Skip to main content
Download PDF

Prevalence of US Adults with Triglycerides ≥ 150 mg/dl: NHANES 2007–2014

Cardiology and Therapy volume 9, pages 207–213 (2020)Cite this article

Abstract

Introduction

Hypertriglyceridemia is associated with increased atherosclerotic cardiovascular disease (ASCVD) event risk, which persists even in statin-treated patients. The objective of this analysis was to estimate the prevalence of triglyceride (TG) levels ≥ 150 mg/dl in statin-treated adults with diabetes or ASCVD in the United States.

Methods

Laboratory data, medical history, and prescription data from 40,617 subjects who participated in the US National Health and Nutrition Examination Survey (NHANES) spanning 8 years (four 2-year surveys; 2007–2014) were analyzed. Patients included were ≥ 20 years old and had morning fasting (at least 8.5 h) TG values available. The proportion and weighted number of individuals in the US population with TG ≥ 150 mg/dl was calculated according to statin use, as well as in key subgroups of statin-treated patients including those with low-density lipoprotein cholesterol (LDL-C) levels < 100 mg/dl, type 2 diabetes, ASCVD, and those with type 2 diabetes and ASCVD.

Results

A total of 9593 subjects, projected to represent 219.9 million Americans, met the study entry criteria and were included in the analysis. Of these, 2523 had TG levels ≥ 150 mg/dl, translating to a prevalence of 25.9% and representing 56.9 million Americans. Among statin-treated adults, the proportion with TG levels ≥ 150 mg/dl was 31.6% (12.3 million) and ranged from 27.6 to 39.5% for those who also had LDL-C levels < 100 mg/dl and type 2 diabetes or ASCVD.

Conclusions

Over 12 million Americans are treated with a statin and have TG levels ≥ 150 mg/dl. Interventions such as icosapent ethyl that have been shown to reduce ASCVD event risk in this elevated TG population with type 2 diabetes or established ASCVD can provide substantial clinical benefit for these patients.

FormalPara Key Summary Points
Why carry out this study?
Hypertriglyceridemia is an important risk factor for atherosclerotic cardiovascular disease (ASCVD) events, even in statin-treated patients.
This study attempted to estimate the prevalence of hypertriglyceridemia in statin-treated patients in the United States, including those with type 2 diabetes or ASCVD.
What was learned from this study?
The overall prevalence of statin-treated patients with triglyceride levels ≥ 150 mg/dl in the United States is 25.9%.
A total of 12.3 million statin-treated patients have triglyceride levels ≥ 150 mg/dl, including as many as 6.4 million with type 2 diabetes or ASCVD.

Introduction

Hypertriglyceridemia is associated with increased atherosclerotic cardiovascular disease (ASCVD) event risk [1,2,3,4], and is highly prevalent in adults in the US due to genetic polymorphisms in triglyceride (TG) metabolism and to the increasing prevalence of obesity, insulin resistance, and diabetes mellitus. Guidelines suggest that target TG levels should be < 150 mg/dl for reduced ASCVD event risk [5]. The American Heart Association suggests that a TG level < 100 mg/dl may be optimal [6]. Elevated ASCVD event risk associated with elevated TG levels persists even in statin-treated patients; in the Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) study, which evaluated atorvastatin and pravastatin, on-treatment TG levels of < 150 mg/dl versus ≥ 150 mg/dl were more predictive of a lower coronary heart disease risk than low-density lipoprotein cholesterol (LDL-C) levels of < 70 mg/dl versus ≥ 70 mg/dl [7]. Recent claims-based database analyses have attempted to quantify the cardiovascular event risk associated with elevated TG levels. In an analysis of the Optum Research Database, patients with TG levels ≥ 150 mg/dl were significantly more likely to have an initial major cardiovascular event than a corresponding propensity-matched cohort with TG levels < 150 mg/dl (hazard ratio [HR] 1.26; 95% confidence interval [CI] 1.19–1.34; P < 0.001) [8]. These analyses also indicated that elevated TG levels (i.e., ≥ 150 mg/dl) significantly predicted new heart failure diagnosis and hospitalization for new-onset kidney disease [9, 10]. The direct healthcare costs associated with TG levels ≥ 150 mg/dl were also significantly increased compared to costs for patients with more desirable TG levels (< 150 mg/dl), with an incremental cost burden across the US of $10.7 billion in statin-treated patients with hypertriglyceridemia [11].

The recent Reduction of Cardiovascular Events With Icosapent Ethyl–Intervention Trial (REDUCE-IT) demonstrated that the purified and stable eicosapentaenoic acid (EPA) formulation icosapent ethyl significantly reduced the risk of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, coronary revascularization, or unstable angina compared with placebo in high-risk, statin-treated patients with TG levels ≥ 150 mg/dl, established cardiovascular disease or diabetes, and well-controlled LDL-C (< 100 mg/dl) (HR 0.75; 95% CI 0.68–0.83; P < 0.001) [12]. As a result, the indication for icosapent ethyl has recently been expanded to include its use as an adjunct to maximally tolerated statin therapy (defined as the highest tolerated intensity and frequency of a statin, even if the dose is zero) for reduction of cardiovascular events among adults with TG levels ≥ 150 mg/dl and either established cardiovascular disease or diabetes mellitus and at least two additional risk factors for ASCVD event-risk reduction, and has been endorsed by multiple society recommendations or guidelines [13,14,15,16]. The objective of this analysis was to estimate the prevalence of TG levels ≥ 150 mg/dl in statin-treated adults with diabetes or ASCVD in the US.

Methods

This analysis included laboratory data, medical history, and prescription data from 40,617 subjects who participated in the US National Health and Nutrition Examination Survey (NHANES) spanning 8 years (four 2-year surveys; 2007–2014). The methodology for NHANES data collection has been described in detail [17]. Subjects who were ≥ 20 years old and had morning fasting (at least 8.5 h) TG values available were included in the analysis.

The prevalence of individuals with TG levels ≥ 150 mg/dl was calculated based on the actual number of participants in NHANES from 2007–2014, for the overall population, and according to statin use, as well as in key subgroups of statin-treated patients including those with LDL-C levels < 100 mg/dl, type 2 diabetes, ASCVD, and those with both type 2 diabetes and ASCVD. The weighted total number of patients in the US in millions was also estimated. Type 2 diabetes was defined as fasting glucose levels ≥ 126 mg/dl, non-fasting glucose levels ≥ 200 mg/dl, the use of insulin or other medications to lower blood sugar, or a diagnosis by a healthcare provider at age ≥ 30 years. LDL-C (mg/dl) was calculated using the Friedewald equation (total cholesterol − high-density lipoprotein cholesterol − [TG/5]).

This article is based on previously conducted studies and does not contain any studies with human participants or animals performed by any of the authors.

Results

The study sample included 40,617 individuals from the NHANES 2007–2014 survey. A total of 9593 subjects met the study entry criteria and were included in the analysis. This group was projected to represent 219.9 million Americans. A total of 2523 individuals from this group had TG levels ≥ 150 mg/dl. As shown in Table 1, this translates to a prevalence of 25.9%, representing 56.9 million Americans. Among statin-treated adults, the proportion with TG levels ≥ 150 mg/dl was 31.6% (12.3 million) and ranged from 27.6 to 39.5% for those who also had LDL-C controlled to < 100 mg/dl with statin therapy and type 2 diabetes or ASCVD (Table 1).

Table 1 Weighted prevalence of TG levels ≥ 150 mg/dl among adults ≥ 20 years of age in NHANES 2007–2014
Full size table

Discussion

More than 25% of all US adults (56.9 million individuals) have TG levels ≥ 150 mg/dl, including 31.6% (12.3 million) of those already being treated with statins. In another recent analysis of this population, 70.5 million US adults were estimated to have TG levels ≥ 135 mg/dl [18]. This lower threshold of moderately elevated TG levels has also been associated with residual cardiovascular event risk, including patients with statin-controlled LDL-C [19]. Taken together, these results indicate a substantial healthcare burden in terms of both cost as well as morbidity and mortality associated with elevated TG levels.

Schwartz et al. [19] demonstrated a significant trend toward increased risk of both short- and long-term ASCVD events following acute coronary syndrome, according to progressively higher tertiles or quintiles of TG concentrations (P = 0.03 and P < 0.001, respectively). This study further reported that the adjusted risk of ASCVD events increased by 1.5 times between the highest (> 175 mg/dl) and lowest (≤ 80 mg/dl) quintiles of TG levels. The cardiovascular event risk associated with TG level, regardless of statin use, was investigated in Danish patients from the Copenhagen City Heart Study and the Copenhagen General Population Study. The results showed a significantly elevated risk of myocardial infarction in patients with TG levels between 89 and 176 mg/dl compared to those with TG levels < 89 mg/dl (HR 1.6; 95% CI 1.4–1.9), indicating substantial risk at lower TG levels [20].

In REDUCE-IT, the ASCVD event risk across strata of baseline TG levels (< 150 mg/dl, ≥ 150 mg/dl, < 200 mg/dl, and ≥ 200 mg/dl) in placebo-treated patients ranged from 21.0 to 22.6% [12]. In another analysis of this study in which patients were stratified according to tertiles of baseline TG levels, ASCVD event risk ranged from 21.1% for those with TG ≤ 190 mg/dl to 23.7% for those with TG > 250 mg/dl [21]. The addition of icosapent ethyl consistently and significantly reduced ASCVD event risk in all TG strata [21]. After stratifying patients by tertiles of baseline TG levels, the associated HRs for the reduction of time to first ASCVD event risk or cardiovascular death with icosapent ethyl treatment were 0.79 (95% CI 0.66–0.94) for those with TG levels ≥ 81 to ≤ 190 mg/dl, 0.80 (95% CI 0.68–0.95) for TG levels > 190 to ≤ 250 mg/dl, and 0.68 (95% CI 0.57–0.80) for TG levels > 250 to ≤ 1401 mg/dl [21]. These results demonstrated that icosapent ethyl reduces ASCVD event risk irrespective of baseline or on-treatment TG levels. Researchers have suggested that anti-platelet and/or anti-inflammatory properties of EPA may help explain this event reduction, although further investigation is warranted [22]. Since the release of the results of REDUCE-IT, subsequent publications discussing health care guidelines have recognized the importance of adding icosapent ethyl therapy to patients with ASCVD or diabetes and multiple risk factors taking maximally tolerated statin therapy with LDL-C levels < 100 mg/dl and moderately elevated TG levels [23, 24].

Other large cardiovascular outcomes trials in patients with hypertriglyceridemia have failed to show ASCVD event-risk reduction with treatments given as adjuncts to statins. In 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) studies, there was no difference between niacin and placebo in terms of endpoints related to cardiovascular events [25, 26]. Similarly, the Action to Control Cardiovascular Risk in Diabetes (ACCORD)–Lipid and the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) studies did not demonstrate any significant differences with fenofibrate treatment in their respective primary cardiovascular endpoints, despite improvements in lipid profiles [27, 28]. In the Vitamin D and Omega-3 Trial (VITAL), 1 g daily (460 mg of EPA and 380 mg of docosahexaenoic acid [DHA]) of concentrated fish oil capsules failed to reduce major adverse cardiovascular events among a primary prevention cohort with no previous history of cardiovascular disease despite a significant reduction in myocardial infarction [29]. Moreover, a meta-analysis of 18 randomized controlled trials indicated a nonsignificant reduction in coronary heart disease risk with EPA + DHA overall (summary relative risk estimate [SRRE] 0.94; 95% CI 0.85–1.05), as well as nonsignificant relative risk reductions among patients with LDL-C levels ≥ 130 mg/dl (SRRE 0.86; 95% CI 0.76–0.98) and TG levels ≥ 150 mg/dl (SRRE 0.84; 95% CI 0.72–0.98) [30]. More recently, the Outcomes Study to Assess Statin Residual Risk Reduction With Epanova in High CV Risk Patients With Hypertriglyceridemia (STRENGTH, NCT02104817), which investigated the impact of adding 4 g/day EPA + DHA to statins, was recently stopped due to a low likelihood of demonstrating a benefit to the patients studied. Although the omega-3 fatty acids EPA and DHA are frequently conflated as having similar biological effects, the halting of the STRENGTH trial may be due to their differences in activity, doses utilized, and achieved blood levels [31]. In addition, given the fact that the majority of combination EPA + DHA trials have been negative to date [29, 32,33,34,35,36], it is possible that DHA exerts effects that may antagonize or even negate the benefit exerted by EPA. An ongoing clinical trial investigating a newer fibrate (pemafibrate) in patients with type 2 diabetes (Pemafibrate to Reduce Cardiovascular Outcomes by Reducing Triglycerides in Patients with Diabetes [PROMINENT]; NCT03071692) may be informative [37].

Conclusions

In summary, more than 12 million Americans are treated with a statin and have TG levels ≥ 150 mg/dl, a degree of hypertriglyceridemia associated with increased ASCVD event risk [8, 19, 20]. New approaches are needed to address residual ASCVD event risk in these patients, including lifestyle modification adherence measures and the use of evidence-based pharmacologic therapies shown to reduce ASCVD event risk. Icosapent ethyl is the first treatment to demonstrate a reduction in cardiovascular death and ischemic disease in statin-treated patients with elevated TG levels and established ASCVD or with type 2 diabetes plus additional risk factors, and should be considered when designing treatment plans for this population based on the expanded FDA indication for this agent.

References

  1. Vallejo-Vaz AJ, Corral P, Schreier L, Ray KK. Triglycerides and residual risk. Curr Opin Endocrinol Diabetes Obes. 2020;27(2):95–103.

    CAS  Article  Google Scholar 

  2. Arbel Y, Klempfner R, Erez A, Goldenberg I, Benzekry S, Shlomo N, et al. Bezafibrate for the treatment of dyslipidemia in patients with coronary artery disease: 20-year mortality follow-up of the BIP randomized control trial. Cardiovasc Diabetol. 2016;15(1):11.

    Article  Google Scholar 

  3. Nordestgaard BG. Triglyceride-rich lipoproteins and atherosclerotic cardiovascular disease: new insights from epidemiology, genetics, and biology. Circ Res. 2016;118(4):547–63.

    CAS  Article  Google Scholar 

  4. Toth PP. Triglyceride-rich lipoproteins as a causal factor for cardiovascular disease. Vasc Health Risk Manag. 2016;12:171–83.

    CAS  Article  Google Scholar 

  5. Jellinger PS, Handelsman Y, Rosenblit PD, Bloomgarden ZT, Fonseca VA, Garber AJ, et al. American Association of Clinical Endocrinologists and American College of Endocrinology guidelines for management of dyslipidemia and prevention of cardiovascular disease: executive summary. Endocr Pract. 2017;23(4):479–97.

    Article  Google Scholar 

  6. Miller M, Stone NJ, Ballantyne C, Bittner V, Criqui MH, Ginsberg HN, et al. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation. 2011;123(20):2292–333.

    Article  Google Scholar 

  7. Miller M, Cannon CP, Murphy SA, Qin J, Ray KK, Braunwald E. Impact of triglyceride levels beyond low-density lipoprotein cholesterol after acute coronary syndrome in the PROVE IT-TIMI 22 trial. J Am Coll Cardiol. 2008;51(7):724–30.

    CAS  Article  Google Scholar 

  8. Toth PP, Philip S, Hull M, Granowitz C. Association of elevated triglycerides with increased cardiovascular risk and direct costs in statin-treated patients. Mayo Clin Proc. 2019;94(9):1670–80.

    CAS  Article  Google Scholar 

  9. Toth PP, Philip S, Hull M, Granowitz C. Elevated triglycerides (≥150 mg/dl) and high triglycerides (200–499 mg/dl) are significant predictors of hospitalization for new-onset kidney disease: a real-world analysis of high-risk statin-treated patients. Cardiorenal Med. 2019;9(6):400–7.

    CAS  Article  Google Scholar 

  10. Toth PP, Philip S, Hull M, Liassou D, Granowitz C. Elevated triglycerides (≥150 mg/dl) and high triglycerides (200–499 mg/dl) are significant predictors of new heart failure diagnosis: a real-world analysis of high-risk statin-treated patients. J Card Fail. 2018;24(8suppl):S32–S33 [Abstract].

    Article  Google Scholar 

  11. Case BC, Bress AP, Kolm P, Philip S, Herrick JS, Granowitz CB, et al. The economic burden of hypertriglyceridemia among US adults with diabetes or atherosclerotic cardiovascular disease on statin therapy. J Clin Lipidol. 2019;13(5):754–61.

    Article  Google Scholar 

  12. Bhatt DL, Steg G, Miller M, Brinton EA, Jacobson TA, Ketchum SB, et al. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med. 2019;380(1):11–22.

    CAS  Article  Google Scholar 

  13. American Diabetes Association (2019) Living standards of medical care in diabetes Arlington County, VA: American Diabetes Association; 2019. Available from: https://care.diabetesjournals.org/living-standards#2018. Updated 31 Jul 2019.

  14. Skulas-Ray AC, Wilson PWF, Harris WS, Brinton EA, Kris-Etherton PM, Richter CK, et al. Omega-3 fatty acids for the management of hypertriglyceridemia: a science advisory from the American Heart Association. Circulation. 2019;140(12):e673–e691691.

    CAS  Article  Google Scholar 

  15. Mach F, Baigent C, Catapano AL, Koskinas KC, Casula M, Badimon L, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk: the task force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS). Eur Heart J. 2020;41(1):111–88.

    Article  Google Scholar 

  16. National Lipid Association. NLA position on the use of icosapent ethyl in high and very-high risk patients Jacksonville, FL: 2019. Available from: https://www.lipid.org/nla/nla-position-use-icosapent-ethyl-high-and-very-high-risk-patients. Accessed 10 Apr 2020.

  17. Centers for Disease Control and Prevention. National Health and Nutrition Examination Survey (NHANES) Laboratory Procedures Manual: 2007. Available from: https://wwwn.cdc.gov/nchs/data/nhanes/2007-2008/manuals/manual_lab.pdf. Accessed 10 Apr 2020.

  18. Fan W, Philip S, Granowitz C, Toth P, Wong N. Hypertriglyceridemia in statin-treated US adults: The National Health and Nutrition Examination Survey. J Clin Lipidol. 2019;13:100–8.

    Article  Google Scholar 

  19. Schwartz GG, Abt M, Bao W, DeMicco D, Kallend D, Miller M, et al. Fasting triglycerides predict recurrent ischemic events in patients with acute coronary syndrome treated with statins. J Am Coll Cardiol. 2015;65(21):2267–75.

    CAS  Article  Google Scholar 

  20. Pedersen SB, Langsted A, Nordestgaard BG. Nonfasting mild-to-moderate hypertriglyceridemia and risk of acute pancreatitis. JAMA Intern Med. 2016;176(12):1834–42.

    Article  Google Scholar 

  21. Bhatt DL, Steg PG, Miller M, Brinton EA, Jacobson TA, Ketchum SB, et al. Reduction in first and total ischemic events with icosapent ethyl across baseline triglyceride tertiles. J Am Coll Cardiol. 2019;74(8):1159–61.

    Article  Google Scholar 

  22. Harris WS. Understanding why REDUCE-IT was positive—mechanistic overview of eicosapentaenoic acid. Prog Cardiovasc Dis. 2019;62(5):401–5.

    Article  Google Scholar 

  23. Robinson JG. Lipid management beyond the guidelines. Prog Cardiovasc Dis. 2019;62(5):384–9.

    Article  Google Scholar 

  24. Bittner V. Implications for REDUCE IT in clinical practice. Prog Cardiovasc Dis. 2019;62(5):395–400.

    Article  Google Scholar 

  25. AIM-HIGH Investigators. The role of niacin in raising high-density lipoprotein cholesterol to reduce cardiovascular events in patients with atherosclerotic cardiovascular disease and optimally treated low-density lipoprotein cholesterol Rationale and study design. The Atherothrombosis Intervention in Metabolic syndrome with low HDL/high triglycerides: Impact on Global Health outcomes (AIM-HIGH). Am Heart J. 2011;161(3):471–7.

    Article  Google Scholar 

  26. The HPS2THRIVE Collaborative Group. Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med. 2014;371(3):203–12.

    Article  Google Scholar 

  27. The FIELD Study Investigators. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet. 2005;366(9500):1849–61.

    Article  Google Scholar 

  28. The ACCORD Study Group. Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med. 2010;362(17):1563–74.

    Article  Google Scholar 

  29. Manson JE, Cook NR, Lee IM, Christen W, Bassuk SS, Mora S, et al. Marine n-3 fatty acids and prevention of cardiovascular disease and cancer. N Engl J Med. 2019;380(1):23–322.

    CAS  Article  Google Scholar 

  30. Alexander DD, Miller PE, Van Elswyk ME, Kuratko CN, Bylsma LC. A meta-analysis of randomized controlled trials and prospective cohort studies of eicosapentaenoic and docosahexaenoic long-chain omega-3 fatty acids and coronary heart disease risk. Mayo Clin Proc. 2017;92(1):15–29.

    CAS  Article  Google Scholar 

  31. Update on Phase III STRENGTH trial for Epanova in mixed dyslipidaemia [press release]: AstraZeneca; 2020. Available from: https://www.astrazeneca.com/media-centre/press-releases/2020/update-on-phase-iii-strength-trial-for-epanova-in-mixed-dyslipidaemia-13012020.html. Accessed 10 Apr 2020.

  32. Kromhout D, Giltay EJ, Geleijnse JM. n-3 Fatty acids and cardiovascular events after myocardial infarction. N Engl J Med. 2010;363(21):2015–26.

    CAS  Article  Google Scholar 

  33. Rauch B, Schiele R, Schneider S, Diller F, Victor N, Gohlke H, et al. OMEGA, a randomized, placebo-controlled trial to test the effect of highly purified omega-3 fatty acids on top of modern guideline-adjusted therapy after myocardial infarction. Circulation. 2010;122(21):2152–9.

    CAS  Article  Google Scholar 

  34. ORIGIN Trial Investigators. n-3 Fatty acids and cardiovascular outcomes in patients with dysglycemia. N Engl J Med. 2012;367(4):309–18.

    Article  Google Scholar 

  35. The Risk and Prevention Study Collaborative Group. n-3 Fatty acids in patients with multiple cardiovascular risk factors: the Risk and Prevention Study Collaborative Group. N Engl J Med. 2013;368:1800–8.

    Article  Google Scholar 

  36. ASCEND Study Collaborative Group. Effects of n-3 fatty acid supplements in diabetes mellitus. N Engl J Med. 2018;379(16):1540–50.

    Article  Google Scholar 

  37. Pradhan AD, Paynter NP, Everett BM, Glynn RJ, Amarenco P, Elam M, et al. Rationale and design of the Pemafibrate to Reduce Cardiovascular Outcomes by Reducing Triglycerides in Patients with Diabetes (PROMINENT) study. Am Heart J. 2018;206:80–93.

    CAS  Article  Google Scholar 

Download references

Acknowledgements

Funding

The study, medical writing assistance, and the journals’ rapid service fee were funded by Amarin Pharma Inc., Bridgewater, NJ, USA.

Medical Writing and Editorial Assistance

Medical writing assistance was provided by Peloton Advantage, LLC, an OPEN Health company, Parsippany, NJ, USA.

Authorship

All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, take responsibility for the integrity of the work as a whole, and have given their approval for this version to be published.

Disclosures

Wenjun Fan has no relationships to disclose. Sephy Philip and Craig Granowitz are employees of Amarin Pharma, Inc. Peter P. Toth is a consultant and speaker for Amarin Pharma, Inc., Amgen, Kowa, and Novo Nordisk. Nathan D. Wong receives research support from Amarin Pharma, Inc., Amgen, Boehringer Ingelheim, Novo Nordisk, and Novartis, and has participated on advisory boards or speakers bureaus for Amarin Pharma, Inc., Sanofi, and Esperion.

Compliance with Ethics Guidelines

This article is based on previously conducted studies and does not contain any studies with human participants or animals performed by any of the authors.

Data Availability

The datasets generated during and/or analyzed during the current study are available in the National Health and Nutrition Examination Survey repository https://wwwn.cdc.gov/nchs/nhanes/Default.aspx.

Open Access

This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.

Author information

Authors and Affiliations

  1. Heart Disease Prevention Program, Division of Cardiology, University of California, Irvine, Irvine, CA, USA

    Wenjun Fan & Nathan D. Wong

  2. Amarin Pharma, Inc, Bridgewater, NJ, USA

    Sephy Philip & Craig Granowitz

  3. Cicarrone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, MD, USA

    Peter P. Toth

Authors
  1. Wenjun Fan
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Sephy Philip
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Craig Granowitz
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Peter P. Toth
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Nathan D. Wong
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Nathan D. Wong.

Additional information

Digital Features

To view digital features for this article go to https://doi.org/10.6084/m9.figshare.12123921.

Rights and permissions

This article is published under an open access license. Please check the 'Copyright Information' section either on this page or in the PDF for details of this license and what re-use is permitted. If your intended use exceeds what is permitted by the license or if you are unable to locate the licence and re-use information, please contact the Rights and Permissions team.

About this article

Verify currency and authenticity via CrossMark

Cite this article

Fan, W., Philip, S., Granowitz, C. et al. Prevalence of US Adults with Triglycerides ≥ 150 mg/dl: NHANES 2007–2014. Cardiol Ther 9, 207–213 (2020). https://doi.org/10.1007/s40119-020-00170-x

Download citation

  • Received:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s40119-020-00170-x

Keywords

  • ASCVD
  • Cardiovascular disease
  • Eicosapentaenoic acid
  • Hypertriglyceridemia
  • Icosapent ethyl