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Effects of Dalcetrapib in Patients with a Recent Acute Coronary Syndrome
Open accessAbstract
BACKGROUND: In observational analyses, higher levels of high-density lipoprotein (HDL) cholesterol have been associated with a lower risk of coronary heart disease events. However, whether raising HDL cholesterol levels therapeutically reduces cardiovascular risk remains uncertain. Inhibition of cholesteryl ester transfer protein (CETP) raises HDL cholesterol levels and might therefore improve cardiovascular outcomes. METHODS: We randomly assigned 15,871 patients who had had a recent acute coronary syndrome to receive the CETP inhibitor dalcetrapib, at a dose of 600 mg daily, or placebo, in addition to the best available evidence-based care. The primary efficacy end point was a composite of death from coronary heart disease, nonfatal myocardial infarction, ischemic stroke, unstable angina, or cardiac arrest with resuscitation. RESULTS: At the time of randomization, the mean HDL cholesterol level was 42 mg per deciliter (1.1 mmol per liter), and the mean low-density lipoprotein (LDL) cholesterol level was 76 mg per deciliter (2.0 mmol per liter). Over the course of the trial, HDL cholesterol levels increased from baseline by 4 to 11% in the placebo group and by 31 to 40% in the dalcetrapib group. Dalcetrapib had a minimal effect on LDL cholesterol levels. Patients were followed for a median of 31 months. At a prespecified interim analysis that included 1135 primary end-point events (71% of the projected total number), the independent data and safety monitoring board recommended termination of the trial for futility. As compared with placebo, dalcetrapib did not alter the risk of the primary end point (cumulative event rate, 8.0% and 8.3%, respectively; hazard ratio with dalcetrapib, 1.04; 95% confidence interval, 0.93 to 1.16; P=0.52) and did not have a significant effect on any component of the primary end point or total mortality. The median C-reactive protein level was 0.2 mg per liter higher and the mean systolic blood pressure was 0.6 mm Hg higher with dalcetrapib as compared with placebo (P<0.001 for both comparisons). CONCLUSIONS: In patients who had had a recent acute coronary syndrome, dalcetrapib increased HDL cholesterol levels but did not reduce the risk of recurrent cardiovascular events. (Funded by F. Hoffmann-La Roche; dal-OUTCOMES ClinicalTrials.gov number, NCT00658515.).
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“The last factor probably also contributed to the rise in LDL cholesterol observed in the placebo group, in the on-treatment analysis in the alirocumab group, and in previous trials involving patients who had an acute coronary syndrome. 5,21”
From Alirocumab and Cardiovascular Outcomes after Acute Coronary Syndrome (2018) · cites this paper as [21]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“three large RCTs of cholesterol ester transfer protein inhibitors (dalcetrapib, evacetrapib, and torcetrapib) did not improve CV outcomes despite substantial increases in plasma HDL-C levels”
From The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk (2019) · cites this paper as [21]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Unfortunately, early generations of CETP inhibitors were either associated with off-target adverse effects with safety concerns, or had no significant or only modest LDL-C lowering and thus failed to demonstrate cardiovascular benefit, leading to a loss of enthusiasm in this drug class [[7], [8], [9], [10]].”
From Efficacy and safety of obicetrapib in patients with dyslipidemia: An updated meta-analysis of randomized controlled trials (2025) · cites this paper as [8]
Experimental — accuracy not yet measuredIn the citing paper
“Furthermore, there is no evidence from randomized trials that therapeutically increasing plasma HDL-C reduces the risk of CV events [63-67].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [64]
In the citing paper
“Similarly, in the Assessment of Clinical Effects of Cholesteryl Ester Transfer Protein Inhibition with Evacetrapib in Patients at a High-Risk for Vascular Outcomes (ACCELERATE) and Randomized Evaluation of the Effects of Anacetrapib Through Lipid Modification (REVEAL) trials, treatment with CETP inhibitors more than doubled HDL-C levels, but did not appear to reduce the risk of ASCVD events beyond”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [64]
In the citing paper
“Anacetrapib reduced major coronary events by 9% over a median of 4.1 years [64].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [64]
In the citing paper
“More recently, the REVEAL study investigated anacetrapib in > 30 000 patients with atherosclerotic vascular disease and resulted in a lower incidence of MACE compared with placebo after 4 years, with no safety concerns [64].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [64]
In the citing paper
“Furthermore, in patients who had experienced a recent ACS, the CETP inhibitor dalcetrapib did not reduce the risk of recurrent CV events. 362”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [362]
In the citing paper
“Furthermore, in patients who had experienced a recent ACS, the CETP inhibitor dalcetrapib did not reduce the risk of recurrent CV events.362”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [362]
In the citing paper
“Colocalization, which is a statistical approach that quantifies the extent to which two traits share the same underlying causal variant, and thus can be used to infer vertical pleiotropy 83-85 , can be used to test for such bias 86 , but can suffer from issues of lack of power and/or availability of suitable data from relevant tissues.”
From Integrating genomics with biomarkers and therapeutic targets to invigorate cardiovascular drug development (2021) · cites this paper as [85]
In the citing paper
“However, three out of four prospective studies with CETP inhibitors had to be terminated due to increased mortality in the treatment group or due to futility (Table 3).”
From HDL cholesterol: reappraisal of its clinical relevance (2017) · cites this paper as [107]
In the citing paper
“outcome trials that have targeted HDL-C pharmacologically and have included patients with low HDL-C at baseline, have not demonstrated reduced CVD risk despite appreciable increases in HDL-C.5-10”
From Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study (2016) · cites this paper as [6]
In the citing paper
“In contrast, recent studies have failed to demonstrate that high HDL-C acquired naturally or pharmacologically, is associated with reduced CVD risk.5-11,18”
From Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study (2016) · cites this paper as [6]
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Citations
Cites
High density lipoprotein as a protective factor against coronary heart disease
Gordon, T., Castelli, W. P., Hjortland, M. C., Kannel, W. B., & Dawber, T. R. (1977) · The American Journal of Medicine · doi:10.1016/0002-9343(77)90874-9 · Cited by 5,059
Helsinki Heart Study: Primary-Prevention Trial with Gemfibrozil in Middle-Aged Men with Dyslipidemia
Frick, M. H., Elo, O., Haapa, K., Heinonen, O. P., Heinsalmi, P., Helo, P., Huttunen, J. K., Kaitaniemi, P., Koskinen, P., Manninen, V., et al. (1987) · New England Journal of Medicine · doi:10.1056/nejm198711123172001 · Cited by 3,881
Rubins, H. B., Robins, S. J., Collins, D., Fye, C. L., Anderson, J. W., Elam, M. B., Faas, F. H., Linares, E., Schaefer, E. J., Schectman, G., et al. (1999) · New England Journal of Medicine · doi:10.1056/nejm199908053410604 · Cited by 3,439
Effects of torcetrapib in patients at high risk for coronary events
Barter, P. J., Caulfield, M., Eriksson, M., Grundy, S. M., Kastelein, J. J. P., Komajda, M., Lopez-Sendon, J., Mosca, L., Tardif, J.-C., Waters, D. D., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa0706628 · Cited by 3,139
Self-citationNiacin in Patients with Low HDL Cholesterol Levels Receiving Intensive Statin Therapy
The AIM-HIGH Investigators (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1107579 · Cited by 2,911
Effects of Combination Lipid Therapy in Type 2 Diabetes Mellitus
(2010) · New England Journal of Medicine · doi:10.1056/nejmoa1001282 · Cited by 2,837
Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis
Khera, A. V., Cuchel, M., de la Llera-Moya, M., Rodrigues, A., Burke, M. F., Jafri, K., French, B. C., Phillips, J. A., Mucksavage, M. L., Wilensky, R. L., et al. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1001689 · Cited by 1,943
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- 10.1016/S0140-6736(12)60312-2 · DOI · Paper page
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Conventional and Novel Lipid Measures and Risk of Peripheral Artery Disease
Kou, M., Ding, N., Ballew, S. H., Salameh, M., Martin, S. S., Selvin, E., HEISS, G. M., Ballantyne, C. M., Matsushita, K., & Hoogeveen, R. C. (2021) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.120.315828 · Cited by 44
Self-citationUraemic dyslipidaemia revisited: role of high-density lipoprotein
Speer, T., Zewinger, S., & Fliser, D. (2013) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gft080 · Cited by 45
Niacin Therapy, HDL Cholesterol, and Cardiovascular Disease: Is the HDL Hypothesis Defunct?
Mani, P., & Rohatgi, A. K. (2015) · Current Atherosclerosis Reports · doi:10.1007/s11883-015-0521-x · Cited by 47
Ip, C.-K., Jin, D.-M., Gao, J.-J., Meng, Z., Meng, J., Tan, Z., Wang, J.-F., & Geng, D.-F. (2015) · International Journal of Cardiology · doi:10.1016/j.ijcard.2015.04.228 · Cited by 43
Cao, J., Nomura, S. O., Steffen, B. T., Guan, W., Remaley, A. T., Karger, A. B., Ouyang, P., Michos, E. D., & Tsai, M. Y. (2020) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2019.11.005 · Cited by 48
Does Elevated High-Density Lipoprotein Cholesterol Protect Against Cardiovascular Disease?
Razavi, A. C., Jain, V., Grandhi, G. R., Patel, P., Karagiannis, A. D., Patel, N. H., Dhindsa, D. S., Liu, C., Desai, S., Almuwaqqat, Z., et al. (2023) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgad406 · Cited by 47
Very Large Database of Lipids: Rationale and Design
Martin, S. S., Blaha, M. J., Toth, P. P., Joshi, P. H., McEvoy, J. W., Ahmed, H. M., Elshazly, M. B., Swiger, K. J., Michos, E. D., Kwiterovich, P. O., et al. (2013) · Clinical Cardiology · doi:10.1002/clc.22214 · Cited by 43
Chandra, A., Neeland, I. J., Das, S. R., Khera, A., Turer, A. T., Ayers, C. R., McGuire, D. K., & Rohatgi, A. K. (2015) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2015.01.015 · Cited by 43
PCSK9 inhibition: the way forward in the treatment of dyslipidemia
Stoekenbroek, R. M., Kastelein, J. J. P., & Huijgen, R. (2015) · BMC Medicine · doi:10.1186/s12916-015-0503-4 · Cited by 45
Serum Lipids, Apolipoproteins, and Mortality among Coronary Artery Disease Patients
Ding, D., Li, X., Qiu, J., Li, R., Zhang, Y., Su, D., Li, Z., Wang, M., Lv, X., Wang, D., et al. (2014) · BioMed Research International · doi:10.1155/2014/709756 · Cited by 43
Apro, J., Tietge, U. J. F., Dikkers, A., Parini, P., Angelin, B., & Rudling, M. (2016) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.116.307385 · Cited by 44
Weight loss surgery in adolescents corrects high-density lipoprotein subspecies and their function
Davidson, W. S., Inge, T. H., Sexmith, H., Heink, A., Elder, D. A., Hui, D. Y., Melchior, J., Kelesidis, T., & Shah, A. S. (2016) · International Journal of Obesity · doi:10.1038/ijo.2016.190 · Cited by 44
Lipid Metabolism and Emerging Targets for Lipid-Lowering Therapy
Gaudet, D., Drouin‐Chartier, J., & Couture, P. (2017) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2016.12.019 · Cited by 43
Nicholls, S. J., Ray, K. K., Ballantyne, C. M., Beacham, L. A., Miller, D. L., Ruotolo, G., Nissen, S. E., & Riesmeyer, J. S. (2017) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2017.04.008 · Cited by 44
Self-citationKaralis, I. K., & Jukema, J. W. (2018) · Current Cardiology Reports · doi:10.1007/s11886-018-1004-9 · Cited by 43
Lipid lowering drugs and inflammatory changes: an impact on cardiovascular outcomes?
Ruscica, M., Ferri, N., Macchi, C., Corsini, A., & Sirtori, C. R. (2018) · Annals of Medicine · doi:10.1080/07853890.2018.1498118 · Cited by 43
Association of an HDL Apolipoproteomic Score With Coronary Atherosclerosis and Cardiovascular Death
Natarajan, P., Collier, T., Jin, Z., Lyass, A., Li, Y., Ibrahim, N. E., Mukai, R., McCarthy, C. P., Massaro, J. M., D’Agostino, R. B., et al. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2019.01.073 · Cited by 45
Li, X., Guan, B., Wang, Y., Tse, G., Zou, F., Waleed, K. B., Xia, Y., Wu, S., & Sun, J. (2019) · Scientific Reports · doi:10.1038/s41598-019-50924-4 · Cited by 43
Niisuke, K., Kuklenyik, Z., Horvath, K. V., Gardner, M. S., Toth, C. A., & Asztalos, B. F. (2020) · Journal of Lipid Research · doi:10.1194/jlr.ra119000258 · Cited by 45
Developing Medicines That Mimic the Natural Successes of the Human Genome
Kathiresan, S. (2015) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2015.02.049 · Cited by 43
The effect of CETP inhibitors on new-onset diabetes: a systematic review and meta-analysis
Dangas, K., Navar, A.-M., & Kastelein, J. J. P. (2022) · European Heart Journal - Cardiovascular Pharmacotherapy · doi:10.1093/ehjcvp/pvac025 · Cited by 44
Poliakova, T., & Wellington, C. L. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00671-y · Cited by 42
eNOS Activation by HDL Is Impaired in Genetic CETP Deficiency
Gomaraschi, M., Ossoli, A., Pozzi, S., Nilsson, P., Cefalu, A. B., Averna, M. R., Kuivenhoven, J. A., Hovingh, G. K., Veglia, F., Franceschini, G., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0095925 · Cited by 42
Rosenthal, E. A., Ranchalis, J., Crosslin, D. R., Burt, A., Brunzell, J. D., Motulsky, A. G., Nickerson, D. A., Wijsman, E. M., & Jarvik, G. P. (2013) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2013.10.019 · Cited by 42
New Therapies for Reducing Low-Density Lipoprotein Cholesterol
Stein, E. A., & Raal, F. J. (2014) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/j.ecl.2014.08.008 · Cited by 42
Singh, S. A., Andraski, A. B., Pieper, B., Goh, W. W. B., Mendivil, C. O., Sacks, F. M., & Aikawa, M. (2016) · Journal of Lipid Research · doi:10.1194/jlr.d061432 · Cited by 42
Kim, D. S., Li, Y. K., Bell, G. A., Burt, A., Vaisar, T., Hutchins, P. M., Furlong, C. E., Otvos, J. D., Polak, J. F., Arnan, M., et al. (2016) · Journal of the American Heart Association · doi:10.1161/jaha.115.002977 · Cited by 42
Elnaem, M. H., Mohamed, M. H. N., Huri, H. Z., Azarisman, S. M., & Elkalmi, R. M. (2017) · Journal of Pharmacy And Bioallied Sciences · doi:10.4103/jpbs.jpbs_30_17 · Cited by 42
Favari, E., Thomas, M. J., & Sorci‐Thomas, M. G. (2018) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0000000000000573 · Cited by 42
Zekavat, S. M., Aragam, K. G., Emdin, C. A., Khera, A. V., Klarin, D. M., Zhao, H., & Natarajan, P. (2019) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.119.312626 · Cited by 40
Ajala, O. N., Demler, O., Liu, Y., Farukhi, Z. M., Adelman, S. J., Collins, H. L., Ridker, P. M., Rader, D. J., Glynn, R. J., & Mora, S. (2020) · Journal of the American Heart Association · doi:10.1161/jaha.119.016507 · Cited by 44
The HDL lipidome is widely remodeled by fast food versus Mediterranean diet in 4 days
Zhu, C., Sawrey-Kubicek, L., Beals, E., Hughes, R. L., Rhodes, C. H., Sacchi, R., & Zivkovic, A. M. (2019) · Metabolomics · doi:10.1007/s11306-019-1579-1 · Cited by 40
Besseling, J., Sjouke, B., & Kastelein, J. J. P. (2015) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.06.011 · Cited by 41
The metabolic vascular syndrome - guide to an individualized treatment
Hanefeld, M., Pistrosch, F., Bornstein, S. R., & Birkenfeld, A. L. (2016) · Reviews in Endocrine and Metabolic Disorders · doi:10.1007/s11154-016-9345-4 · Cited by 44
ABCA1-Derived Nascent High-Density Lipoprotein–Apolipoprotein AI and Lipids Metabolically Segregate
Xu, B., Gillard, B. K., Gotto, A. M., Rosales, C., & Pownall, H. J. (2017) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.117.310290 · Cited by 41
Reversal of coronary atherosclerosis: Role of life style and medical management
Parsons, C. E., Agasthi, P., Mookadam, F., & Arsanjani, R. (2018) · Trends in Cardiovascular Medicine · doi:10.1016/j.tcm.2018.05.002 · Cited by 43
Current and Emerging Reconstituted HDL-apoA-I and HDL-apoE Approaches to Treat Atherosclerosis
Valanti, E.-K., Dalakoura-Karagkouni, K., & Sanoudou, D. (2018) · Journal of Personalized Medicine · doi:10.3390/jpm8040034 · Cited by 41
Lorkowski, S. W., Brubaker, G., Rotroff, D. M., Kashyap, S. R., Bhatt, D. L., Nissen, S. E., Schauer, P. R., Aminian, A., & Smith, J. D. (2020) · Biomolecules · doi:10.3390/biom10040551 · Cited by 45
Wu, Z., Lou, Y., Qiu, X., Liu, Y., Lu, L., Chen, Q., & Jin, W. (2014) · BMC Medical Genetics · doi:10.1186/s12881-014-0118-1 · Cited by 40
“Subsequently, another large randomized trial performed in ACS patients showed that another CETP inhibitor, dalcetrapib, increased HDL-C levels, but did not reduce the risk of recurrent cardiovascular events [9].”
Pharmacogenetics-guided dalcetrapib therapy after an acute coronary syndrome: the dal-GenE trial
Tardif, J., Pfeffer, M. A., Kouz, S., Köenig, W., Maggioni, A. P., McMurray, J. J. V., Mooser, V., Waters, D. D., Grégoire, J. C., L’Allier, P. L., et al. (2022) · European Heart Journal · doi:10.1093/eurheartj/ehac374 · Cited by 40
Self-citationAhmad, W. N. H. W., Sakri, F. H., Mokhsin, A., Rahman, T. H. A., Nasir, N. M., Abdul-Razak, S., Yasin, M. M., Ismail, A. M., Ismail, Z., & Nawawi, H. M. (2015) · PLoS ONE · doi:10.1371/journal.pone.0116867 · Cited by 40
The Role of Early LDL Lowering to Prevent the Onset of Atherosclerotic Disease
Ference, B. A., & Mahajan, N. (2013) · Current Atherosclerosis Reports · doi:10.1007/s11883-013-0312-1 · Cited by 41
RVX 208: A novel BET protein inhibitor, role as an inducer of apo A‐I/ HDL and beyond
Ghosh, G. C., Bhadra, R., Ghosh, R. K., Banerjee, K., & Gupta, A. (2017) · Cardiovascular Therapeutics · doi:10.1111/1755-5922.12265 · Cited by 42
Koekemoer, A. L., Codd, V., Masca, N. G. D., Nelson, C. P., Musameh, M. D., Kaess, B. M., Hengstenberg, C., Rader, D. J., & Samani, N. J. (2017) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.117.309201 · Cited by 40
Genga, K. R., Trinder, M., Kong, H. J., Li, X., Leung, A. K. K., Shimada, T., Walley, K. R., Russell, J. A., Francis, G. A., Brunham, L. R., et al. (2018) · Scientific Reports · doi:10.1038/s41598-018-35261-2 · Cited by 43
A Novel Role for CETP as Immunological Gatekeeper: Raising HDL to Cure Sepsis?
Blauw, L. L., Wang, Y., van Dijk, K. W., & Rensen, P. C. N. (2020) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2020.01.003 · Cited by 40
Wang, M., Liu, M., Li, F., Guo, C., Liu, Z., Pan, Y., Liu, Y., Liu, F., Cai, H., Wu, Y., et al. (2020) · Lipids in Health and Disease · doi:10.1186/s12944-020-01313-8 · Cited by 42
Schillemans, T., Donat‐Vargas, C., Lindh, C. H., de Faire, U., Wolk, A., Leander, K., & Åkesson, A. (2022) · Environmental Health Perspectives · doi:10.1289/ehp9791 · Cited by 39
HDL cholesterol levels and susceptibility to COVID-19
Chidambaram, V., Kumar, A., Majella, M. G., Seth, B., Sivakumar, R. K., Voruganti, D. C., Bavineni, M., Baghal, A., Gates, K., Kumari, A., et al. (2022) · EBioMedicine · doi:10.1016/j.ebiom.2022.104166 · Cited by 40
Novel and Emerging LDL-C Lowering Strategies: A New Era of Dyslipidemia Management
Agnello, F., Ingala, S., Laterra, G., Scalia, L., & Barbanti, M. (2024) · Journal of Clinical Medicine · doi:10.3390/jcm13051251 · Cited by 39
HDL-Cholesterol and Triglycerides Dynamics: Essential Players in Metabolic Syndrome
Alcover, S., Ramos-Regalado, L., Girón, G., Muñoz‐García, N., & Vilahur, G. (2025) · Antioxidants · doi:10.3390/antiox14040434 · Cited by 50
Dysfunctional high-density lipoprotein: an updated review
Ouyang, F. W., Chiang, H., Hsu, W., Tsai, M.-H., Huang, C.-Y., Remaley, A. T., Akyol, Ö., & Chen, C. (2025) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2025.1713387 · Cited by 40
Extended-Release Niacin Therapy and Risk of Ischemic Stroke in Patients With Cardiovascular Disease
Teo, K. K., Goldstein, L. B., CHAITMAN, B. R., Grant, S., Weintraub, W. S., Anderson, D. C., Sila, C. A., Cruz‐Flores, S., Padley, R. J., Kostuk, W. J., et al. (2013) · Stroke · doi:10.1161/strokeaha.113.001529 · Cited by 39
Self-citationvan Capelleveen, J. C., Kastelein, J. J. P., Zwinderman, A. H., van Deventer, S. J. H., Collins, H. L., Adelman, S. J., Round, P., Ford, J., Rader, D. J., & Hovingh, G. K. (2016) · Journal of clinical lipidology · doi:10.1016/j.jacl.2016.06.006 · Cited by 42
Influence of HDL particles on cell-cholesterol efflux under various pathological conditions
Asztalos, B. F., Horvath, K. V., Mehan, M. R., Yokota, Y., & Schaefer, E. J. (2017) · Journal of Lipid Research · doi:10.1194/jlr.m075648 · Cited by 39
Farràs, M., Fernández‐Castillejo, S., Rubió, L., Arranz, S., Catalán, Ú., Subirana, I., Romero, M.-P., Castañer, O., Pedret, A., Blanchart, G., et al. (2017) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2017.09.010 · Cited by 39
Wacker, B. K., Dronadula, N., Bi, L., Stamatikos, A., & Dichek, D. A. (2017) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.117.309565 · Cited by 39
Shishikura, D., Kataoka, Y., Honda, S., Takata, K., Kim, S. W., Andrews, J., Psaltis, P. J., Sweeney, M., Kulikowski, E., Johansson, J., et al. (2018) · American Journal of Cardiovascular Drugs · doi:10.1007/s40256-018-0298-8 · Cited by 39
Self-citationLymphatic system identification, pathophysiology and therapy in the cardiovascular diseases
Hu, D. M., Li, L., Li, S., Wu, M., Ge, N., Cui, Y., Lian, Z., Song, J., & Chen, H. (2019) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2019.06.002 · Cited by 44
Streja, E., Kovesdy, C. P., Streja, D. A., Moradi, H., Kalantar‐Zadeh, K., & Kashyap, M. L. (2015) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2014.11.033 · Cited by 39
Ewang-Emukowhate, M., & Wierzbicki, A. S. (2013) · Journal of Cardiovascular Pharmacology and Therapeutics · doi:10.1177/1074248413492906 · Cited by 39
Dullaart, R. P. F., Annema, W., Tio, R. A., & Tietge, U. J. F. (2014) · Clinica Chimica Acta · doi:10.1016/j.cca.2014.02.026 · Cited by 41
Palmisano, B. T., Le, T. D. V., Zhu, L., Lee, Y., & Stafford, J. M. (2016) · Journal of Lipid Research · doi:10.1194/jlr.m069013 · Cited by 39
The Therapeutic Potential of Anti-Inflammatory Exerkines in the Treatment of Atherosclerosis
Yu, M., Tsai, S., & Kuo, Y. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18061260 · Cited by 39
Noninvasive Plaque Imaging to Accelerate Coronary Artery Disease Drug Development
Figtree, G. A., Adamson, P. D., Antoniades, C. A., Blumenthal, R. S., Blaha, M. J., Budoff, M. J., Celermajer, D. S., Chan, M. Y., Chow, C. K., Dey, D., et al. (2022) · Circulation · doi:10.1161/circulationaha.122.060308 · Cited by 38
Self-citationMørland, J. G., Magnus, P. M., Vollset, S. E., Leon, D. A., Selmer, R. M., & Tverdal, A. (2023) · International Journal of Epidemiology · doi:10.1093/ije/dyad011 · Cited by 40
Photocatalytic Phosphine-Mediated Thioesterification of Carboxylic Acids with Disulfides
Su, J., Chen, A., Zhang, G., Jiang, Z., & Zhao, J. (2023) · Organic Letters · doi:10.1021/acs.orglett.3c03249 · Cited by 38
Impact of Obicetrapib on Major Adverse Cardiovascular Events in High-Risk Patients
Nicholls, S. J., Nelson, A. J., Ray, K. K., Ballantyne, C. M., Ditmarsch, M., Kling, D. F., Hsieh, A., Szarek, M. J., Kastelein, J. J. P., & Davidson, M. H. (2025) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2025.07.056 · Cited by 39
Self-citationUpdate on Lipoprotein(a) as a Cardiovascular Risk Factor and Mediator
Boffa, M. B., & Koschinsky, M. L. (2013) · Current Atherosclerosis Reports · doi:10.1007/s11883-013-0360-6 · Cited by 38
Vilahur, G., Gutiérrez, M., Casaní, L., Cubedo, J., Capdevila, A., Pons‐Lladó, G., Carreras, F., Hidalgo, A., & Badimón, L. (2015) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2015.08.901 · Cited by 38
Reyes‐Soffer, G., Millar, J. S., Ngai, C. I., Jumes, P. A., Coromilas, E. J., Asztalos, B. F., Johnson‐Levonas, A. O., Wagner, J. A., Donovan, D. S., Karmally, W., et al. (2016) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.115.306680 · Cited by 38
Halcox, J., & Misra, A. (2014) · Metabolic Syndrome and Related Disorders · doi:10.1089/met.2014.0049 · Cited by 38
Mendelian randomization reveals unexpected effects of CETP on the lipoprotein profile
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Gibson, C. M., Kernéis, M., Yee, M. K., Daaboul, Y., Korjian, S., Mehr, A. P., Tricoci, P., Alexander, J. H., Kastelein, J. J. P., Mehran, R., et al. (2018) · American Heart Journal · doi:10.1016/j.ahj.2018.11.008 · Cited by 38
Yamashita, S., Arai, H., Bujo, H., Masuda, D., Ohama, T., Ishibashi, T., Yanagi, K., Doi, Y., Nakagawa, S., Yamashiro, K., et al. (2020) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.55327 · Cited by 40
HDL, cholesterol efflux, and ABCA1: Free from good and evil dualism
Ogura, M. (2022) · Journal of Pharmacological Sciences · doi:10.1016/j.jphs.2022.07.004 · Cited by 44
The mechanistic pathways of oxidative stress in aortic stenosis and clinical implications
Phua, K., Chew, N., Kong, W. K. F., Tan, R., Ye, L., & Poh, K. K. (2022) · Theranostics · doi:10.7150/thno.71813 · Cited by 41
Structure-based mechanism and inhibition of cholesteryl ester transfer protein
Han, X. M., Zhang, M., Liu, J., Wang, J., & Ren, G. (2023) · Current Atherosclerosis Reports · doi:10.1007/s11883-023-01087-1 · Cited by 37
Implications of reverse cholesterol transport: Recent studies
Levinson, S. S., & Wagner, S. G. (2014) · Clinica Chimica Acta · doi:10.1016/j.cca.2014.10.018 · Cited by 36
Pharmacogenetic Markers of Drug Efficacy and Toxicity
Yip, V., Hawcutt, D. B., & Pirmohamed, M. (2015) · Clinical Pharmacology & Therapeutics · doi:10.1002/cpt.135 · Cited by 38
Mantlo, N. B., & Escribano, A. (2013) · Journal of Medicinal Chemistry · doi:10.1021/jm400574e · Cited by 37
Recent clinical trials evaluating benefit of drug therapy for modification of HDL cholesterol
Wright, R. S. (2013) · Current Opinion in Cardiology · doi:10.1097/hco.0b013e328362059d · Cited by 37
Self-citationCholesteryl ester transfer protein: An enigmatic pharmacology – Antagonists and agonists
Yamashita, S., Ruscica, M., Macchi, C., Corsini, A., Matsuzawa, Y., & Sirtori, C. R. (2018) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2018.09.035 · Cited by 37
Hannon, B. A., Khan, N. A., & Terán-Garcı́a, M. (2018) · Nutrients · doi:10.3390/nu10101404 · Cited by 45
Lipidome Abnormalities and Cardiovascular Disease Risk in HIV Infection
Bowman, E., & Funderburg, N. (2019) · Current HIV/AIDS Reports · doi:10.1007/s11904-019-00442-9 · Cited by 38
Lipid efflux mechanisms, relation to disease and potential therapeutic aspects
Castaño, D., Rattanasopa, C., Monteiro-Cardoso, V. F., Corlianò, M., Liu, Y., Zhong, A., Rusu, M., Liehn, E. A., & Singaraja, R. R. (2020) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2020.04.013 · Cited by 37
Xue, H., & Pan, W. (2020) · PLoS Genetics · doi:10.1371/journal.pgen.1009105 · Cited by 37
High-Density Lipoprotein Subclasses, Coronary Artery Disease, and Cardiovascular Mortality
Silbernagel, G., Pagel, P., Pfahlert, V., Genser, B., Scharnagl, H., Kleber, M. E., Delgado, G., Ohrui, H., Ritsch, A., Grammer, T. B., et al. (2017) · Clinical Chemistry · doi:10.1373/clinchem.2017.275636 · Cited by 38
Cholesteryl Ester Transfer Protein Inhibition Is Not Yet Dead—Pro
Barter, P. J., & Rye, K. (2016) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.115.306879 · Cited by 36
Self-citationObicetrapib—the Rebirth of CETP Inhibitors?
Chang, B. J., Laffin, L. J., Sarraju, A., & Nissen, S. E. (2024) · Current Atherosclerosis Reports · doi:10.1007/s11883-024-01231-5 · Cited by 36
Lu, J. J.-Q., Hübner, K., Nanjee, M. N., Brinton, E. A., & Mazer, N. A. (2014) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1003509 · Cited by 37
Kawaguchi, H., Yamada, T., Miura, N., Ayaori, M., Uto‐Kondo, H., Ikegawa, M., Noguchi, M., Wang, K., Izumi, H., & Tanimoto, A. (2013) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.21246 · Cited by 36
Battaggia, A., Donzelli, A., Font, M., Molteni, D., & Galvano, A. (2015) · PLOS ONE · doi:10.1371/journal.pone.0124587 · Cited by 36
Suico, J. G., Wang, M., Friedrich, S. W., Cannady, E. A., Konkoy, C. S., Ruotolo, G., & Krueger, K. A. (2014) · Journal of Pharmacy and Pharmacology · doi:10.1111/jphp.12287 · Cited by 36
Linden, F., Domschke, G., Erbel, C., Akhavanpoor, M., Katus, H. A., & Gleissner, C. A. (2014) · Frontiers in Physiology · doi:10.3389/fphys.2014.00455 · Cited by 35
New directions for pharmacotherapy in the treatment of acute coronary syndrome
Adamski, P., Adamska, U., Ostrowska, M., Koziński, M., & Kubica, J. (2016) · Expert Opinion on Pharmacotherapy · doi:10.1080/14656566.2016.1241234 · Cited by 36
Rautureau, Y., Deschambault, V., Higgins, M., Rivas, D., Mecteau, M., Geoffroy, P., Miquel, G., Uy, K., Sánchez, R., Lavoie, V., et al. (2018) · Circulation · doi:10.1161/circulationaha.117.031134 · Cited by 36
Self-citationZhu, L., Luu, T. N., Emfinger, C. H., Parks, B. A., Shi, J., Trefts, E., Zeng, F., Kuklenyik, Z., Harris, R. C., Wasserman, D. H., et al. (2018) · Diabetes · doi:10.2337/db18-0474 · Cited by 36
Impact of ADCY9 Genotype on Response to Anacetrapib
Hopewell, J. C., Ibrahim, M. A.-H., Hill, M., Shaw, P. M., D, E. B. M., Blaustein, R. O., Bowman, L. J., Landray, M., Sabatine, M. S., Collins, R., et al. (2019) · Circulation · doi:10.1161/circulationaha.119.041546 · Cited by 36
Self-citationTeis, A., Cediel, G., Amigó, N., Julve, J., Aranyo, J. A., Andrés-Cordón, J. F., Puig-Jové, C., Castelblanco, E., Gual‐Capllonch, F., Ferrer‐Sistach, E., et al. (2021) · Scientific Reports · doi:10.1038/s41598-021-82861-6 · Cited by 36
Metadata
- Authors
- Schwartz, G. G., Olsson, A. G., Abt, M., Ballantyne, C. M., Barter, P. J., Brumm, J., Chaitman, B. R., Holme, I. M., Kallend, D., Leiter, L. A., Leitersdorf, E., McMurray, J. J. V., Mundl, H., Nicholls, S. J., Shah, P. K., Tardif, J.-C., & Wright, R. S.
- Affiliations
- Denver VA Medical Center (US)
- Linköping University (SE)
- F. Hoffmann-La Roche AG (CH)
- Baylor College of Medicine (US)
- University of Zurich (CH)
- Oslo University Hospital (NO)
- St. Michael's Hospital (CA)
- Mayo Clinic (US)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2012-11-29
- Volume
- 367
- Issue
- 22
- Pages
- 2089-2099
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2118825330
- Cited by
- 2,022
- References
- 35
- Citations by year
- 2026: 66 · 2025: 82 · 2024: 81 · 2023: 89 · 2022: 103 · 2021: 128 · 2020: 109 · 2019: 141 · 2018: 164 · 2017: 195 · 2016: 222 · 2015: 244 · 2014: 191 · 2013: 190 · 2012: 7
- FWCI
- 206.17
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
- Research Bank (Australian Catholic University) (submittedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Archivio Istituzionale della Ricerca - Università degli Studi della Campania "Luigi Vanvitelli" (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- Amgen
- Bristol-Myers Squibb
- Eli Lilly and Company
- Pfizer
- AstraZeneca
- GlaxoSmithKline
- Sanofi
- F. Hoffmann-La Roche
- CSL Behring
- Amarin Corporation
- Anthera
- Kowa Company
- Servier
- Esperion Therapeutics
- Genentech
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- dalcetrapib, cholesteryl ester transfer protein inhibition, HDL cholesterol, acute coronary syndrome, cardiovascular risk, futility, LDL cholesterol, C-reactive protein, systolic blood pressure, myocardial infarction, ischemic stroke, unstable angina, cardiovascular mortality, lipid-lowering therapy
- MeSH terms
- Aged, Amides, Anticholesteremic Agents, Apolipoproteins, Blood Pressure, C-Reactive Protein, Cardiovascular Diseases, Esters, Female, Humans, Cholesterol, HDL, Cholesterol, LDL, Male, Middle Aged, Risk, Sulfhydryl Compounds, Triglycerides, Biomarkers, Cholesterol Ester Transfer Proteins, Acute Coronary Syndrome, Secondary Prevention
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