Impact of triglyceride levels beyond low-density lipoprotein cholesterol after acute coronary syndrome in the PROVE IT-TIMI 22 trial
Open accessAbstract
Objectives The purpose of this study was to assess the impact of on-treatment triglycerides (TG) on coronary heart disease (CHD) risk after an acute coronary syndrome (ACS).Background The PROVE IT-TIMI (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) 22 trial demonstrated that low-density lipoprotein cholesterol (LDL-C) <70 mg/dl was associated with greater CHD event reduction than LDL-C <100 mg/dl after ACS. However, the impact of low on-treatment TG on CHD risk beyond LDL-C <70 mg/dl has not been explored.Methods The PROVE IT-TIMI 22 trial evaluated 4,162 patients hospitalized for ACS and randomized to atorvastatin 80 mg or pravastatin 40 mg daily. The relationship between on-treatment levels of TG and LDL-C and the composite end point of death, myocardial infarction (MI), and recurrent ACS were assessed 30 days after initial presentation.Results Low on-treatment TG (<150 mg/dl) was associated with reduced CHD risk compared with higher TG in univariate analysis (hazard ratio [HR] 0.73, 95% confidence interval [CI] 0.62 to 0.87; p < 0.001) and in adjusted analysis (HR 0.80, 95% CI 0.66 to 0.97; p = 0.025). For each 10-mg/dl decrement in on-treatment TG, the incidence of death, MI, and recurrent ACS was lower by 1.6% or 1.4% after adjustment for LDL-C or non-high-density lipoprotein cholesterol and other covariates (p < 0.001 and p = 0.01, respectively). Lower CHD risk was also observed with TG <150 mg/dl and LDL-C <70 mg/dl (HR 0.72, 95% CI 0.54 to 0.94; p = 0.017) or low on-treatment TG, LDL-C, and C-reactive protein (<2 mg/l) (HR 0.59, 95% CI 0.41 to 0.83; p = 0.002) compared with higher levels of each variable in adjusted analysis.Conclusions On-treatment TG <150 mg/dl was independently associated with a lower risk of recurrent CHD events, lending support to the concept that achieving low TG may be an additional consideration beyond low LDL-C in patients after ACS.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In PROVE IT-TIMI 22, patients with higher triglyceride levels at baseline still derived substantial event reduction with intensive statin therapy.
“Moreover, in the PROVE IT–TIMI 22 trial, patients with higher triglyceride levels at baseline still derived substantial event reduction with intensive statin therapy [84].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [84]
The Study population and protocol section (page unavailable) confirms that PROVE IT–TIMI 22 compared intensive atorvastatin with standard pravastatin. The Discussion and Effect of lowering TG levels on the composite end point sections (pages unavailable) associate lower on-treatment triglycerides with fewer events, but do not show that patients with higher triglycerides at baseline specifically derived substantial event reduction from intensive versus standard statin therapy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredStatins remain first-line therapy for patients with hypertriglyceridemia, having demonstrated consistent reductions in ASCVD events across a wide range of populations, including those with elevated triglycerides.
“Statins remain the first-line therapy for patients with hypertriglyceridemia, having demonstrated consistent reductions in ASCVD events across a wide range of populations, including those with elevated triglycerides.”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [84]
The Conclusions (p. not available in our copy) report that, among statin-treated patients after acute coronary syndrome, lower on-treatment triglycerides were associated with fewer recurrent coronary events. The study population and protocol describe a comparison of intensive and standard statin therapy in that specific population. These passages do not establish that statins are first-line therapy for hypertriglyceridemia or that they consistently reduce ASCVD events across a wide range of populations, including people with elevated triglycerides. (LLM, conf=0.85)
Experimental — accuracy not yet measuredObservational cohorts demonstrate that higher TG and remnant cholesterol predict cardiovascular events independently of LDL-C.
“Observational cohorts demonstrate that higher TG and remnant cholesterol predict cardiovascular events independently of LDL-C, while Mendelian randomization analyses confirm a causal relationship between lifelong TRL elevation and ASCVD.”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [34]
The Discussion reports prospective studies linking higher TG to CHD risk and finds that on-treatment TG predicts recurrent events independently of LDL-C in patients after acute coronary syndrome. It discusses cholesterol-enriched remnants as a possible mechanism, but does not show that remnant cholesterol independently predicts cardiovascular events. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIn the PROVE IT-TIMI 22 trial, LDL-C <70 mg/dL was associated with greater coronary heart disease event reduction compared with LDL-C <100 mg/dL after acute coronary syndrome.
“In the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22) trial, LDL-C <70 mg/dL was associated with greater coronary heart disease event reduction compared with LDL-C <100 mg/dL after acute coronary syndrome (5).”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [5]
The Discussion and Abstract report lower CHD risk after acute coronary syndrome when LDL-C <70 mg/dL was achieved together with low triglycerides. The paper does not report the claimed comparison with LDL-C <100 mg/dL; its analyses use a 70 mg/dL LDL-C cut-point, while the 100 mg/dL cut-points concern triglycerides or non-HDL-C. Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe association between triglycerides and cardiovascular risk is well established from epidemiological studies, genome-wide analyses, and Mendelian randomization studies.
“The association between triglycerides and cardiovascular (CV) risk is well established from epidemiological studies,1-5 genome-wide analyses,6-8 and Mendelian randomization studies.9,10”
Despite statin therapy, ASCVD event rates remain high in patients with elevated triglycerides.
“Studies have shown that despite the use of statin therapy, ASCVD event rates remain high in patients with elevated triglycerides (5,6).”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [5]
In PROVE IT-TIMI 22, an on-treatment triglyceride level <150 mg/dL was independently associated with a lower risk of recurrent coronary heart disease events compared with a triglyceride level ≥150 mg/dL in univariate analysis (HR: 0.73; 95% CI: 0.62-0.87; P < 0.001) and in adjusted analysis (HR: 0.80; 95% CI: 0.66-0.97; P = 0.025).
“An on-treatment triglyceride level <150 mg/dL was independently associated with a lower risk of recurrent coronary heart disease events compared with a triglyceride level ≥150 mg/dL in univariate analysis (HR: 0.73; 95% CI: 0.62-0.87; P < 0.001) and in adjusted analysis (HR: 0.80; 95% CI: 0.66-0.97; P = 0.025).”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [5]
Reductions in plasma triglyceride are associated with reduction in the risk of atherosclerotic cardiovascular disease events after adjustment for statin-induced LDL-C lowering.
“There is also evidence that reductions in plasma TG are associated with reduction in the risk of ASCVD events after adjustment for statin-induced LDL-C lowering.39–42”
Patients with elevated triglycerides, atherosclerosis, or diabetes receiving statins are at substantial risk for recurrent, potentially fatal ischemic events.
“In addition to their initial events, such patients are at substantial risk for recurrent, potentially fatal events.”
From Effects of Icosapent Ethyl on Total Ischemic Events (2019) · cites this paper as [8]
The observed annualized primary endpoint event rate for placebo patients in REDUCE-IT is consistent with historical cardiovascular outcome studies with comparable patient populations and expanded or hard MACE.
“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 [8]
In the PROVE IT-TIMI 22 trial, serum TG, regardless of LDL-C concentration, had a substantial impact on CV outcomes in patients with acute coronary syndromes.
“Data from the secondary prevention PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22) trial revealed that serum TG, regardless of LDL-C concentration, had a substantial impact on CV outcomes in patients with acute coronary syndromes (20).”
From Triglycerides and residual atherosclerotic risk (2021) · cites this paper as [20]
Among statin-treated patients, on-treatment TG <150 mg/dl was associated with reduced CV risk independently of LDL-C concentration.
“Notably, among statin-treated patients, on-treatment TG <150 mg/dl was associated with reduced CV risk independently of LDL-C concentration.”
From Triglycerides and residual atherosclerotic risk (2021) · cites this paper as [20]
The beneficial effect of reducing LDL-C to <70 mg/dl was highest in individuals with TG <150 mg/dl.
“Furthermore, the beneficial effect of reducing LDL-C to <70 mg/dl was highest in individuals with TG <150 mg/dl (20).”
From Triglycerides and residual atherosclerotic risk (2021) · cites this paper as [20]
Prior studies demonstrate an approximate 10-20% increase in CVD risk when TG exceeded 150 mg/dL compared to <100 mg/dL.
“and an approximate 10-20% increase in CVD risk when TG exceeded 150 mg/dL compared to < 100 mg/dL.19”
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 [19]
Post-hoc analyses found TG to be more accurate than HDL-C in predicting recurrent CVD events after an acute coronary syndrome.
“and post-hoc analyses found TG to be more accurate than HDL-C in predicting recurrent CVD events after an acute coronary syndrome.19,31”
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 [19]
Observational studies and clinical trials have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.
“observational studies and clinical trials 3,232,367,374 -380 that have consistently demonstrated the lowest risk of incident and recurrent CVD in association with the lowest fasting triglyceride levels.”
From Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association (2011) · cites this paper as [379]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
Friedewald, W. T., Levy, R. I., & Fredrickson, D. S. (1972) · Clinical Chemistry · doi:10.1093/clinchem/18.6.499 · Cited by 32,423 · see citing works
Grundy, S. M., Cleeman, J. I., Merz, C. N. B., Brewer, H. B., Clark, L. T., Hunninghake, D. B., Pasternak, R. C., Smith, S. C., & Stone, N. J. (2004) · Circulation · doi:10.1161/01.cir.0000133317.49796.0e · Cited by 6,902 · see citing works
Epstein, F. H., Steinberg, D. I., Parthasarathy, S., Carew, T. E., Khoo, J. C., & Witztum, J. L. (1989) · New England Journal of Medicine · doi:10.1056/nejm198904063201407 · Cited by 6,425 · see citing works
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 · see citing works
Self-citationYokoyama, M., Origasa, H., Matsuzaki, M., Matsuzawa, Y., Saito, Y., Ishikawa, Y., Oikawa, S., Sasaki, J., Hishida, H., Itakura, H., et al. (2007) · The Lancet · doi:10.1016/s0140-6736(07)60527-3 · Cited by 2,516 · see citing works
C-Reactive Protein Levels and Outcomes after Statin Therapy
Ridker, P. M., Cannon, C. P., Morrow, D., Rifai, N., Rose, L. M., McCabe, C. H., Pfeffer, M. A., & Braunwald, E. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa042378 · Cited by 2,292 · see citing works
Self-citationGrundy, S. M., Cleeman, J. I., Bairey Merz, C. N., Brewer, H. B., Clark, L. T., Hunninghake, D. B., Pasternak, R. C., Smith, S. C., & Stone, N. J. (2004) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2004.07.001 · Cited by 1,550 · see citing works
Atherogenic lipoprotein phenotype. A proposed genetic marker for coronary heart disease risk
Austin, M. A., King, M. C., Vranizan, K. M., & Krauss, R. M. (1990) · Circulation · doi:10.1161/01.cir.82.2.495 · Cited by 1,411 · see citing works
Sarwar, N., Danesh, J., Eiriksdottir, G., Sigurdsson, G., Wareham, N., Bingham, S., Boekholdt, S. M., Khaw, K.-T., & Gudnason, V. (2007) · Circulation · doi:10.1161/circulationaha.106.637793 · Cited by 1,408 · see citing works
Manninen, V, Tenkanen, L., Koskinen, P., Huttunen, J. K., Mänttäri, M., Heinonen, O. P., & Frick, M. H. (1992) · Circulation · doi:10.1161/01.cir.85.1.37 · Cited by 1,329 · see citing works
Effect of Statins on Risk of Coronary Disease: A Meta-analysis of Randomized Controlled Trials
LaRosa, J. C., He, J., & Vupputuri, S. (1999) · JAMA · doi:10.1001/jama.282.24.2340 · Cited by 1,246 · see citing works
Action to Control Cardiovascular Risk in Diabetes (ACCORD) Trial: Design and Methods
Buse, J. B. (2007) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2007.03.003 · Cited by 661 · see citing works
Fasting Triglycerides, High-Density Lipoprotein, and Risk of Myocardial Infarction
Gaziano, J. M., Hennekens, C. H., O’Donnell, C. J., Breslow, J. L., & Buring, J. E. (1997) · Circulation · doi:10.1161/01.cir.96.8.2520 · Cited by 602 · see citing works
Sacks, F., & Katan, M. (2002) · American Journal of Medicine · doi:10.1016/s0002-9343(01)00987-1 · Cited by 523 · see citing works
Plasma Triglyceride Level and Mortality from Coronary Heart Disease
Criqui, M. H., HEISS, G. M., Cohn, R. D., Cowan, L. D., Suchindran, C., Bangdiwala, S. I., Kritchevsky, S., Jacobs, D. R., O'Grady, H. K., & DAVIS, C. E. (1993) · New England Journal of Medicine · doi:10.1056/nejm199304293281702 · Cited by 418 · see citing works
Why do omega-3 fatty acids lower serum triglycerides?
Harris, W. S., & Bulchandani, D. (2006) · Current Opinion in Lipidology · doi:10.1097/01.mol.0000236363.63840.16 · Cited by 398 · see citing works
Manninen, V., Tenkanen, L., Koskinen, P., Huttunen, J. K., Mänttäri, M., Op, H., & Frick, H. M. (1992) · Circulation · Cited by 360 · see citing works
Early and Late Benefits of High-Dose Atorvastatin in Patients With Acute Coronary Syndromes
Ray, K. K., Cannon, C. P., McCabe, C. H., Cairns, R., Tonkin, A. M., Sacks, F. M., Jackson, G., & Braunwald, E. (2005) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2005.03.077 · Cited by 356 · see citing works
Self-citationHYPERTRIGLYCERIDAEMIA AND HYPERCOAGULABILITY
Simpson, H. C. R., Meade, T. W., Stirling, Y., Mann, J. I., Chakrabarti, R., & Woolf, L. (1983) · The Lancet · doi:10.1016/s0140-6736(83)91849-4 · Cited by 286 · see citing works
Ridker, P. M., Morrow, D. A., Rose, L. M., Rifai, N., Cannon, C. P., & D, E. B. M. (2005) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2005.02.080 · Cited by 235 · see citing works
Self-citationInfluence of Low HDL on Progression of Coronary Artery Disease and Response to Fluvastatin Therapy
Ballantyne, C. M., Herd, J. A., Ferlic, L. L., Dunn, J. K., Farmer, J. A., Jones, P. H., Schein, J. R., & Gotto, A. M. (1999) · Circulation · doi:10.1161/01.cir.99.6.736 · Cited by 198 · see citing works
Miller, M., Seidler, A., Moalemi, A., & Pearson, T. A. (1998) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(98)00083-7 · Cited by 193 · see citing works
Self-citationRezaie-Majd, A., Prager, G. W., Bucek, R. A., Schernthaner, G.-H., Maca, T., Kress, H. G., Valent, P., Binder, B. R., Minar, E., & Baghestanian, M. (2003) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000059384.34874.f0 · Cited by 146 · see citing works
Postprandial lipoproteins and atherosclerosis
Kenneth, C.-W. Y. (2001) · Frontiers in bioscience · doi:10.2741/yu · Cited by 145 · see citing works
Greene, D. J., Skeggs, J. W., & Morton, R. E. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m008725200 · Cited by 133 · see citing works
Pleiotropic effects of thiazolidinediones: Taking a look beyond antidiabetic activity
Giannini, S., Serio, M., & Galli, A. (2004) · Journal of Endocrinological Investigation · doi:10.1007/bf03347546 · Cited by 132 · see citing works
Design of the Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE IT)—TIMI 22 trial
Cannon, C. P., McCabe, C. H., Belder, R., Breen, J. D., & D, E. B. M. (2002) · The American Journal of Cardiology · doi:10.1016/s0002-9149(02)02201-4 · Cited by 125 · see citing works
Self-citationElevated Soluble Cellular Adhesion Molecules in Subjects With Low HDL-Cholesterol
Calabresi, L., Gomaraschi, M., Villa, B., Omoboni, L., Dmitrieff, C., & Franceschini, G. (2002) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/hq0402.105901 · Cited by 125 · see citing works
Ray, K. K., Cannon, C. P., Cairns, R., Morrow, D. A., Rifai, N., Kirtane, A. J., McCabe, C. H., Skene, A. M., Gibson, C. M., Ridker, P. M., et al. (2005) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2005.08.024 · Cited by 123 · see citing works
Self-citationThe role of fibrates in managing hyperlipidemia: Mechanisms of action and clinical efficacy
Fazio, S., & Linton, M. F. (2004) · Current Atherosclerosis Reports · doi:10.1007/s11883-004-0104-8 · Cited by 118 · see citing works
Gelfand, E. V., & Cannon, C. P. (2006) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2005.12.067 · Cited by 118 · see citing works
Self-citationAre Remnant-Like Particles Independent Predictors of Coronary Heart Disease Incidence?
Imke, C., Rodríguez, B. L., Grove, J., McNamara, J. R., Waslien, C., Katz, A. R., Willcox, B. J., Yano, K., & Curb, J. D. (2005) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000173310.85845.7b · Cited by 89 · see citing works
LDL and HDL enriched in triglyceride promote abnormal cholesterol transport
Skeggs, J. W., & Morton, R. E. (2002) · Journal of Lipid Research · doi:10.1194/jlr.m100431-jlr200 · Cited by 73 · see citing works
The Year in Non–ST-Segment Elevation Acute Coronary Syndrome
Giugliano, R. P., & D, E. B. M. (2010) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2010.09.016 · Cited by 72 · see citing works
Benefits of achieving the NCEP optional LDL-C goal among elderly patients with ACS
Ray, K. K. (2006) · European Heart Journal · doi:10.1093/eurheartj/ehl180 · Cited by 71 · see citing works
Self-citationFamilial lipoprotein disorders and premature coronary artery disease
Schaefer, E. J., Genest, J. J., Ordovás, J. M., Salem, D. N., & Wilson, P. W. F. (1994) · Atherosclerosis · doi:10.1016/0021-9150(94)90152-x · Cited by 68 · see citing works
Atorvastatin Improves Postprandial Lipoprotein Metabolism in Normolipidemic Subjects1
Parhofer, K. G., Barrett, P. H. R., & SCHWANDT, P. (2000) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.85.11.6978 · Cited by 65 · see citing works
Assmann, G. (2001) · The American Journal of Cardiology · doi:10.1016/s0002-9149(01)01448-5 · Cited by 57 · see citing works
Triglyceride and coronary heart disease mortality in a 24-year follow-up study in Xi'an, China
He, Y., Lam, T. H., Li, L. S., Li, L. S., He, S. F., & Liang, B. Q. (2003) · Annals of Epidemiology · doi:10.1016/s1047-2797(03)00069-3 · Cited by 44 · see citing works
Ray, K., & Cannon, C. (2004) · Journal of Thrombosis and Thrombolysis · doi:10.1007/s11239-004-0205-9 · Cited by 43 · see citing works
Self-citationCurrent perspectives on the management of hypertriglyceridemia
Miller, M. J. (2000) · American Heart Journal · doi:10.1067/mhj.2000.108001 · Cited by 40 · see citing works
Self-citationUnderstanding risk in hypercholesterolemia
LaRosa, J. C. (2003) · Clinical Cardiology · doi:10.1002/clc.4960261303 · Cited by 23 · see citing works
Familial lipoprotein disorders and premature coronary artery disease
Schaefer, E. J. (1994) · Medical Clinics of North America · doi:10.1016/s0025-7125(16)30175-4 · Cited by 21 · see citing works
Thrombophilia in Patients with Hypertriglyceridemia
Chan, P., Huang, T.-Y., Shieh, S., Lin, T., & Tsai, C.-W. (1997) · Journal of Thrombosis and Thrombolysis · doi:10.1023/a:1008857618659 · Cited by 16 · see citing works
The Year in Non–ST-Segment Elevation Acute Coronary Syndromes
Giugliano, R. P., & D, E. B. M. (2006) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2006.05.040 · Cited by 5 · see citing works
The Evolving Role of High‐Density Lipoprotein in Reducing Cardiovascular Risk
Ballantyne, C. M., & Rangaraj, G. (2001) · Preventive Cardiology · doi:10.1111/j.1520-037x.2001.00556.x · Cited by 4 · see citing works
Some concerns about the future of the practice of cardiovascular medicine
Miller, A. J. (2003) · Clinical Cardiology · doi:10.1002/clc.4960261012 · Cited by 4 · see citing works
Brown, B. G. (2005) · Nature Clinical Practice Cardiovascular Medicine · doi:10.1038/ncpcardio0189 · Cited by 2 · see citing works
Flagged first, then by citations
Research works printed but not linked: 2
- [18]18. Assmann G. Pro and con: high-density lipoprotein, triglycerides, and other lipid subfractions are the future of lipid management. Am J Cardiol 2001;87:2B-7B.
- [35]35. Parhofer KG, Barrett PH, Schwandt P. Atorvastatin improves post- prandial lipoprotein metabolism in normolipidemlic subjects. J Clin Endocrinol Metab 2000;85:4224 -30.
Cited by
Sorted by citations
Kernan, W. N., Ovbiagele, B., Black, H. R., Bravata, D. M., Chimowitz, M. I., Ezekowitz, M. D., Fang, M. C., Fisher, M., Furie, K. L., Heck, D. V., et al. (2014) · Stroke · doi:10.1161/str.0000000000000024 · Cited by 5,170 · see citing works
Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association
Miller, M., Stone, N. J., Ballantyne, C., Bittner, V., Criqui, M. H., Ginsberg, H. N., Goldberg, A. C., Howard, W. J., Jacobson, M. S., Kris-Etherton, P. M., et al. (2011) · Circulation · doi:10.1161/cir.0b013e3182160726 · Cited by 1,871 · see citing works
Self-citationChapman, M. J., Ginsberg, H. N., Amarenco, P., Andreotti, F., Borén, J., Catapano, A. L., Descamps, O. S., Fisher, E., Kovanen, P. T., Kuivenhoven, J. A., et al. (2011) · European Heart Journal · doi:10.1093/eurheartj/ehr112 · Cited by 1,227 · see citing works
Self-citationNordestgaard, B. G. (2016) · Circulation Research · doi:10.1161/circresaha.115.306249 · Cited by 1,116 · see citing works
Ginsberg, H. N., Packard, C. J., Chapman, M. J., Borén, J., Aguilar-Salinas, C. A., Averna, M., Ference, B. A., Gaudet, D., Hegele, R. A., Kersten, S., et al. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab551 · Cited by 979 · see citing works
Pollin, T. I., Damcott, C. M., Shen, H., Ott, S. H., Shelton, J., Horenstein, R. B., Post, W., McLenithan, J. C., Bielak, L. F., Peyser, P. A., et al. (2008) · Science · doi:10.1126/science.1161524 · Cited by 688 · see citing works
Self-citationSandesara, P. B., Virani, S. S., Fazio, S., & Shapiro, M. D. (2019) · Endocrine Reviews · doi:10.1210/er.2018-00184 · Cited by 626 · see citing works
Fruchart, J.-C., Sacks, F., Hermans, M. P., Assmann, G., Brown, W. V., Ceska, R., Chapman, M. J., Dodson, P. M., Fioretto, P., Ginsberg, H. N., et al. (2008) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2008.10.002 · Cited by 463 · see citing works
Sampson, U. K., Fazio, S., & Linton, M. F. (2012) · Current Atherosclerosis Reports · doi:10.1007/s11883-011-0219-7 · Cited by 439 · see citing works
Beyond Low-Density Lipoprotein Cholesterol
Arsenault, B. J., Rana, J. S., Stroes, E. S. G., Després, J.-P., Shah, P. K., Kastelein, J. J. P., Wareham, N. J., Boekholdt, S. M., & Khaw, K.-T. (2009) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2009.07.057 · Cited by 342 · see citing works
Virani, S. S., Morris, P. B., Agarwala, A., Ballantyne, C. M., Birtcher, K. K., Kris-Etherton, P. M., Ladden-Stirling, A. B., Miller, M., Orringer, C. E., & Stone, N. J. (2021) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2021.06.011 · Cited by 341 · see citing works
Self-citationMarston, N. A., Giugliano, R. P., Im, K., Silverman, M. G., O’Donoghue, M. L., Wiviott, S. D., Ference, B. A., & Sabatine, M. S. (2019) · Circulation · doi:10.1161/circulationaha.119.041998 · Cited by 301 · see citing works
Chapman, M. J., Le Goff, W., Guerin, M., & Kontush, A. (2010) · European Heart Journal · doi:10.1093/eurheartj/ehp399 · Cited by 298 · see citing works
Gaudet, D., Karwatowska-Prokopczuk, E., Baum, S. J., Hurh, E., Kingsbury, J., Bartlett, V. J., Figueroa, A. L., Piscitelli, P., Singleton, W., Witztum, J. L., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehaa689 · Cited by 279 · see citing works
Schwartz, G. G., Abt, M., Bao, W., DeMicco, D., Kallend, D., Miller, M., Mundl, H., & Olsson, A. G. (2015) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2015.03.544 · Cited by 272 · see citing works
Self-citationFruchart, J.-C., Sacks, F. M., Hermans, M. P., Assmann, G., Brown, W. V., Ceska, R., Chapman, M. J., Dodson, P. M., Fioretto, P., Ginsberg, H. N., et al. (2008) · Diabetes and Vascular Disease Research · doi:10.3132/dvdr.2008.046 · Cited by 260 · see citing works
Effects of Icosapent Ethyl on Total Ischemic Events
Bhatt, D. L., Steg, P. G., Miller, M., Brinton, E. A., Jacobson, T. A., Ketchum, S. B., Doyle, R. T., Juliano, R. A., Jiao, L., Granowitz, C., et al. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2019.02.032 · Cited by 259 · see citing works
Self-citationTriglycerides and residual atherosclerotic risk
Raposeiras-Roubin, S., Rosselló, X., Oliva, B., Fernández-Friera, L., Mendiguren, J. M., Andrés, V., Bueno, H., Sanz, J., Martínez de Vega, V., Abu-Assi, E., et al. (2021) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2021.04.059 · Cited by 254 · see citing works
Lee, M., Saver, J. L., Towfighi, A., Chow, J., & Ovbiagele, B. (2011) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2011.04.020 · Cited by 240 · see citing works
Triglyceride-rich lipoproteins as a causal factor for cardiovascular disease
Toth, P. (2016) · Vascular Health and Risk Management · doi:10.2147/vhrm.s104369 · Cited by 237 · see citing works
Fruchart, J.-C. (2009) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2009.03.008 · Cited by 233 · see citing works
Niacin and fibrates in atherogenic dyslipidemia: pharmacotherapy to reduce cardiovascular risk
Chapman, M. J., Redfern, J. S., McGovern, M. E., & Giral, P. (2010) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2010.01.008 · Cited by 227 · see citing works
Jepsen, A.-M. K., Langsted, A., Varbo, A., Bang, L. E., Kamstrup, P. R., & Nordestgaard, B. G. (2016) · Clinical Chemistry · doi:10.1373/clinchem.2015.253757 · Cited by 218 · see citing works
Plozasiran, an RNA Interference Agent Targeting APOC3, for Mixed Hyperlipidemia
Ballantyne, C. M., Vasas, S., Azizad, M., Clifton, P., Rosenson, R. S., Chang, T., Melquist, S., Zhou, R., Mushin, M., Leeper, N. J., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2404143 · Cited by 210 · see citing works
Unmet Need for Adjunctive Dyslipidemia Therapy in Hypertriglyceridemia Management
Ganda, O. P., Bhatt, D. L., Mason, R. P., Miller, M., & Boden, W. E. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.04.061 · Cited by 195 · see citing works
Self-citationThe clinical relevance of omega-3 fatty acids in the management of hypertriglyceridemia
Backes, J., Anzalone, D., Hilleman, D., & Catini, J. (2016) · Lipids in Health and Disease · doi:10.1186/s12944-016-0286-4 · Cited by 195 · see citing works
Postprandial hypertriglyceridemia as a coronary risk factor
Borén, J., Matikainen, N., Adiels, M., & Taskinen, M.-R. (2014) · Clinica Chimica Acta · doi:10.1016/j.cca.2014.01.015 · Cited by 182 · see citing works
Faergeman, O., Holme, I., Fayyad, R., Bhatia, S., Grundy, S. M., Kastelein, J. J. P., LaRosa, J. C., Larsen, M. L., Lindahl, C., Olsson, A. G., et al. (2009) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2009.04.008 · Cited by 154 · see citing works
Triglycerides as vascular risk factors: new epidemiologic insights.
Kannel, W. B., & Vasan, R. S. (2009) · Current Opinion in Cardiology · doi:10.1097/hco.0b013e32832c1284 · Cited by 149 · see citing works
Fruchart, J.-C., Santos, R. D., Aguilar-Salinas, C., Aikawa, M., Al Rasadi, K., Amarenco, P., Barter, P. J., Ceska, R., Corsini, A., Després, J.-P., et al. (2019) · Cardiovascular Diabetology · doi:10.1186/s12933-019-0864-7 · Cited by 140 · see citing works
Self-citationTriglycerides and HDL Cholesterol
Bitzur, R., Cohen, H., Kamari, Y., Shaish, A., & Harats, D. (2009) · Diabetes Care · doi:10.2337/dc09-s343 · Cited by 132 · see citing works
Lawler, P. R., Kotrri, G., Koh, M., Goodman, S. G., Farkouh, M. E., Lee, D. S., Austin, P. C., Udell, J. A., & Ko, D. T. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz767 · Cited by 113 · see citing works
Demystifying the management of hypertriglyceridaemia
Watts, G. F., Ooi, E. M. M., & Chan, D. C. (2013) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2013.140 · Cited by 115 · see citing works
Gjuladin-Hellon, T., Davies, I. G., Penson, P., & Amiri Baghbadorani, R. (2019) · Nutrition Reviews · doi:10.1093/nutrit/nuy049 · Cited by 108 · see citing works
Orringer, C. E., Jacobson, T. A., & Maki, K. C. (2019) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2019.10.014 · Cited by 103 · see citing works
Nichols, G. A., Philip, S., Reynolds, K., Granowitz, C. B., & Fazio, S. (2018) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2018-00470 · Cited by 102 · see citing works
Combined therapy in the treatment of dyslipidemia
Reiner, Ž. (2010) · Fundamental & Clinical Pharmacology · doi:10.1111/j.1472-8206.2009.00764.x · Cited by 100 · see citing works
Watts, G. F., & Karpe, F. (2011) · Heart · doi:10.1136/hrt.2010.204990 · Cited by 97 · see citing works
Bartlett, J., Predazzi, I. M., Williams, S. M., Bush, W. S., Kim, Y., Havas, S., Toth, P. P., Fazio, S., & Miller, M. (2016) · Circulation: Cardiovascular Quality and Outcomes · doi:10.1161/circoutcomes.115.002436 · Cited by 96 · see citing works
Self-citationAdvanced lipoprotein testing and subfractionation are not (yet) ready for routine clinical use
Mora, S. (2009) · Circulation · doi:10.1161/circulationaha.108.819359 · Cited by 89 · see citing works
Maki, K. C., Bays, H. E., & Dicklin, M. R. (2012) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2012.04.003 · Cited by 83 · see citing works
Fan, W., Philip, S., Granowitz, C., Toth, P. P., & Wong, N. D. (2019) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2018.11.008 · Cited by 67 · see citing works
Berge, R. K., Ramsvik, M. S., Bohov, P., Svardal, A., Nordrehaug, J. E., Rostrup, E., Bruheim, I., & Bjørndal, B. (2015) · Lipids in Health and Disease · doi:10.1186/s12944-015-0162-7 · Cited by 51 · see citing works
Rubenfire, M., Brook, R. D., & Rosenson, R. S. (2010) · The American Journal of Medicine · doi:10.1016/j.amjmed.2010.03.024 · Cited by 40 · see citing works
Bashir, B., Schofield, J., Downie, P., France, M., Ashcroft, D. M., Wright, A. K., Romeo, S., Gouni-Berthold, I., Maan, A., Durrington, P. N., et al. (2024) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2024.1389106 · Cited by 40 · see citing works
Huang, X., Zhao, S., Bai, L., Hu, M., Zhao, W., & Zhang, Q. (2009) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2009.00350.x · Cited by 36 · see citing works
Nguyen, S. V., Nakamura, T., & Kugiyama, K. (2014) · Circulation Journal · doi:10.1253/circj.cj-14-0380 · Cited by 34 · see citing works
Lorenzatti, A. J., Monsalvo, M. L., López, J. A. G., Wang, H., & Rosenson, R. S. (2021) · Cardiovascular Diabetology · doi:10.1186/s12933-021-01287-6 · Cited by 34 · see citing works
Toh, D. W. K., Koh, E. S., & Kim, J. E. (2020) · Nutrition Reviews · doi:10.1093/nutrit/nuz104 · Cited by 33 · see citing works
Can pleiotropic effects of eicosapentaenoic acid (EPA) impact residual cardiovascular risk?
Nelson, J. R., True, W. S., Le, V., & Mason, R. P. (2017) · Postgraduate Medicine · doi:10.1080/00325481.2017.1385365 · Cited by 27 · see citing works
Targeting RNA to lower triglycerides: long strides from short molecules
Qamar, A., Libby, P., & Bhatt, D. L. (2019) · European Heart Journal · doi:10.1093/eurheartj/ehz321 · Cited by 14 · see citing works
Risk prediction with triglycerides in patients with stable coronary disease on statin treatment
Werner, C., Filmer, A., Fritsch, M., Groenewold, S., Gräber, S., Böhm, M., & Laufs, U. (2014) · Clinical Research in Cardiology · doi:10.1007/s00392-014-0740-0 · Cited by 13 · see citing works
Alam, U., Mathai, S. V., Filtz, A., Kuno, T., Badimon, J. J., Sniderman, A. D., Virani, S. S., Toth, P. P., Shapiro, M. D., Lavie, C. J., et al. (2026) · Current Cardiology Reports · doi:10.1007/s11886-025-02337-1 · Cited by 4 · see citing works
Targeting triglycerides for cardiovascular risk reduction
Maiorca, C., Tramontano, D., Di Costanzo, A., & D’Erasmo, L. (2026) · Internal and Emergency Medicine · doi:10.1007/s11739-026-04383-1
- Authors
- Miller, M., Cannon, C. P., Murphy, S. A., Qin, J., Ray, K. K., & Braunwald, E.
- Affiliations
- University of Maryland Medical Center (US)
- Brigham and Women's Hospital (US)
- University of Cambridge (GB)
- Corresponding author
- Miller, Michael
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2008-02
- Volume
- 51
- Issue
- 7
- Pages
- 724-730
- ISSN
- 0735-1097 (ISSN-L)
- OpenAlex
- W2006551863
- Cited by
- 610
- References
- 50
- Citations by year
- 2026: 11 · 2025: 20 · 2024: 28 · 2023: 30 · 2022: 31 · 2021: 39 · 2020: 40 · 2019: 43 · 2018: 30 · 2017: 25 · 2016: 40 · 2015: 29 · 2014: 33 · 2013: 32 · 2012: 30
- FWCI
- 52.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- Bristol-Myers Squibb
- Pfizer
- AstraZeneca
- GlaxoSmithKline
- Sanofi
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL061369, HL61369)
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Antiplatelet Therapy and Cardiovascular Diseases
- Keywords
- triglycerides, acute coronary syndrome, LDL cholesterol, atorvastatin, pravastatin, coronary heart disease risk, non-HDL cholesterol, C-reactive protein, PROVE IT-TIMI 22, statin therapy, reinfarction, mortality, lipid-lowering therapy, triglyceride-lowering therapy, secondary prevention, dyslipidemia
- MeSH terms
- Atorvastatin, Anticholesteremic Agents, Coronary Disease, Female, Heptanoic Acids, Humans, Cholesterol, LDL, Male, Middle Aged, Myocardial Infarction, Pyrroles, Recurrence, Triglycerides, Proportional Hazards Models, Pravastatin, Risk Assessment, Acute Coronary Syndrome
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
