is associated with decreased incidence of diabetes (log-odds ratio) compared to control (Effect size: −0.068; 95% CI: −0.115 to −0.021; p-value: 4.44E-03) and SGLT2 inhibition alone (Effect size: −0.062; 95% CI: −0.112 to −0.012; p-value: 0.0149). CONCLUSIONS AND RELEVANCE: Our results suggest that CETP and SGLT2 inhibitor therapy may improve glycemic control over SGLT2 inhibitors alone. Future clinical trials can explore whether CETP inhibitors can be repurposed to treat metabolic disease and provide an oral therapeutic option to benefit high-risk patients before escalation to injectable drugs such as insulin or glucagon-like peptide 1 (GLP1) receptor agonists.

Published
2023

9. PEGOZAFERMIN PROVIDES BENEFICIAL LIPID EFFECTS IN SUBJECTS WITH SEVERE HYPERTRIGLYCERIDEMIA REGARDLESS OF BACKGROUND LIPID MODIFYING THERAPY STATUS: AN ANALYSIS OF THE PHASE 2 ENTRIGUE STUDY

Author

Bhatt, Deepak L., primary, Bays, Harold E., additional, Miller, Michael, additional, Parli, Teresa, additional, Feng, Shibao, additional, Sterling, Lulu, additional, Hartsfield, Cynthia, additional, Agollah, Germaine, additional, Mansbach, Hank, additional, and Kastelein, John J.P., additional

Published
2023
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10. Intima-media thickness at the near or far wall of the common carotid artery in cardiovascular risk assessment

Author

Seekircher, Lisa, Tschiderer, Lena, Lind, Lars, Safarova, Maya S., Kavousi, Maryam, Ikram, M. Arfan, Lonn, Eva, Yusuf, Salim, Grobbee, Diederick E., Kastelein, John J.P., Visseren, Frank L.J., Walters, Matthew, Dawson, Jesse, Higgins, Peter, Agewall, Stefan, Catapano, Alberico, De Groot, Eric, Espeland, Mark A., Klingenschmid, Gerhard, Magliano, Dianna, Olsen, Michael H., Preiss, David, Sander, Dirk, Skilton, Michael, Zozulińska-Ziółkiewicz, Dorota A., Grooteman, Muriel P.C., Blankestijn, Peter J., Kitagawa, Kazuo, Okazaki, Shuhei, Manzi, Maria V., Mancusi, Costantino, Izzo, Raffaele, Desvarieux, Moise, Rundek, Tatjana, Gerstein, Hertzel C., Bots, Michiel L., Sweeting, Michael J., Lorenz, Matthias W., Willeit, Peter, Seekircher, Lisa, Tschiderer, Lena, Lind, Lars, Safarova, Maya S., Kavousi, Maryam, Ikram, M. Arfan, Lonn, Eva, Yusuf, Salim, Grobbee, Diederick E., Kastelein, John J.P., Visseren, Frank L.J., Walters, Matthew, Dawson, Jesse, Higgins, Peter, Agewall, Stefan, Catapano, Alberico, De Groot, Eric, Espeland, Mark A., Klingenschmid, Gerhard, Magliano, Dianna, Olsen, Michael H., Preiss, David, Sander, Dirk, Skilton, Michael, Zozulińska-Ziółkiewicz, Dorota A., Grooteman, Muriel P.C., Blankestijn, Peter J., Kitagawa, Kazuo, Okazaki, Shuhei, Manzi, Maria V., Mancusi, Costantino, Izzo, Raffaele, Desvarieux, Moise, Rundek, Tatjana, Gerstein, Hertzel C., Bots, Michiel L., Sweeting, Michael J., Lorenz, Matthias W., and Willeit, Peter

Abstract

Aims: Current guidelines recommend measuring carotid intima-media thickness (IMT) at the far wall of the common carotid artery (CCA). We aimed to precisely quantify associations of near vs. far wall CCA-IMT with the risk for atherosclerotic cardiovascular disease (CVD, defined as coronary heart disease or stroke) and their added predictive values. Methods and results: We analysed individual records of 41 941 participants from 16 prospective studies in the Proof-ATHERO consortium {mean age 61 years [standard deviation (SD) = 11]; 53% female; 16% prior CVD}. Mean baseline values of near and far wall CCA-IMT were 0.83 (SD = 0.28) and 0.82 (SD = 0.27) mm, differed by a mean of 0.02 mm (95% limits of agreement: -0.40 to 0.43), and were moderately correlated [r = 0.44; 95% confidence interval (CI): 0.39-0.49). Over a median follow-up of 9.3 years, we recorded 10 423 CVD events. We pooled study-specific hazard ratios for CVD using random-effects meta-analysis. Near and far wall CCA-IMT values were approximately linearly associated with CVD risk. The respective hazard ratios per SD higher value were 1.18 (95% CI: 1.14-1.22; I² = 30.7%) and 1.20 (1.18-1.23; I² = 5.3%) when adjusted for age, sex, and prior CVD and 1.09 (1.07-1.12; I² = 8.4%) and 1.14 (1.12-1.16; I²=1.3%) upon multivariable adjustment (all P < 0.001). Assessing CCA-IMT at both walls provided a greater C-index improvement than assessing CCA-IMT at one wall only [+0.0046 vs. +0.0023 for near (P < 0.001), +0.0037 for far wall (P = 0.006)]. Conclusions: The associations of near and far wall CCA-IMT with incident CVD were positive, approximately linear, and similarly strong. Improvement in risk discrimination was highest when CCA-IMT was measured at both walls.

Published
2023

11. Intima-media thickness at the near or far wall of the common carotid artery in cardiovascular risk assessment

Author

Global Health, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, Interne Geneeskunde Vasculaire, Nefro Vasculaire Geneeskunde, Cardiovasculaire Epi Team 5, Cardiovasculaire Epidemiologie, Seekircher, Lisa, Tschiderer, Lena, Lind, Lars, Safarova, Maya S., Kavousi, Maryam, Ikram, M. Arfan, Lonn, Eva, Yusuf, Salim, Grobbee, Diederick E., Kastelein, John J.P., Visseren, Frank L.J., Walters, Matthew, Dawson, Jesse, Higgins, Peter, Agewall, Stefan, Catapano, Alberico, De Groot, Eric, Espeland, Mark A., Klingenschmid, Gerhard, Magliano, Dianna, Olsen, Michael H., Preiss, David, Sander, Dirk, Skilton, Michael, Zozulińska-Ziółkiewicz, Dorota A., Grooteman, Muriel P.C., Blankestijn, Peter J., Kitagawa, Kazuo, Okazaki, Shuhei, Manzi, Maria V., Mancusi, Costantino, Izzo, Raffaele, Desvarieux, Moise, Rundek, Tatjana, Gerstein, Hertzel C., Bots, Michiel L., Sweeting, Michael J., Lorenz, Matthias W., Willeit, Peter, Global Health, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, Interne Geneeskunde Vasculaire, Nefro Vasculaire Geneeskunde, Cardiovasculaire Epi Team 5, Cardiovasculaire Epidemiologie, Seekircher, Lisa, Tschiderer, Lena, Lind, Lars, Safarova, Maya S., Kavousi, Maryam, Ikram, M. Arfan, Lonn, Eva, Yusuf, Salim, Grobbee, Diederick E., Kastelein, John J.P., Visseren, Frank L.J., Walters, Matthew, Dawson, Jesse, Higgins, Peter, Agewall, Stefan, Catapano, Alberico, De Groot, Eric, Espeland, Mark A., Klingenschmid, Gerhard, Magliano, Dianna, Olsen, Michael H., Preiss, David, Sander, Dirk, Skilton, Michael, Zozulińska-Ziółkiewicz, Dorota A., Grooteman, Muriel P.C., Blankestijn, Peter J., Kitagawa, Kazuo, Okazaki, Shuhei, Manzi, Maria V., Mancusi, Costantino, Izzo, Raffaele, Desvarieux, Moise, Rundek, Tatjana, Gerstein, Hertzel C., Bots, Michiel L., Sweeting, Michael J., Lorenz, Matthias W., and Willeit, Peter

Published
2023

15. Response by Kusters et al to Letter Regarding Article, “Effect of Rosuvastatin on Carotid Intima-Media Thickness in Children With Heterozygous Familial Hypercholesterolemia: The CHARON Study (Hypercholesterolemia in Children and Adolescents Taking Rosuvastatin Open Label)”

Author

Kusters, D. Meeike, Braamskamp, Marjet J.A.M., Langslet, Gisle, McCrindle, Brian W., Cassiman, David, Francis, Gordon A., Gagne, Claude, Gaudet, Daniel, Morrison, Katherine M., Wiegman, Albert, Turner, Traci, Miller, Elinor, Raichlen, Joel, Martin, Paul D., Stein, Evan A., Kastelein, John J.P., and Hutten, Barbara A.

Published
2018
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19. EVOLOCUMAB IN PEDIATRIC HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA: RESULTS FROM THE HAUSER OPEN-LABEL EXTENSION STUDY

Author

Santos, Raul, primary, Ruzza, Andrea, additional, Hovingh, G Kees, additional, Stefanutti, Claudia, additional, Mach, François, additional, Descamps, Olivier, additional, Bergeron, Jean, additional, Wang, Bei, additional, Bartuli, Andrea, additional, Buonuomo, Paola Sabrina, additional, Greber-Platzer, Susanne, additional, Luirink, Ilse, additional, Raal, Frederick J., additional, Kastelein, John J.P., additional, Wiegman, Albert, additional, and Gaudet, Daniel, additional

Published
2022
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24. New and Emerging Therapies for Reduction of LDL-Cholesterol and Apolipoprotein B:JACC Focus Seminar 1/4

Author

Nurmohamed, Nick S., Navar, Ann Marie, and Kastelein, John J.P.

Abstract

Adding to the foundation of statins, ezetimibe and proprotein convertase subtilisin–kexin type 9 inhibitors (PCSK9i), novel, emerging low-density lipoprotein cholesterol (LDL-C)–lowering therapies are under development for the prevention of cardiovascular disease. Inclisiran, a small interfering RNA molecule that inhibits PCSK9, only needs to be dosed twice a year and has the potential to help overcome current barriers to persistence and adherence to lipid-lowering therapies. Bempedoic acid, which lowers LDL-C upstream from statins, provides a novel alternative for patients with statin intolerance. Angiopoetin-like 3 protein (ANGPTL3) inhibitors have been shown to provide potent LDL-C lowering in patients with homozygous familial hypercholesterolemia without major adverse effects as seen with lomitapide and mipomersen, and may reduce the need for apheresis. Finally, CETP inhibitors may yet be effective with the development of obicetrapib. These novel agents provide the clinician the tools to effectively lower LDL-C across the entire range of LDL-C–induced elevation of cardiovascular risk, from primary prevention and secondary prevention to null-null homozygous familial hypercholesterolemia patients.

Published
2021

26. A meta-analysis of medications directed against PCSK9 in familial hypercholesterolemia

Author

Universidad de Sevilla. Departamento de Medicina, Brandts, Julia, Dharmayat, Kanika I., Vallejo Vaz, Antonio Javier, Azar Sharabiani, Mansour Taghavi, Jones, Rebecca, Kastelein, John J.P., Raal, Frederick J., Ray, Kausik K., Universidad de Sevilla. Departamento de Medicina, Brandts, Julia, Dharmayat, Kanika I., Vallejo Vaz, Antonio Javier, Azar Sharabiani, Mansour Taghavi, Jones, Rebecca, Kastelein, John J.P., Raal, Frederick J., and Ray, Kausik K.

Abstract

Background and aims Several medications targeting PCSK9 reduce LDL-cholesterol (LDL-C) in heterozygous familial hypercholesterolemia (HeFH). We aimed to assess in patients diagnosed clinically as HeFH, whether LDL-C reduction varied by different therapeutic approaches to PCSK9-targeting or by the underlying genetic variant. Methods We conducted a random-effects meta-analysis of randomised clinical trials assessing PCSK9-targeting therapies, namely alirocumab, evolocumab and inclisiran, in patients with clinically diagnosed HeFH and restricted analyses to those patients in whom genotypic data were available. A search of MEDLINE and Embase identified eligible trials published between inception and June 29, 2020. We included trials of sufficient duration to allow for a stable treatment effect: ~12 weeks for monoclonal antibodies (mAbs) (alirocumab, evolocumab) and ~1 year for small interfering RNA (siRNA) (inclisiran). Single-moderator meta-regression comparing mean percentage LDL-C reduction between mAbs and siRNA as well as PCSK9-targeting therapies between different genotypes was used to assess heterogeneity. Results Eight trials of HeFH met our inclusion criteria, including 1887 genotyped patients. Among monogenic HeFH cases (N = 1347) the LDL-C reduction from baseline was 46.12% (95%CI 48.4-43.9) for siRNA and 50.4% (59.3-41.4) for mAbs compared to control, without evidence of significant heterogeneity between treatment (QM = 0.32, df = 1, p = 0.57). Irrespective of therapeutic approach to PCSK9-targeting, reductions in LDL-C were generally consistent across genetic variants (LDL-Receptor variants, LDL-Receptor variants of unknown significance, Apolipoprotein B variants, two variants and no variant) (QM = 8.3, df = 4, p = 0.08). Conclusions Among patients with HeFH, the LDL-C-lowering effect of PCSK9-targeting medications did not show statistical heterogeneity across different drug-classes and across genetic variants.

Published
2021

31. Intensive lipid lowering with atorvastatin in patients with coronary artery disease, diabetes, and chronic kidney disease

Author

Shepherd, James, Kastelein, John J.P., Bittmer, Vera A., Carmena, Rafael, Deedwania, Prakash C., Breazna, Andrei, Dobson, Stephen, Wilson, Daniel J., Zuckerman, Andrea L., and Wenger, Nanette K.

Subjects
Lipids -- Control, Coronary heart disease -- Drug therapy, Coronary heart disease -- Patient outcomes, Type 2 diabetes -- Drug therapy, Type 2 diabetes -- Patient outcomes, Chronic kidney failure -- Drug therapy, Chronic kidney failure -- Patient outcomes
Abstract

OBJECTIVE: To investigate the effect of intensive lipid lowering with high-dose atorvastatin on the incidence of major cardiovascular events compared with low-dose atorvastatin in patients with coronary artery disease and [...]

Published
2008

32. Evolocumab in Pediatric Heterozygous Familial Hypercholesterolemia

Author

Santos, Raul D., Ruzza, Andrea, Hovingh, G. Kees, Wiegman, Albert, Mach, François, Kurtz, Christopher E., Hamer, Andrew, Bridges, Ian, Bartuli, Andrea, Bergeron, Jean, Szamosi, Tamás, Santra, Saikat, Stefanutti, Claudia, Descamps, Olivier S., Greber-Platzer, Susanne, Luirink, Ilse, Kastelein, John J.P., Gaudet, Daniel, HAUSER-RCT INVESTIGATORS, Stéphenne, Xavier, Sokal, Etienne, UCL - SSS/IREC/PEDI - Pôle de Pédiatrie, UCL - (SLuc) Service de gastro-entérologie et hépatologie pédiatrique, Experimental Vascular Medicine, Vascular Medicine, ACS - Atherosclerosis & ischemic syndromes, Paediatric Metabolic Diseases, General Paediatrics, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, APH - Methodology, APH - Quality of Care, ACS - Heart failure & arrhythmias, ACS - Diabetes & metabolism, and ACS - Pulmonary hypertension & thrombosis

Subjects
Male, medicine.medical_specialty, Heterozygote, animal structures, Adolescent, medicine.drug_class, Familial hypercholesterolemia, 030204 cardiovascular system & hematology, Monoclonal antibody, Antibodies, LDL, Hyperlipoproteinemia Type II, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Double-Blind Method, Drug Therapy, Internal medicine, Monoclonal, medicine, Humans, 030212 general & internal medicine, Child, Humanized, biology, Cholesterol, business.industry, Anticholesteremic Agents, fungi, Antibodies, Monoclonal, Humanized, Cholesterol, LDL, Drug Therapy, Combination, Female, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Lipids, Proprotein Convertase 9, Treatment Outcome, General Medicine, Proprotein convertase, medicine.disease, Evolocumab, Endocrinology, chemistry, Combination, biology.protein, lipids (amino acids, peptides, and proteins), Antibody, business, Lipoprotein
Abstract

Background: Evolocumab, a fully human monoclonal antibody directed against proprotein convertase subtilisin-kexin type 9, is widely used in adult patients to lower low-density lipoprotein (LDL) cholesterol levels. Its effects in pediatric patients with heterozygous familial hypercholesterolemia are not known. Methods: We conducted a 24-week, randomized, double-blind, placebo-controlled trial to evaluate the efficacy and safety of evolocumab in pediatric patients with heterozygous familial hypercholesterolemia. Patients 10 to 17 years of age who had received stable lipid-lowering treatment for at least 4 weeks before screening and who had an LDL cholesterol level of 130 mg per deciliter (3.4 mmol per liter) or more and a triglyceride level of 400 mg per deciliter (4.5 mmol per liter) or less were randomly assigned in a 2:1 ratio to receive monthly subcutaneous injections of evolocumab (420 mg) or placebo. The primary end point was the percent change in LDL cholesterol level from baseline to week 24; key secondary end points were the mean percent change in LDL cholesterol level from baseline to weeks 22 and 24 and the absolute change in LDL cholesterol level from baseline to week 24. Results: A total of 157 patients underwent randomization and received evolocumab (104 patients) or placebo (53 patients). At week 24, the mean percent change from baseline in LDL cholesterol level was -44.5% in the evolocumab group and -6.2% in the placebo group, for a difference of -38.3 percentage points (P

Published
2020

34. Low plasma adiponectin exacerbates the risk of premature coronary heart disease in familial hypercholesterolemia

Author

Perron, Patrice, Brisson, Diane, Laprise, Catherine, St-Pierre, Julie, Gaudet, Daniel, Tremblay, Gérald, Bouhali, Tarek, Vohl, Marie-Claude, Després, Jean-Pierre, Vissers, Maud N., Hutten, Barbara A., Kastelein, John J.P., Perron, Patrice, Brisson, Diane, Laprise, Catherine, St-Pierre, Julie, Gaudet, Daniel, Tremblay, Gérald, Bouhali, Tarek, Vohl, Marie-Claude, Després, Jean-Pierre, Vissers, Maud N., Hutten, Barbara A., and Kastelein, John J.P.

Abstract

Familial hypercholesterolemia (FH) is characterized by increased risk for premature coronary artery disease (CAD). This risk is exacerbated in the presence of abdominal obesity and insulin resistance. Low adiponectin is part of the clustering of metabolic abnormalities associated with abdominal obesity and insulin resistance. The present study, therefore, aims to examine the relationship between plasma adiponectin and age at CAD diagnosis in FH patients. Plasma adiponectin was measured by ELISA in 568 non-diabetic FH individuals of French-Canadian origin. CAD was defined according to strict clinical criteria. Prior to analyses, patients were grouped according to age and gender-specific tertiles of plasma adiponectin levels. Multivariate Cox proportional hazards regression was used to estimate the association between plasma adiponectin levels and age at diagnosis of CAD. Overall, FH patients in the lowest tertile of plasma adiponectin exhibited CAD at a significantly younger age (hazard ratio = 1.73, confidence interval 95%: [1.19–2.53]; p = 0.004). These results suggest that low plasma adiponectin is associated with an increased risk of premature CAD over and above the already exaggerated risk seen in FH patients.

Published
2020

39. Loci influencing blood pressure identified using a cardiovascular gene-centric array

Author

Ganesh, Santhi K., Tragante, Vinicius, Guo, Wei, Guo, Yiran, Lanktree, Matthew B., Smith, Erin N., Johnson, Toby, Castillo, Berta Almoguera, Barnard, John, Baumert, Jens, Chang, Yen-Pei Christy, Elbers, Clara C., Farrall, Martin, Fischer, Mary E., Franceschini, Nora, Gaunt, Tom R., Gho, Johannes M.I.H., Gieger, Christian, Gong, Yan, Isaacs, Aaron, Kleber, Marcus E., Leach, Irene Mateo, McDonough, Caitrin W., Meijs, Matthijs F.L., Mellander, Olle, Molony, Cliona M., Nolte, Ilja M., Padmanabhan, Sandosh, Price, Tom S., Rajagopalan, Ramakrishnan, Shaffer, Jonathan, Shah, Sonia, Shen, Haiqing, Soranzo, Nicole, van der Most, Peter J., Van Iperen, Erik P.A., Van Setten, Jessic A., Vonk, Judith M., Zhang, Li, Beitelshees, Amber L., Berenson, Gerald S., Bhatt, Deepak L., Boer, Jolanda M.A., Boerwinkle, Eric, Burkley, Ben, Burt, Amber, Chakravarti, Aravinda, Chen, Wei, Cooper-DeHoff, Rhonda M., Curtis, Sean P., Dreisbach, Albert, Duggan, David, Ehret, Georg B., Fabsitz, Richard R., Fornage, Myriam, Fox, Ervin, Furlong, Clement E., Gansevoort, Ron T., Hofker, Marten H., Hovingh, G. Kees, Kirkland, Susan A., Kottke-Marchant, Kandice, Kutlar, Abdullah, LaCroix, Andrea Z., Langaee, Taimour Y., Li, Yun R., Lin, Honghuang, Liu, Kiang, Maiwald, Steffi, Malik, Rainer, Murugesan, Gurunathan, Newton-Cheh, Christopher, OʼConnell, Jeffery R., Onland-Moret, N. Charlotte, Ouwehand, Willem H., Palmas, Walter, Penninx, Brenda W., Pepine, Carl J., Pettinger, Mary, Polak, Joseph F., Ramachandran, Vasan S., Ranchalis, Jane, Redline, Susan, Ridker, Paul M., Rose, Lynda M., Scharnag, Hubert, Schork, Nicholas J., Shimbo, Daichi, Shuldiner, Alan R., Srinivasan, Sathanur R., Stolk, Ronald P., Taylor, Herman A., Thorand, Barbara, Trip, Mieke D., van Duijn, Cornelia M., Verschuren, W. Monique, Wijmenga, Cisca, Winkelmann, Bernhard R., Wyatt, Sharon, Young, J. Hunter, Boehm, Bernhard O., Caulfield, Mark J., Chasman, Daniel I., Davidson, Karina W., Doevendans, Pieter A., FitzGerald, Garret A., Gums, John G., Hakonarson, Hakon, Hillege, Hans L., Illig, Thomas, Jarvik, Gail P., Johnson, Julie A., Kastelein, John J.P., Koenig, Wolfgang, März, Winfried, Mitchell, Braxton D., Murray, Sarah S., Oldehinkel, Albertine J., Rader, Daniel J., Reilly, Muredach P., Reiner, Alex P., Schadt, Eric E., Silverstein, Roy L., Snieder, Harold, Stanton, Alice V., Uitterlinden, André G., van der Harst, Pim, van der Schouw, Yvonne T., Samani, Nilesh J., Johnson, Andrew D., Munroe, Patricia B., de Bakker, Paul I.W., Zhu, Xiaofeng, Levy, Daniel, Keating, Brendan J., and Asselbergs, Folkert W.

Published
2013
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