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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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“Patients without elevated cardiac biomarkers were qualified to participate if symptoms of acute myocardial ischemia were accompanied by a new onset electrocardiographic changes [4].”
BackgroundTardif, J., Rhainds, D., Rhéaume, É., & Dubé, M. (2017) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.116.307122 · Cited by 32
Self-citationHDL Hypothesis: Where Do We Stand Now?
Tariq, S. M., Sidhu, M. S., Toth, P. P., & Boden, W. E. (2014) · Current Atherosclerosis Reports · doi:10.1007/s11883-014-0398-0 · Cited by 31
Hovingh, G. K., Ray, K. K., & Boekholdt, S. M. (2015) · Circulation · doi:10.1161/circulationaha.115.014026 · Cited by 31
“The dal-oUTCoMES trial was stopped for futility after an average of 3 years of follow up.(45) When subgroups such as those with low baseline HDL-C or high LDL-C were assessed, there was no evidence that dalcetrapib had a beneficial effect.”
BackgroundMethodResidual cardiovascular risk of lipid origin. Components and pathophysiological aspects
Mijares, A. H., Ascaso, J. F., Blasco, M., Brea, Á., Díaz, Á., Mantilla, T., Pedro‐Botet, J., Pintó, X., & Millán, J. (2019) · Clínica e Investigación en Arteriosclerosis (English Edition) · doi:10.1016/j.artere.2019.02.002 · Cited by 31
Morvaridzadeh, M., Zoubdane, N., Heshmati, J., Alami, M., Berrougui, H., & Khalil, A. (2024) · Nutrients · doi:10.3390/nu16050653 · Cited by 39
“This trial was also terminated early due to futility, with a hazard ratio (HR) for the primary endpoint of major vascular events of 1.04 [118].”
BackgroundInfluentialHDL-C: clinical equipoise and vascular endothelial function
Campbell, S., & Genest, J. J. (2013) · Expert Review of Cardiovascular Therapy · doi:10.1586/erc.13.17 · Cited by 30
Ducrocq, G., Bhatt, D. L., Labreuche, J., Corbalan, R. L., Porath, A., Gao, R., Панченко, Е. П., Cs, L., Ikeda, Y., Goto, S., et al. (2013) · European Journal of Preventive Cardiology · doi:10.1177/2047487313501278 · Cited by 30
“Most large recent randomized controlled trials (RCTs) have enrolled patients in various regions of the world.(2,3) (1)Université Paris-Diderot, Sorbonne Paris Cité, France; AP-HP, Hopital Bichat - Paris, France; INSERM U-698, France (2)VA Boston Healthcare System, Brigham and Women’s Hospital, Harvard Medical School,…”
BackgroundKoba, S., Ayaori, M., Uto‐Kondo, H., Furuyama, F., Yokota, Y., Tsunoda, F., Shoji, M., Ikewaki, K., & Kobayashi, Y. (2016) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.34454 · Cited by 31
Lei, D., Rames, M. J., Zhang, X., Zhang, L., Zhang, S., & Ren, G. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.715565 · Cited by 31
“Although anacetrapib is still being tested in clinical studies, the failures of torcetrapib (due to off-target effects) (7) and dalcetrapib and evacetrapib (due to their unexpected low efficacy) (8, 11) highlight that the detailed mechanism underlying the CETP-mediated transfer of CE molecules between HDL and LDL/VLDL…”
BackgroundLeveraging human genetics to guide drug target discovery
Stitziel, N. O., & Kathiresan, S. (2016) · Trends in Cardiovascular Medicine · doi:10.1016/j.tcm.2016.08.008 · Cited by 31
“therapeutically raising HDL have failed to demonstrate reduction in risk of CHD[13, 14].”
Metabolic and Molecular Imaging of Atherosclerosis and Venous Thromboembolism
Osborn, E. A., Kessinger, C. W., Tawakol, A. A., & Jaffer, F. A. (2017) · Journal of Nuclear Medicine · doi:10.2967/jnumed.116.182873 · Cited by 31
Brassard, D., Arsenault, B. J., Boyer, M., Bernic, D., Tessier‐Grenier, M., Talbot, D. C., Tremblay, A., Levy, E. H., Asztalos, B. F., Jones, P. J. H., et al. (2018) · Journal of Nutrition · doi:10.1093/jn/nxy014 · Cited by 30
“The neutral effect of SFAs from cheese on HDLmediated CEC as well as on LDL-cholesterol concentrations (28) is consistent with the absence of an association between cheese consumption and CAD risk.”
BackgroundInfluentialJonas, K., & Kopeć, G. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20143514 · Cited by 31
“Previous trials with CETP inhibitors: Torcetrapib and dalcetrapib failed to show the beneficial effect of increasing HDL on cardiovascular risk [15,16].”
Aghasizadeh, M., Samadi, S., Sahebkar, A., Miri‐Moghaddam, E., Esmaily, H., Souktanloo, M., Avan, A., Mansoori, A., Ferns, G. A., Kazemi, T., et al. (2021) · Journal of Clinical Laboratory Analysis · doi:10.1002/jcla.23770 · Cited by 32
“concentration according to the last literature (16).”
Gracia‐Rubio, I., Martı́n, C., Civeira, F., & Cenarro, A. (2021) · Biomedicines · doi:10.3390/biomedicines9060612 · Cited by 32
“However, Mendelian randomization studies [9,10] and pharmacological interventional studies [11,12] do not support the concept that HDLc directly reduces the risk of CVD [8].”
BackgroundMultitrait GWAS to connect disease variants and biological mechanisms
Julienne, H., Laville, V., McCaw, Z. R., He, Z., Guillemot, V., Lasry, C., Ziyatdinov, A., Nerin, C., Vaysse, A., Lechat, P., et al. (2021) · PLoS Genetics · doi:10.1371/journal.pgen.1009713 · Cited by 35
European guidelines for the treatment of dyslipidaemias: New concepts and future challenges
Pirillo, A., Casula, M., & Catapano, A. L. (2023) · Pharmacological Research · doi:10.1016/j.phrs.2023.106936 · Cited by 38
Self-Evaluation of Voice as a Treatment Outcome Measure
Laukkanen, A.-M., Leppänen, K., & Ilomäki, I. (2009) · Folia Phoniatrica et Logopaedica · doi:10.1159/000201000 · Cited by 31
HDL quality and functionality: what can proteins and genes predict?
Karavia, E. A., Zvintzou, E., Πετροπούλου, Π.-Ι., Xepapadaki, E., Constantinou, C., & Kypreos, K. E. (2014) · Expert Review of Cardiovascular Therapy · doi:10.1586/14779072.2014.896741 · Cited by 31
“Though two large clinical trials that involve increasing HDL-C levels by pharmacological means (REVEAL and ACCELERATE) are still under way [21], the failure of high-dose niacin to reduce the risk for cardiovascular events [22], the increased CHD-related mortality seen in patients treated with Torcetrapib [23,24] and t…”
BackgroundSemenkovich, C. F., Goldberg, A. C., & Goldberg, I. J. (2011) · Elsevier eBooks · doi:10.1016/b978-1-4377-0324-5.00037-7 · Cited by 32
Biology, pathophysiology and current therapies that affect lipoprotein (a) levels
Rawther, T., & Tabet, F. (2019) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2019.04.005 · Cited by 31
Zein, M. A., Khazzeka, A., Khoury, A. E., Zein, J. A., Dima, Z., & Eid, A. H. (2024) · Progress in Cardiovascular Diseases · doi:10.1016/j.pcad.2024.10.009 · Cited by 35
HDL particle functionality as a primary pharmacological target for HDL-based therapies
Kypreos, K. E., Gkizas, S., Rallidis, L. S., & Karagiannides, I. (2013) · Biochemical Pharmacology · doi:10.1016/j.bcp.2013.03.004 · Cited by 30
“trial showed that dalcetrapib did not reduce the risk of recurrent cardiovascular events in patients with acute coronary syndrome despite a significant increase in HDL-C [25].”
BackgroundResultDyslipidemia in Patients with Chronic and End-Stage Kidney Disease
Omran, J., Al‐Dadah, A., & Dellsperger, K. C. (2013) · Cardiorenal Medicine · doi:10.1159/000351985 · Cited by 30
Current guidelines for high-density lipoprotein cholesterol in therapy and future directions
Michos, E. D., Subedi, B. H., Joshi, P. H., Jones, S. R., Martin, S. S., & Blaha, M. J. (2014) · Vascular Health and Risk Management · doi:10.2147/vhrm.s45648 · Cited by 31
Padala, S. K., Sidhu, M. S., & Boden, W. E. (2016) · Springer eBooks · doi:10.1007/978-3-642-37393-0_70-2 · Cited by 30
“Despite a significant increase in on-treatment HDL-C levels of 31–40 % (with no change in LDL-C levels), there was no difference in the cardiovascular outcomes or mortality (Schwartz et al. 2012).”
BackgroundPlaque imaging to refine indications for emerging lipid-lowering drugs
Alkhalil, M., Chai, J. T., & Choudhury, R. P. (2016) · European Heart Journal - Cardiovascular Pharmacotherapy · doi:10.1093/ehjcvp/pvw034 · Cited by 30
“However, other CETP inhibitors which do not share molecular similarity as torcetrapib were also unsuccessful in reducing CV risk.(39)”
BackgroundDavidson, W. S., Heink, A., Sexmith, H., Dolan, L. M., Gordon, S. M., Otvos, J. D., Melchior, J., Elder, D. A., Khoury, J. C., Geh, E. N., et al. (2017) · Journal of Lipid Research · doi:10.1194/jlr.m078667 · Cited by 30
Examining the paradox of high high-density lipoprotein and elevated cardiovascular risk
Singh, K., & Rohatgi, A. K. (2018) · Journal of Thoracic Disease · doi:10.21037/jtd.2017.12.97 · Cited by 30
“As described above, CETP inhibitors were studied in large outcomes trials with the first three resulting in either harm or no benefit despite increases in HDL-C as high as 70% (12,13,29).”
BackgroundAssessment of HDL Cholesterol Removal Capacity: Toward Clinical Application
Toh, R. (2018) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.rv17028 · Cited by 31
Gonna, H., & Ray, K. K. (2019) · Diabetes Obesity and Metabolism · doi:10.1111/dom.13691 · Cited by 30
“Dalcetrapib had little or no effect on apoB and LDL-C but increased HDL-C by about 30%.(117) Evacetrapib reduced LDL by about 30% and raised HDL-C by about 133% and did not reduce CVD.”
BackgroundTardif, J., Dubé, M., Pfeffer, M. A., Waters, D. D., Köenig, W., Maggioni, A. P., McMurray, J. J. V., Mooser, V., White, H. D., Heinonen, T. M., et al. (2020) · American Heart Journal · doi:10.1016/j.ahj.2020.01.007 · Cited by 30
Self-citationTreating Coronary Artery Disease: Beyond Statins, Ezetimibe, and PCSK9 Inhibition
Musunuru, K. (2020) · Annual Review of Medicine · doi:10.1146/annurev-med-080819-044918 · Cited by 32
Hafiane, A., Bielicki, J. K., Johansson, J. O., & Genest, J. J. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2014.07.018 · Cited by 30
Batuca, J. R., Amaral, M., Favas, C., Paula, F. S., Ames, P. R. J., Papoila, A. L., & Alves, J. D. (2016) · British Journal of Clinical Pharmacology · doi:10.1111/bcp.13198 · Cited by 31
Tsai, C.-W., Huang, H.-C., Chiang, H.-Y., Chung, C.-W., Chang, S.-N., Chu, P.-L., & Kuo, C.-C. (2019) · Journal of Lipid Research · doi:10.1194/jlr.p084590 · Cited by 28
Causal Effect of Lipids and Lipoproteins on Atherosclerosis
Ference, B. A. (2018) · Cardiology Clinics · doi:10.1016/j.ccl.2017.12.001 · Cited by 28
Helgadottir, A., Thorleifsson, G., Snaebjarnarson, A., Stefansdottir, L., Sveinbjornsson, G., Tragante, V., Björnsson, E., Steinthorsdottir, V., Gretarsdottir, S., Helgason, H., et al. (2022) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwac219 · Cited by 30
The Role of Selected lncRNAs in Lipid Metabolism and Cardiovascular Disease Risk
Gluba-Brzózka, A., Franczyk, B., Rysz-Górzyńska, A., Olszewski, R., & Rysz, J. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25179244 · Cited by 32
Teramoto, T., Takeuchi, M., Morisaki, Y., Ruotolo, G., & Krueger, K. A. (2014) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2014.03.045 · Cited by 29
“It is worth noting that evacetrapib did not have any adverse effects on mineralocorticoid or electrolyte measures, thus agreeing with data reported in the phase 2 study of evacetrapib in the United States and Europe,(6) in the phase 2 study of anacetrapib,(17) and in the phase 3 study of dalcetrapib.(18)The lack of un…”
ResultYadav, R., Liu, Y., Kwok, S., Hama, S., France, M. W., Eatough, R., Pemberton, P., Schofield, J. D., Siahmansur, T. J., Malik, R. A., et al. (2015) · Journal of the American Heart Association · doi:10.1161/jaha.114.001508 · Cited by 29
“Our results also show that ERN/LRP significantly reduces CETP activity and increases HDL cholesterol efflux capacity, explaining the increase in HDL-C.”
BackgroundMethodInfluentialYakushiji, E., Ayaori, M., Nishida, T., Shiotani, K., Takiguchi, S., Nakaya, K., Uto‐Kondo, H., Ogura, M., Sasaki, M., Yogo, M., et al. (2016) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.115.306376 · Cited by 29
“In this regard, inhibition of cholesteryl ester transfer protein has been unsuccessful to date in achieving a beneficial clinical outcome.(15,16) One might raise the argument that functional aspects of HDL should be targeted rather than merely increasing HDLcholesterol to achieve clinical benefits, specifically focusi…”
BackgroundThe Future of Cardiovascular Therapeutics
MacRae, C. A., Roden, D. M., & Loscalzo, J. (2016) · Circulation · doi:10.1161/circulationaha.116.023555 · Cited by 29
Yamashita, S., & Matsuzawa, Y. (2016) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000332 · Cited by 30
“In dal-OUTCOMES [67], patients with recent acute coronary syndrome received dalcetrapib or placebo.”
MethodEyvazian, V. A., & Frishman, W. H. (2017) · Cardiology in Review · doi:10.1097/crd.0000000000000137 · Cited by 31
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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