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Niacin in Patients with Low HDL Cholesterol Levels Receiving Intensive Statin Therapy
Open accessAbstract
BACKGROUND: In patients with established cardiovascular disease, residual cardiovascular risk persists despite the achievement of target low-density lipoprotein (LDL) cholesterol levels with statin therapy. It is unclear whether extended-release niacin added to simvastatin to raise low levels of high-density lipoprotein (HDL) cholesterol is superior to simvastatin alone in reducing such residual risk. METHODS: We randomly assigned eligible patients to receive extended-release niacin, 1500 to 2000 mg per day, or matching placebo. All patients received simvastatin, 40 to 80 mg per day, plus ezetimibe, 10 mg per day, if needed, to maintain an LDL cholesterol level of 40 to 80 mg per deciliter (1.03 to 2.07 mmol per liter). The primary end point was the first event of the composite of death from coronary heart disease, nonfatal myocardial infarction, ischemic stroke, hospitalization for an acute coronary syndrome, or symptom-driven coronary or cerebral revascularization. RESULTS: A total of 3414 patients were randomly assigned to receive niacin (1718) or placebo (1696). The trial was stopped after a mean follow-up period of 3 years owing to a lack of efficacy. At 2 years, niacin therapy had significantly increased the median HDL cholesterol level from 35 mg per deciliter (0.91 mmol per liter) to 42 mg per deciliter (1.08 mmol per liter), lowered the triglyceride level from 164 mg per deciliter (1.85 mmol per liter) to 122 mg per deciliter (1.38 mmol per liter), and lowered the LDL cholesterol level from 74 mg per deciliter (1.91 mmol per liter) to 62 mg per deciliter (1.60 mmol per liter). The primary end point occurred in 282 patients in the niacin group (16.4%) and in 274 patients in the placebo group (16.2%) (hazard ratio, 1.02; 95% confidence interval, 0.87 to 1.21; P=0.79 by the log-rank test). CONCLUSIONS: Among patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of less than 70 mg per deciliter (1.81 mmol per liter), there was no incremental clinical benefit from the addition of niacin to statin therapy during a 36-month follow-up period, despite significant improvements in HDL cholesterol and triglyceride levels. (Funded by the National Heart, Lung, and Blood Institute and Abbott Laboratories; AIM-HIGH ClinicalTrials.gov number, NCT00120289.).
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In the citing paper
“Nonetheless, these studies also did not prospectively enroll patients with elevated TG levels despite statin therapy,6, 12, 13, 14, 15”
From Rationale and design of REDUCE‐IT : Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (2017) · cites this paper as [15]
Checked by a reasoning model — may be wrong.
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
“Post hoc and prespecified subgroup analyses and meta-analyses of 5 major fibrate trialsdHelsinki Heart Study, Veterans Affairs HDL Intervention Trial, Bezafibrate Infarction Project, FIELD, and ACCORD-Lipiddhave shown a CV benefit in persons with moderate dyslipidemia (triglycerides >200 mg/dL and HDL-C <40 mg/dL, either isolated or together) but not in persons without dyslipidemia.”
From American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update. (2022) · cites this paper as [378]
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
“In the EU, treatment with niacin was stopped after the AIM-HIGH and HPS2-THRIVE trials showed no improvement in MACE and an increased occurrence of undesirable side effects [123, 124].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [123]
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
“Similarly, a previous trial of niacin 4 and two previous trials of fenofibrate 5,6 showed no significant decrease in cardiovascular risk, although triglyceride levels were lowered by 26%, 29%, and 26%, respectively.”
From Triglyceride Lowering with Pemafibrate to Reduce Cardiovascular Risk (2022) · cites this paper as [4]
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
“With the exception of the FIELD trial, all these trials involved patients who were receiving statins.”
From Triglyceride Lowering with Pemafibrate to Reduce Cardiovascular Risk (2022) · cites this paper as [4]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Prior CV outcome studies that administered therapies with TG‐lowering effects (niacin or fenofibrate) on top of statin therapy did not reach their primary endpoints.”
From Rationale and design of REDUCE‐IT : Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (2017) · cites this paper as [15]
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
“Benefits in outcome studies appear limited to subgroups with high TG and low HDL-C, highlighting the complexity of translating TG reduction into ASCVD risk reduction [61, 74–77].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [75]
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
“Conversely, traditional TG-lowering agents, such as fibrates and niacin, have demonstrated inconsistent CVD benefits in randomized trials, even when lipid changes were robust.”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [75]
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
“Two large randomized controlled trials (RCTs) evaluating the efficacy of extended-release niacin vs placebo on background statin therapy in individuals with established ASCVD did not demonstrate a reduction in vascular events”
From The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk (2019) · cites this paper as [18]
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
“Large clinical trials, including the Atherothrombosis Intervention in Metabolic Syndrome With Low HDL/High Triglycerides: Impact on Global Health Outcomes (AIM-HIGH) and Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE) trials, failed to demonstrate a benefit of adding niacin to individuals on appropriate statin therapy.”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2025 (2025) · cites this paper as [160]
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
“Large clinical trials, including the Atherothrombosis Intervention in Metabolic Syndrome With Low HDL/High Triglycerides: Impact on Global Health Outcomes (AIM-HIGH) and Heart Protection Study 2–Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE) trials, failed to demonstrate a benefit of adding niacin to individuals on appropriate statin therapy.”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2026 (2026) · cites this paper as [154]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“However, the recently concluded AIM-HIGH study did not report any further benefits with regard to cardiovascular events when niacin was added to a statin in patients with median triglyceride level of about 160 mg/dl in the mild hypertriglyceridemia range and average LDL cholesterol levels below 80 mg/dl (177).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [177]
The cited source says what the claim attributes to it.
In the citing paper
“whether lowering these levels would also lower the incidence of cardiovascular events remains controversial.”
From Triglyceride Lowering with Pemafibrate to Reduce Cardiovascular Risk (2022) · cites this paper as [4]
The cited source says what the claim attributes to it.
In the citing paper
“These neutral findings with pemafibrate are consistent with those from the contemporary Outcomes Study to Assess Statin Residual Risk Reduction with Epanova in High Cardiovascular Risk Patients with Hypertriglyceridemia (STRENGTH) trial 2 of high-dose n-3 fatty acids, the previous Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health Outcomes”
From Triglyceride Lowering with Pemafibrate to Reduce Cardiovascular Risk (2022) · cites this paper as [4]
The cited source says what the claim attributes to it.
In the citing paper
“In fact, there was a possible increased risk of ischemic stroke in the AIM-HIGH trial (160)”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2025 (2025) · cites this paper as [160]
The cited source says what the claim attributes to it.
In the citing paper
“In fact, there was a possible increased risk of ischemic stroke in the AIM-HIGH trial (154) and an increased incidence of new-onset diabetes (absolute excess, 1.3 percentage points; P < 0.001) and disturbances in diabetes management among those with diabetes in the HPS2-THRIVE trial in those on combination therapy (155).”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2026 (2026) · cites this paper as [154]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Studies, such as the Copenhagen City Heart Study involving 9330 individuals, indicate a progressive rise in myocardial infarction risk over a decade with increasing Lp(a) levels [13].”
From Residual Cardiovascular Risk: Role of Remnants Cholesterol, Monocyte/HDL Ratio and Lipoprotein Ratios on Personalized Cardiovascular Prevention (2024) · cites this paper as [13]
Experimental — accuracy not yet measuredIn the citing paper
“The observed annualized primary endpoint event rate for placebo patients in REDUCE-IT was 5.74%, which is consistent with historical cardiovascular outcome studies, including those published since the design of REDUCE-IT, with comparable patient populations and expanded or hard major adverse cardiovascular events (MACE) (4,8,9,30-44).”
From Effects of Icosapent Ethyl on Total Ischemic Events (2019) · cites this paper as [30]
In the citing paper
“Combinations of statins with fibrates, niacin, or fish oil have thus far generally failed to demonstrate cardiovascular benefits beyond that achieved with statins alone.128–132”
From Clinical management of stable coronary artery disease in patients with type 2 diabetes mellitus: a scientific statement from the American Heart Association (2020) · cites this paper as [129]
In 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 [65]
In the citing paper
“In the Effects of Dalcetrapib in Patients with a Recent Acute Coronary Syndrome (dal-OUTCOMES) trial, treatment with the cholesteryl ester transfer protein (CETP) inhibitor dalcetrapib increased HDL-C without any effect on LDL-C or ApoB, but did not reduce the risk of major CV events [65].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [65]
In the citing paper
“The CETP inhibitors dalcetrapib (in > 30 000 patients with recent ACS [65]) and evacetrapib (in > 12 000 high-risk patients [63]) were investigated in 2012 and 2017, respectively. Neither clinical study was able to show any clinical benefit associated with CETP inhibitors [65].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [65]
In the citing paper
“Niacin also lowers LDL-C levels by 15–20%,49 but recent large randomized trials showed a significant excess of adverse effects and no significant CVD benefit when added to background statin treatment; therefore, niacin derivatives are no longer available for prescription in Europe.50,51”
In the citing paper
“After two large studies with nicotinic acid, one with extended-release niacin 251 and one with niacin plus laropiprant, 252 showed no beneficial effect, but rather an increased frequency of serious adverse effects, no medication containing nicotinic acid is currently approved in Europe.”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [251]
In the citing paper
“Twolarge randomized clinical trials [the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health Outcomes (AIM-HIGH) and the Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE)] using, respectively, extended release (ER) nicotinic acid vs. placebo in addition to simvastatin, and ER nicotinic acid/l”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [251]
In the citing paper
“Two large randomized clinical trials [the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health Outcomes (AIM-HIGH) and the Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE)] using, respectively, extended release (ER) nicotinic acid vs. placebo in addition to simvastatin, and ER nicotinic acid/l”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [251]
In the citing paper
“After two large studies with nicotinic acid, one with extended-release niacin 251 and one with niacin plus laropiprant, 252 showed no beneficial effect, but rather an increased frequency of serious adverse effects, no medication containing nicotinic acid is currently approved in Europe.”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [251]
In the citing paper
“Modest regression of carotid atherosclerosis with niacin in most (but not all) imaging studies was not supported by clinical benefit in the AIM-HIGH and HPS2-THRIVE trials.251,252”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [251]
In the citing paper
“Niacin did not reduce stroke over longterm follow-up in patients with CVD in the AIM-HIGH and HPS2-THRIVE trials.251,252”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [251]
In the citing paper
“With respect to primary endpoints of these studies, although the effectiveness of fenofibrate was not demonstrated, a meta-analysis in primary prevention using fibrates revealed that deaths from cerebrovascular and cardiovascular diseases, non-fatal myocardial infarction, and non-fatal stroke significantly decreased by 16%651).”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [651]
In the citing paper
“Combination therapy using ethyl icosapentate (EPA) preparation or fibrate with statin is effective in suppressing ASCVD incidence. (Evidence level 2, recommendation level B).”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [696]
In the citing paper
“In a sub-analysis of JELIS study696) which enrolled subjects with hypercholesterolemia, it was shown that EPA administration added-on to statins prevented coronary event incidence for patients in primary prevention whose TG and HDL-C levels were ≥ 151 mg/dL and < 40 mg/dL, respectively.”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [696]
In the citing paper
“Meta-analyses of studies with niacin (mostly without simultaneous administration of statins) indicate a decrease in cardiovascular events [92–94].”
From HDL cholesterol: reappraisal of its clinical relevance (2017) · cites this paper as [92]
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 [7]
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 [7]
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Cholesterol Treatment Trialists' (CTT) Collaboration (2010) · The Lancet · doi:10.1016/s0140-6736(10)61350-5 · Cited by 6,550
Heart Disease and Stroke Statistics—2010 Update: A Report From the American Heart Association
WRITING GROUP MEMBERS, Lloyd-Jones, D., Adams, R. J., Brown, T. M., Carnethon, M., Dai, S., De Simone, G., Ferguson, T. B., Ford, E., Furie, K., et al. (2010) · Circulation · doi:10.1161/circulationaha.109.192667 · Cited by 5,700
Intensive versus Moderate Lipid Lowering with Statins after Acute Coronary Syndromes
Cannon, C. P., Braunwald, E., McCabe, C. H., Rader, D. J., Rouleau, J. L., Belder, R., Joyal, S. V., Hill, K. A., Pfeffer, M. A., & Skene, A. M. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040583 · Cited by 4,938
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
Brown, B. G., Zhao, X.-Q., Chait, A., Fisher, L. D., Cheung, M. C., Morse, J. S., Dowdy, A. A., Marino, E. K., Bolson, E. L., Alaupovic, P., et al. (2001) · New England Journal of Medicine · doi:10.1056/nejmoa011090 · Cited by 1,979
Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin
Canner, P. L., Berge, K. G., Wenger, N. K., Stamler, J., Friedman, L., Prineas, R. J., & Friedewald, W. (1986) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(86)80293-5 · Cited by 1,824
Clofibrate and Niacin in Coronary Heart Disease
Stamler, J. (1975) · JAMA · doi:10.1001/jama.1975.03240160024021 · Cited by 1,750
HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events
Barter, P., Gotto, A. M., LaRosa, J. C., Maroni, J., Szarek, M., Grundy, S. M., Kastelein, J. J. P., Bittner, V., & Fruchart, J.-C. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa064278 · Cited by 1,610
Prevalence of Conventional Risk Factors in Patients With Coronary Heart Disease
Khot, U. N. (2003) · JAMA · doi:10.1001/jama.290.7.898 · Cited by 1,494
Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) 2
Taylor, A. J., Sullenberger, L. E., Lee, H. J., Lee, J. K., & Grace, K. A. (2004) · Circulation · doi:10.1161/01.cir.0000148955.19792.8d · Cited by 888
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- Castelli WP, 1988, Can J Cardiol, 4, 5A
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Song, W., & FitzGerald, G. A. (2013) · Journal of Lipid Research · doi:10.1194/jlr.r040592 · Cited by 70
High-Density Lipoprotein Particle Subclass Heterogeneity and Incident Coronary Heart Disease
Akinkuolie, A. O., Paynter, N. P., Padmanabhan, L., & Mora, S. (2013) · Circulation Cardiovascular Quality and Outcomes · doi:10.1161/circoutcomes.113.000675 · Cited by 69
Salicylate improves macrophage cholesterol homeostasis via activation of Ampk
Fullerton, M. D., Ford, R. J., McGregor, C., LeBlond, N. D., Snider, S. A., Stypa, S., Day, E. A., Lhoták, Š., Schertzer, J. D., Austin, R. C., et al. (2015) · Journal of Lipid Research · doi:10.1194/jlr.m058875 · Cited by 70
Temel, R. E., & Brown, J. M. (2015) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2015.04.002 · Cited by 75
Hewing, B., Moore, K. J., & Fisher, E. A. A. (2012) · Circulation Research · doi:10.1161/circresaha.112.280958 · Cited by 67
Markers of Atherosclerosis: Part 1 – Serological Markers
Tibaut, M., Čaprnda, M., Kubatka, P., Sinkovič, A., Valentová, V., Filipová, S., Gazdíková, K., Gašpar, Ľ., Mozos, I. M., Egom, E. E. A., et al. (2018) · Heart Lung and Circulation · doi:10.1016/j.hlc.2018.06.1057 · Cited by 74
Michos, E. D., Sibley, C. T., Baer, J., Blaha, M. J., & Blumenthal, R. S. (2012) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2012.01.045 · Cited by 68
Landray, M., & REVEAL Collaborative Group (2017) · American Heart Journal · doi:10.1016/j.ahj.2017.02.021 · Cited by 72
Obicetrapib: Reversing the Tide of CETP Inhibitor Disappointments
Kastelein, J. J. P., Hsieh, A., Dicklin, M. R., Ditmarsch, M., & Davidson, M. H. (2023) · Current Atherosclerosis Reports · doi:10.1007/s11883-023-01184-1 · Cited by 69
Mendelian randomisation applied to drug development in cardiovascular disease: a review
Mokry, L. E., Ahmad, O. S., Forgetta, V., Thanassoulis, G., & Richards, J. B. (2014) · Journal of Medical Genetics · doi:10.1136/jmedgenet-2014-102438 · Cited by 67
Bochem, A. E., van Wijk, D. F., Holleboom, A. G., Duivenvoorden, R., Motazacker, M. M., Dallinga‐Thie, G. M., de Groot, E., Kastelein, J. J. P., Nederveen, A. J., Hovingh, G. K., et al. (2012) · European Heart Journal · doi:10.1093/eurheartj/ehs376 · Cited by 70
Karalis, D. G., Victor, B. M., Ahedor, L., & Liu, L. (2012) · Cholesterol · doi:10.1155/2012/861924 · Cited by 68
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Papakonstantinou, E., Lambadiari, V., Dimitriadis, G., & Zampelas, A. (2014) · Current Vascular Pharmacology · doi:10.2174/15701611113116660176 · Cited by 67
Chang, T. I., Streja, E., Soohoo, M., Kim, T., Rhee, C. M., Kovesdy, C. P., Kashyap, M. L., Vaziri, N. D., Kalantar‐Zadeh, K., & Moradi, H. (2017) · Clinical Journal of the American Society of Nephrology · doi:10.2215/cjn.08730816 · Cited by 67
HDL abnormalities in familial hypercholesterolemia: Focus on biological functions
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Barylski, M., Toth, P. P., Nikolic, D., Banach, M., Rizzo, M., & Montalto, G. (2014) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2013.11.001 · Cited by 67
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Sando, K. R., & Knight, M. (2015) · Clinical Therapeutics · doi:10.1016/j.clinthera.2015.09.001 · Cited by 69
Management of dyslipidemia in adult solid organ transplant recipients
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Should low high-density lipoprotein cholesterol (HDL-C) be treated?
Toth, P. P., Barylski, M., Nikolić, D., Rizzo, M., Montalto, G., & Banach, M. (2013) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2013.11.002 · Cited by 67
HDL and atherosclerosis: Insights from inherited HDL disorders
Calabresi, L., Gomaraschi, M., Simonelli, S., Bernini, F., & Franceschini, G. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2014.07.015 · Cited by 67
Genotype-Dependent Effects of Dalcetrapib on Cholesterol Efflux and Inflammation
Tardif, J., Rhainds, D., Brodeur, M. R., Zada, Y. F., Fouodjio, R., Provost, S., Boulé, M., Alem, S., Grégoire, J. C., L’Allier, P. L., et al. (2016) · Circulation Cardiovascular Genetics · doi:10.1161/circgenetics.116.001405 · Cited by 69
Unravelling HDL—Looking beyond the Cholesterol Surface to the Quality Within
Kajani, S., Curley, S., & McGillicuddy, F. C. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19071971 · Cited by 70
Sherratt, S. C. R., Juliano, R. A., & Mason, R. P. (2020) · Biochimica et Biophysica Acta (BBA) - Biomembranes · doi:10.1016/j.bbamem.2020.183254 · Cited by 68
HDL particle subpopulations: Focus on biological function
Rached, F. H., Chapman, M. J., & Kontush, A. (2015) · BioFactors · doi:10.1002/biof.1202 · Cited by 73
Tall, A. R., Yvan‐Charvet, L., Westerterp, M., & Murphy, A. J. (2012) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.112.300134 · Cited by 67
HDL mimetic CER-001 targets atherosclerotic plaques in patients
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Wierzbicki, A. S., Hardman, T. C., & Viljoen, A. (2012) · International Journal of Clinical Practice · doi:10.1111/j.1742-1241.2011.02867.x · Cited by 65
Hsu, S., Ton, V., Ashen, M. D., Martin, S. S., Gluckman, T. J., Kohli, P., Sisson, S. D., Blumenthal, R. S., & Blaha, M. J. (2013) · Clinical Cardiology · doi:10.1002/clc.22137 · Cited by 67
Wang, Y., You, Y., Tian, Y., Sun, H., Li, X., Wang, X., Wang, Y., & Liu, J. (2020) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.0c05060 · Cited by 65
Ito, M. K. (2015) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.06.012 · Cited by 68
Moreno, G., & Mangione, C. M. (2013) · Journal of the American Geriatrics Society · doi:10.1111/jgs.12513 · Cited by 65
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Lim, S. K., Park, Y. M., Sakuma, I., & Koh, K. K. (2012) · International Journal of Cardiology · doi:10.1016/j.ijcard.2012.03.127 · Cited by 64
Kalil, R. S., Wang, J., de Boer, I. H., Mathew, R. O., Ix, J. H., Asif, A., Shi, X., & Boden, W. E. (2015) · Kidney International · doi:10.1038/ki.2014.383 · Cited by 66
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Khoudary, S. R. E., Hutchins, P. M., Matthews, K. A., Brooks, M. M., Orchard, T. J., Ronsein, G. E., & Heinecke, J. W. (2016) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2016-2144 · Cited by 66
HDL cholesterol and ASCVD risk stratification: A debate
Barter, P. J., & Genest, J. J. (2019) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2019.01.001 · Cited by 68
Lin, A., Nerlekar, N., Rajagopalan, A., Yuvaraj, J., Modi, R., Mirzaee, S., Munnur, R. K., Seckington, M., Doery, J. C. G., SENEVIRATNE, S. K., et al. (2019) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2019.02.019 · Cited by 65
Taddei, C., Jackson, R., Zhou, B., Bixby, H., Danaei, G., Cesare, M. D., Kuulasmaa, K., Hajifathalian, K., Bentham, J., Bennett, J. E., et al. (2019) · International Journal of Epidemiology · doi:10.1093/ije/dyz099 · Cited by 65
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Gutstein, D. E., Krishna, R., Johns, D. G., Surks, H. K., Dansky, H. M., Shah, S., Mitchel, Y., Arena, J. P., & Wagner, J. A. (2011) · Clinical Pharmacology & Therapeutics · doi:10.1038/clpt.2011.271 · Cited by 64
Robinson, J. G., & Stone, N. J. (2015) · European Heart Journal · doi:10.1093/eurheartj/ehv182 · Cited by 65
Bennett, A. N., Dyball, D. M., Boos, C. J., Fear, N. T., Schofield, S. J., Bull, A. M. J., & Cullinan, P. (2020) · BMJ Open · doi:10.1136/bmjopen-2020-037850 · Cited by 66
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Sosale, A., Saboo, B., & Sosale, B. (2015) · Diabetes Metabolic Syndrome and Obesity · doi:10.2147/dmso.s49592 · Cited by 65
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Smith, S. C., & Grundy, S. M. (2014) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2014.06.1159 · Cited by 65
Hegele, R. A., Gidding, S. S., Ginsberg, H. N., McPherson, R., Raal, F. J., Rader, D. J., Robinson, J. G., & Welty, F. K. (2015) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.115.306442 · Cited by 63
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American heart association scientific sessions 2011.
Alexander, W. (2012) · PubMed Central · Cited by 63
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Park, J., Lee, J., & Ovbiagele, B. (2014) · Stroke · doi:10.1161/strokeaha.114.006827 · Cited by 62
Belalcazar, L. M., Haffner, S. M., Lang, W., Hoogeveen, R. C., Rushing, J., Schwenke, D. C., Tracy, R. P., Pi‐Sunyer, F. X., Kriska, A. M., & Ballantyne, C. M. (2013) · Obesity · doi:10.1002/oby.20431 · Cited by 62
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Bhatt, A. B., & Rohatgi, A. K. (2015) · Current Atherosclerosis Reports · doi:10.1007/s11883-015-0554-1 · Cited by 65
Maki, K. C., Guyton, J. R., Orringer, C. E., Hamilton-Craig, I., Alexander, D. D., & Davidson, M. H. (2016) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2016.03.008 · Cited by 62
Riaz, H., Khan, S. U., Rahman, H., Shah, N. P., Kaluski, E., Lincoff, A. M., & Nissen, S. E. (2019) · European Journal of Preventive Cardiology · doi:10.1177/2047487318816495 · Cited by 61
Emerging therapeutic agents to lower lipoprotein (a) levels
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Novel pharmacological targets for calcific aortic valve disease: Prevention and treatments
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Lorenzatti, A. J., & Toth, P. P. (2020) · European Cardiology Review · doi:10.15420/ecr.2019.06 · Cited by 62
Liu, Q. K. (2021) · Journal of clinical lipidology · doi:10.1016/j.jacl.2021.05.007 · Cited by 65
Croyal, M., Ouguerram, K., Passard, M., Ferchaud‐Roucher, V., Chétiveaux, M., Billon‐Crossouard, S., de Gouville, A., Lambert, G. C., Krempf, M., & Nobécourt, E. (2015) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.115.305835 · Cited by 62
Eliasson, B., Guðbjörnsdóttir, S., Zethelius, B., Eeg‐Olofsson, K., & Cederholm, J. (2013) · European Journal of Preventive Cardiology · doi:10.1177/2047487313494292 · Cited by 62
Colhoun, H. M., Robinson, J. G., Farnier, M., Cariou, B., Blom, D. J., Kereiakes, D. J., Lorenzato, C., Pordy, R. C., & Chaudhari, U. (2014) · BMC Cardiovascular Disorders · doi:10.1186/1471-2261-14-121 · Cited by 61
Kawachi, K., Kataoka, H., Manabe, S., Mochizuki, T., & Nitta, K. (2019) · Heart and Vessels · doi:10.1007/s00380-019-01375-4 · Cited by 60
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Future of High-Density Lipoprotein Infusion Therapies
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Bikdeli, B., Punnanithinont, N., Akram, Y., Lee, I., Desai, N. R., Ross, J. S., & Krumholz, H. M. (2017) · Journal of the American Heart Association · doi:10.1161/jaha.116.005285 · Cited by 58
ApoCIII enrichment in HDL impairs HDL-mediated cholesterol efflux capacity
Luo, M., Liu, A., Wang, S., Wang, T., Hu, D., Wu, S., & Peng, D. (2017) · Scientific Reports · doi:10.1038/s41598-017-02601-7 · Cited by 62
Hunter, W. G., McGarrah, R. W., Kelly, J. P., Khouri, M. G., Craig, D. M., Haynes, C. S., Felker, G. M., Hernandez, A. F., Velazquez, E. J., Kraus, W. E., et al. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.10.059 · Cited by 60
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Hafiane, A., Jabor, B., Ruel, I. L., Ling, J., & Genest, J. J. (2013) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2013.09.006 · Cited by 59
Statin Use and Adrenal Aldosterone Production in Hypertensive and Diabetic Subjects
Baudrand, R. F., Pojoga, L. H., Vaidya, A., Garza, A., Vöhringer, P. A., Jeunemaı̂tre, X., Hopkins, P. N., Yao, T. M., Williams, J. S., Adler, G. K., et al. (2015) · Circulation · doi:10.1161/circulationaha.115.016759 · Cited by 60
Serum Lipid Profile of Newly Diagnosed Hypertensive Patients inNnewi, South‐East Nigeria
Osuji, C. U., Omejua, E. G., Onwubuya, E. I., & Ahaneku, G. I. (2012) · International Journal of Hypertension · doi:10.1155/2012/710486 · Cited by 59
New Era of Lipid-Lowering Drugs
Barter, P. J., & Rye, K. (2016) · Pharmacological Reviews · doi:10.1124/pr.115.012203 · Cited by 59
Otvos, J. D., Guyton, J. R., Connelly, M. A., Akapame, S., Bittner, V., Kopecky, S. L., Lacy, M., Marcovina, S. M., Muhlestein, J. B., & Boden, W. E. (2018) · Journal of clinical lipidology · doi:10.1016/j.jacl.2018.01.002 · Cited by 58
Horimatsu, T., Blomkalns, A. L., Ogbi, M., Moses, M. M., Kim, D. S., Patel, S. Y., Gilreath, N., Reid, L. E., Benson, T. W., Pye, J., et al. (2019) · Cardiovascular Research · doi:10.1093/cvr/cvz303 · Cited by 57
HDL Proteome and Alzheimer’s Disease: Evidence of a Link
Marsillach, J., Adorni, M. P., Zimetti, F., Papotti, B., Zuliani, G., & Cervellati, C. (2020) · Antioxidants · doi:10.3390/antiox9121224 · Cited by 62
Statin Intolerance: the Clinician’s Perspective
Štulc, T., Češka, R., & Gotto, A. M. (2015) · Current Atherosclerosis Reports · doi:10.1007/s11883-015-0552-3 · Cited by 59
What do we know about the role of lipoprotein(a) in atherogenesis 57 years after its discovery?
Cybulska, B., Kłosiewicz−Latoszek, L., Penson, P. E., & Banach, M. (2020) · Progress in Cardiovascular Diseases · doi:10.1016/j.pcad.2020.04.004 · Cited by 59
Sacks, F. M., Liang, L., Furtado, J. D., Cai, T., Davidson, W. S., He, Z., McClelland, R. L., Rimm, E. B., & Jensen, M. K. (2020) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.120.314609 · Cited by 57
Joseph, L., & Robinson, J. G. (2015) · Progress in Cardiovascular Diseases · doi:10.1016/j.pcad.2015.04.004 · Cited by 59
Tehrani, D. M., Gardin, J. M., Yanez, D., Hirsch, C. H., Lloyd‐Jones, D. M., Stein, P. K., & Wong, N. D. (2013) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2013.08.036 · Cited by 57
Tan, J. T. M., Prosser, H. C. G., Vanags, L. Z., Monger, S., Ng, M., & Bursill, C. A. (2013) · The FASEB Journal · doi:10.1096/fj.13-233874 · Cited by 59
Murphy, A. J., Funt, S. A., Gorman, D. J., Tall, A. R., & Wang, N. (2013) · Circulation Research · doi:10.1161/circresaha.113.301112 · Cited by 57
Metadata
- Authors
- The AIM-HIGH Investigators
- Corresponding author
- The AIM-HIGH Investigators
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2011-12-15
- Volume
- 365
- Issue
- 24
- Pages
- 2255-2267
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2165605025
- Semantic Scholar
- d76ac03611110eeffa5c3ad8b47d06f372d84eb6
- Cited by
- 2,911
- References
- 19
- Citations by year
- 2026: 79 · 2025: 90 · 2024: 138 · 2023: 133 · 2022: 138 · 2021: 165 · 2020: 146 · 2019: 181 · 2018: 208 · 2017: 203 · 2016: 264 · 2015: 302 · 2014: 316 · 2013: 333 · 2012: 192
- FWCI
- 280.19
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Abbott Laboratories
- Eli Lilly and Company
- Pfizer
- Sanofi
- Genentech
- National Heart, Lung, and Blood Institute
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- nicotinic acid, simvastatin, HDL cholesterol, low HDL cholesterol, residual cardiovascular risk, atherosclerotic cardiovascular disease, extended-release niacin, ezetimibe, LDL cholesterol, triglycerides, major adverse cardiovascular events, cardiovascular risk reduction, statin therapy, coronary artery disease, myocardial infarction, ischemic stroke, acute coronary syndrome, revascularization
- MeSH terms
- Aged, Hypolipidemic Agents, Cardiovascular Diseases, Brain Ischemia, Drug Therapy, Combination, Female, Humans, Cholesterol, HDL, Cholesterol, LDL, Male, Middle Aged, Muscular Diseases, Niacin, Triglycerides, Proportional Hazards Models, Treatment Failure, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Simvastatin, Atherosclerosis, Kaplan-Meier Estimate, Medication Adherence
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