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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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“An outcomes trial using dalcetrapib, an agent with modest HDL-raising effects and essentially no effect on LDL cholesterol, was stopped for futility.(104) Two other compounds, anacetrapib and evacetrapib, remain under active investigation; both have substantial”
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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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