Skip to main content
Log in

Changes in triglyceride, HDL-C, and non-HDL-C levels in patients with acute coronary syndrome

  • original article
  • Published:
Wiener klinische Wochenschrift Aims and scope Submit manuscript



Changes in high-density lipoprotein cholesterol (HDL-C) and triglyceride (TG) levels have been linked to residual cardiovascular risk, whereas non-HDL-C levels have been shown to be more predictive of cardiovascular risk than are low-density lipoprotein cholesterol (LDL-C) levels. We aimed to investigate the impact of HDL-C, TG, and non-HDL-C levels on acute coronary syndrome (ACS) risk with on-target LDL-C levels.


In all, 424 Caucasian patients aged over 50 years who had LDL-C levels below 3.4 mmol/l with a first or subsequent ACS event were enrolled in a multicenter, retrospective study. Lipid samples were collected within 4 days after the cardiovascular event. The subjects of the age-matched, gender-balanced control group (n = 443) had LDL-C levels below 3.4 mmol/l and were free of cardiovascular diseases.


Patients with ACS had significantly higher TG and lower HDL-C levels compared with the control patients; however, we did not find any significant difference regarding non-HDL-C levels between the two groups. In regression analysis, the risk of coronary heart disease increased significantly with 1 standard deviation (SD) increase in TG and 1 SD decrease in HDL-C levels.


High TG and low HDL-C levels may contribute to residual cardiovascular risk in patients with well-controlled LDL-C levels; however, non-HDL-C levels at admission did not seem to be predictive for patients with ACS. Detection and treatment of secondary lipid targets such as high TG and low HDL-C levels may be important for the prevention of cardiovascular diseases.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others


  1. Reiner Z, Catapano AL, De Backer G, European Association for Cardiovascular Prevention & Rehabilitation, et al. ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS). Eur Heart J. 2011;32:1769–818.

    Article  PubMed  Google Scholar 

  2. Baigent C, Keech A, Kearney PM, Cholesterol Treatment Trialists’ (CTT) Collaborators, et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet. 2005;366:1267–78.

    Article  CAS  PubMed  Google Scholar 

  3. Kearney PM, Blackwell L, Collins R, Cholesterol Treatment Trialists’ (CTT) Collaborators, et al. Efficacy of cholesterol-lowering therapy in 18,686 people with diabetes in 14 randomised trials of statins: a meta-analysis. Lancet. 2008;371:117–25.

    Article  CAS  PubMed  Google Scholar 

  4. Hayward RA, Hofer TP, Vijan S. Narrative review: lack of evidence for recommended low-density lipoprotein treatment targets: a solvable problem. Ann Intern Med. 2006;145:520–30.

    Article  PubMed  Google Scholar 

  5. Assmann G, Schulte H. Relation of high-density lipoprotein cholesterol and triglycerides to incidence of atherosclerotic coronary artery disease (the PROCAM experience). Prospective Cardiovascular Münster study. Am J Cardiol. 1992;70:733–7.

    Article  CAS  PubMed  Google Scholar 

  6. Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007;298:299–308.

    Article  CAS  PubMed  Google Scholar 

  7. Ji MS, Jeong MH, Ahn YK, et al. Impact of low level of high-density lipoprotein-cholesterol sampled in overnight fasting state on the clinical outcomes in patients with acute myocardial infarction (difference between ST-segment and non-ST-segment-elevation myocardial infarction). J Cardiol. 2014;65(1):63–70.

    Article  PubMed  Google Scholar 

  8. Welty FK. How do elevated triglycerides and low HDL-cholesterol affect inflammation and atherothrombosis? Curr Cardiol Rep. 2013;15:400.

    Article  PubMed  PubMed Central  Google Scholar 

  9. Fukuda S, Shimada K, Fujita M, et al. Changes in serum cholesterol levels determine future risk of cardiovascular events in patients with acute coronary syndrome in the Japanese Coronary Artery Disease (JCAD) Study. J Cardiol. 2013;61:387–92.

    Article  PubMed  Google Scholar 

  10. Sacks FM, Tonkin AM, Craven T, et al. Coronary heart disease in patients with low LDL-cholesterol: benefit of pravastatin in diabetics and enhanced role for HDL-cholesterol and triglycerides as risk factors. Circulation. 2002;105:1424–8.

    Article  CAS  PubMed  Google Scholar 

  11. Barter P, Gotto AM, LaRosa JC, et al. HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events. N Engl J Med. 2007;357:1301–10.

    Article  CAS  PubMed  Google Scholar 

  12. Gordon DJ, Probstfield JL, Garrison RJ, et al. High-density lipoprotein cholesterol and cardiovascular disease. Four prospective american studies. Circulation. 1989;79:8–15.

    Article  CAS  PubMed  Google Scholar 

  13. Sarwar N, Danesh J, Eiriksdottir G, et al. Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 western prospective studies. Circulation. 2007;115:450–8.

    Article  CAS  PubMed  Google Scholar 

  14. Ginsberg HN, Bonds DE, Lovato LC, et al. Evolution of the lipid trial protocol of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial. Am J Cardiol. 2007;99:56i–67i.

    Article  PubMed  Google Scholar 

  15. Brown BG, Boden WE, Probstfield JR, AIM-HIGH Investigators, et al. 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: baseline characteristics of study partici. Am Heart J. 2011;161:538–43.

    Article  Google Scholar 

  16. Haynes R, Jiang L, Hopewell JC, et al. HPS2-THRIVE Collaborative Group. HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment. Eur Heart J. 2013;34:1279–91.

    Article  CAS  PubMed Central  Google Scholar 

  17. Stauffer ME, Weisenfluh L, Morrison A. Association between triglycerides and cardiovascular events in primary populations: a meta-regression analysis and synthesis of evidence. Vasc Health Risk Manag. 2013;9:671–80.

    Article  PubMed  PubMed Central  Google Scholar 

  18. Carey VJ, Bishop L, Laranjo N, Harshfield BJ, Kwiat C, Sacks FM. Contribution of high plasma triglycerides and low high-density lipoprotein cholesterol to residual risk of coronary heart disease after establishment of low-density lipoprotein cholesterol control. Am J Cardiol. 2010;106:757–63.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  19. Orakzai SH, Nasir K, Blaha M, Blumenthal RS, Raggi P. Non-HDL cholesterol is strongly associated with coronary artery calcification in asymptomatic individuals. Atherosclerosis. 2009;202:289–95.

    Article  CAS  PubMed  Google Scholar 

  20. Liu J, Sempos CT, Donahue RP, Dorn J, Trevisan M, Grundy SM. Non-high-density lipoprotein and very-low-density lipoprotein cholesterol and their risk predictive values in coronary heart disease. Am J Cardiol. 2006;98:1363–8.

    Article  CAS  PubMed  Google Scholar 

  21. Boekholdt SM, Arsenault BJ, Mora S, et al. Association of LDL cholesterol, non-HDL cholesterol, and apolipoprotein B levels with risk of cardiovascular events among patients treated with statins: a meta-analysis. JAMA. 2012;307:1302–9.

    Article  CAS  PubMed  Google Scholar 

  22. Cohen M, Diez JE, Levine GN, et al. Pharmacoinvasive management of acute coronary syndrome: incorporating the 2007 ACC/AHA guidelines: the CATH (cardiac catheterization and antithrombotic therapy in the hospital) Clinical Consensus Panel Report--III. J Invasive Cardiol. 2007;19:525–38.

    PubMed  Google Scholar 

  23. Gotto AM, Moon JE. Pharmacotherapies for lipid modification: beyond the statins. Nat Rev Cardiol. 2013;10:560–70.

    Article  CAS  PubMed  Google Scholar 

  24. Pintó X, Millán J, Muñoz A, et al. A very high prevalence of low HDL cholesterol in Spanish patients with acute coronary syndromes. Clin Cardiol. 2010;33:418–23.

    Article  PubMed  Google Scholar 

  25. Seo SM, Choo EH, Koh YS, et al. High-density lipoprotein cholesterol as a predictor of clinical outcomes in patients achieving low-density lipoprotein cholesterol targets with statins after percutaneous coronary intervention. Heart. 2011;97:1943–50.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Schwartz GG. High-density lipoprotein cholesterol as a risk factor and target of therapy after acute coronary syndrome. Am J Cardiol. 2009;104:46E–51E.

    Article  CAS  PubMed  Google Scholar 

  27. Olsson AG, Schwartz GG, Szarek M, et al. High-density lipoprotein, but not low-density lipoprotein cholesterol levels influence short-term prognosis after acute coronary syndrome: results from the MIRACL trial. Eur Heart J. 2005;26:890–6.

    Article  CAS  PubMed  Google Scholar 

  28. Felix-Getzik EM, Kuvin JT, Karas RH. Nonoptimal high-density lipoprotein cholesterol levels are highly prevalent in patients presenting with acute coronary syndromes and well-controlled low-density lipoprotein cholesterol levels. J Clin Lipidol. 2010;4:265–71.

    Article  PubMed  Google Scholar 

  29. Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004;350:1495–504.

    Article  CAS  PubMed  Google Scholar 

  30. Tornvall P, Olivecrona G, Karpe F, Hamsten A, Olivecrona T. Lipoprotein lipase mass and activity in plasma and their increase after heparin are separate parameters with different relations to plasma lipoproteins. Arterioscler Thromb Vasc Biol. 1995;15:1086–93.

    Article  CAS  PubMed  Google Scholar 

  31. Pitt B, Loscalzo J, Ycas J, Raichlen JS. Lipid levels after acute coronary syndromes. J Am Coll Cardiol. 2008;51:1440–5.

    Article  CAS  PubMed  Google Scholar 

  32. Khawaja OA, Hatahet H, Cavalcante J, Khanal S, Al-Mallah MH. Low admission triglyceride and mortality in acute coronary syndrome patients. Cardiol J. 2011;18:297–303.

    PubMed  Google Scholar 

  33. Henkin Y, Crystal E, Goldberg Y, et al. Usefulness of lipoprotein changes during acute coronary syndromes for predicting postdischarge lipoprotein levels. Am J Cardiol. 2002;89:7–11.

    Article  CAS  PubMed  Google Scholar 

  34. Manfrini O, Pizzi C, Trerè D, Fontana F, Bugiardini R. Parasympathetic failure and risk of subsequent coronary events in unstable angina and non-ST-segment elevation myocardial infarction. Eur Heart J. 2003;24:1560–6.

    Article  PubMed  Google Scholar 

  35. Klingenspor M, Ebbinghaus C, Hülshorst G, et al. Multiple regulatory steps are involved in the control of lipoprotein lipase activity in brown adipose tissue. J Lipid Res. 1996;37:1685–95.

    CAS  PubMed  Google Scholar 

  36. Pecquery R, Leneveu MC, Giudicelli Y. In vivo desensitization of the beta, but not the alpha 2‑adrenoreceptor-coupled-adenylate cyclase system in hamster white adipocytes after administration of epinephrine. Endocrinology. 1984;114:1576–83.

    Article  CAS  PubMed  Google Scholar 

  37. Yamauchi T, Iwai M, Kobayashi N, Shimazu T. Noradrenaline and ATP decrease the secretion of triglyceride and apoprotein B from perfused rat liver. Pflugers Arch. 1998;435:368–74.

    Article  CAS  PubMed  Google Scholar 

  38. Krauss RM. Lipoprotein subfractions and cardiovascular disease risk. Curr Opin Lipidol. 2010;21:305–11.

    Article  CAS  PubMed  Google Scholar 

  39. Mertens A, Holvoet P. Oxidized LDL and HDL: antagonists in atherothrombosis. FASEB J. 2001;15:2073–84.

    Article  CAS  PubMed  Google Scholar 

Download references


This research was supported by the European Union and the State of Hungary, co-financed by the European Social Fund in the framework of TÁMOP-4.2.2/B-10/1-2010-0024. We would like to thank Zsolt Karányi for his help in the statistical analyses (Department of Medicine, Faculty of Medicine, University of Debrecen).

Author information

Authors and Affiliations


Corresponding author

Correspondence to György Paragh MD DSc.

Ethics declarations

Conflict of interest

P. Koncsos, P. Fülöp, I. Juhász, K. Bíró, L. Márk, MDG. Simonyi, and G. Paragh declare that they have no competing interests.

Ethical standards

All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2008.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Koncsos, P., Fülöp, P., Juhász, I. et al. Changes in triglyceride, HDL-C, and non-HDL-C levels in patients with acute coronary syndrome. Wien Klin Wochenschr 128, 858–863 (2016).

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: