HDL-particle subfractions in heart failure
Authors:
Murín J. 1; Bulas J. 1; Gašpar Ľ. 1; Klabník A. 2; Wawruch M. 3
Authors‘ workplace:
I. interná klinika LF UK a UN Bratislava
1; Kardiologická ambulancia, Oravská poliklinika, Námestovo
2; Ústav farmakológie a klinickej farmakológie LF UK, Bratislava
3
Published in:
Kardiol Rev Int Med 2019, 21(3): 168-170
Overview
For some decades there has been an interest in investigating the role of HDL particles in cardiovascular diseases. The Framingham Heart Study discovered that people with high serum HDL-C levels usually have low cardiovascular risk. This was the background of ‘HDL – hypothesis’: that with an increase of serum HDL-C levels, we can reduce cardiovascular morbidity and mortality. The hypothesis was not confirmed by large clinical trials (with niacin, with CETP inhibitors), even though there was an increase of serum HDL-C level detected. These results stimulated analysis of HDL particles and their pleiotropic actions were discovered: small and more dense HDL particles had greater cholesterol efflux, together with anti-inflammatory and anti-oxidative activities, than the larger and less dense HDL particles. In patients with an increase of small and dense HDL particles in serum, there was lower risk of ischaemic heart disease, carotid atherosclerosis and of cardiovascular events and death. In this paper, we present data about subfractions of HDL particles in heart failure (782 patient with systolic heart failure and 1,004 patients with diastolic heart failure): 1. larger HDL particles were observed in patients with systolic heart failure and smaller HDL particles were observed in patients with diastolic heart failure; 2. The presence of small HDL particles in serum of patients with heart failure improved the patients’ prognosis, as these patients suffered from less cardivascular events during the follow-up. Therefore, the presence of HDL subfractions is a marker of residual cardiovascular risk in heart failure patients.
Keywords:
treatment – HDL particle – HDL subfractions – cardiovascular events
Sources
1. Gordon T, Castelli WP, Hjortland MC et al. High density lipoprotein as a protective factor against coronary heart disease. The Framingham Study. Am J Med 1977; 62(5): 707– 714. doi: 10.1016/ 0002-9343(77)90874-9.
2. Toth PP, Barter PJ, Rosenson RS et al. High-density lipoproteins: a consensus statement from the National Lipid Association. J Clin Lipidol 2013; 7(5): 484– 525. doi: 10.1016/ j.jacl.2013.08.001.
3. Boden WE, Probstfield JL, Anderson T et al. AIM-HIGH Investigators. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med 2011; 365(24): 2255– 2267. doi: 10.1056/ NEJMoa1107579.
4. Schwartz GG, Olsson AG, Abt M et al. Effects of dalcetrapib in patients with a recent acute coronary syndrome. N Engl J Med 2012; 367(22): 2089– 2099. doi: 10.1056/ NEJMoa1206797.
5. Barter PJ, Caulfield M, Erikssson M et al. Effects of torcetrapib in patients at high risk for coronary events. N Engl J Med 2007; 357(21): 2109– 2122. doi :10.1056/ NEJMoa0706628.
6. HPS2-THRIVE Collaborative Group. HPS2-THRIVE randomized placebo-controlled tiral in 25 673 high-risk patietns of ER niacin/ laropiprant: trial design, pre-specified muscle and liver out-comes, and reasons for stopping study treatment. Eur Heart J 2013; 34(17): 1279– 1291. doi: 10.1093/ eurheartj/ eht055.
7. Lincoff AM, Nicholls SJ, Riesmeyer JS et al. Evacetrapib and cardiovascular outcomes in high-risk vascular disease. N Engl J Med 2017; 376(20): 1933– 1942. doi: 10.1056/ NEJMoa1609581.
8. Kingwell BA, Chapman MJ, Kontush A et al. HDL-targeted therapies: progess, failures and future. Nat Rev Drug Discov 2014; 13(6): 445– 464. doi: 10.1038/ nrd4279.
9. McGarrah RW. Refocusing the AIM on HDL in the metabolic syndrome. Atherosclerosis 2016; 251: 531– 533. doi: 10.1016/ j.atherosclerosis.2016.06.051.
10. Mackey RH, Greenland P, Goff DC et al. High-density lipoprotein cholesterol and particle concentrations, carotid atherosclerosis, and coronary events: MESA (Multi-Ethnic Study of Atherosclerosis). J Am Coll Cardiol 2012; 60(6): 508– 516. doi: 10.1016/ j.jacc.2012.03.060.
11. Yu S, Yarnell JW, Sweetnam P et al. High density lipoprotein subfractions and the risk of coronary heart disease: 9-years follow-up in the Caerphilly Study. Atherosclerosis 2003; 166(2): 331– 338. doi: 10.1016/ s0021-9150(02)00361-1
12. Kim DS, Burt AA, Rosenthal EA et al. HDL-3 is a superior predictor of carotid artery disease in a case-control cohort of 1725 participants. J Am Heart Assoc 2014; 3(3): e000902. doi: 10.1161/ JAHA.114.000902.
13. Martin SS, Khokhar AA, May HT et al. HDL cholesterol subclasses, myocardial infarction, and mortality in secondary prevention: the Lipoprotein Investigators Collaborative. Eur Heart J 2015; 36(1): 22– 30. doi: 10.1093/ eurheartj/ ehu264.
14. McGarrah RW, Craig DM, Haynes C et al. High-density lipoprotein subclass measurements improve mortality risk prediction, discrimination and reclassification in a cardiac catheterization cohort. Atherosclerosis 2016; 246: 229– 235. doi: 10.1016/ j.atherosclerosis.2016.01.012.
15. Chapman MJ, Kontush A. Biological activities of HDL subpopulations and their relevance to cardiovascular disease. Trends Mol Med 2011; 17(10): 594– 603. doi: 10.1016/ j.molmed.2011.05.013.
16. Jeyarajah EJ, Cromwell WC, Otvos JD. Lipoprotein particle analysis by nuclear magnetic resonance spectroscopy. Clin Lab Med 2006; 26(4): 847– 870. doi: 10.1016/ j.cll.2006.07.006.
17. Hunter WG, McGarrah RW, Kelly JP et al. High-density lipoprotein particle subfractions in Heart Failure with preserved or reduced ejection fraction. J Am Coll Cardiol 2019; 73(2): 177– 186. doi: 10.1016/ j.jacc.2018.10.059.
18. Shah SH, Granger CB, Hauser ER et al. Reclassification of cardiovascular risk using integrated clinical and molecular biosignatures: design of and rationale for the Measurement to Understand the Reclassification od Disease of Cabarrus and Kannapolis (MURDOCK) Horizon 1 Cardiovascular Disease-Study. Am Heart J 2010; 160(3): 371– 379.e372. doi: 10.1016/ j.ahj.2010.06.051.
19. Kraus WE, Granger CB, Sketch MH Jr et al. A guide for a cardiovascular genomics biorepository: the CATHGEN experience. J Cardiovasc Transl Res 2015; 8(8): 449– 457. doi: 10.1007/ s12265-015-9648-y.
20. Akinkuolie AO, Buring JE, Ridker PM et al. A novel protein glycan biomarker and future cardiovascular disease events. J Am Heart Assoc 2014; 3(5): e001221. doi: 10.1161/ JAHA.114.001221.
21. McGarrah RW, Kelly JP, Craig DM et al. A novel protein glycan-derived inflammation biomarker independently predicts cardiovascular disease and modifies the association of HDL subclasses with mortality. Clin Chem 2017; 63(1): 288– 296. doi: 10.1373/ clinchem.2016.261636.
22. Potočnjak I, Degoricija V, Trbušič M et al. Serum concentration of HDL particles predicts mortality in acute heart failure patients. Sci Rep 2017; 7: 46642. doi: 10.1038/ srep46642.
23. Akinkuolie AO, Paynter NP, Padmanabhan L et al. High-density lipoprotein particle subclass heterogeneity and incident coronary heart disease. Circ Cardiovasc Qual Outcomes 2014; 7(1): 55– 63. doi: 10.1161/ CIRCOUTCOMES.113.000675.
24. El Harchaoui K, Arsenault BJ, Franssen R et al. High-density lipoprotein particle size and concentration and coronary risk. Ann Intern Med 2009; 150(2): 84– 93. doi: 10.7326/ 0003-4819-150-2-200901200-00006.
25. Cockerill GW, Rye KA, Gamble JR et al. High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules. Arterioscler Thromb Vasc Biol 1995; 15(11): 1987– 1994.
26. Cockerill GW, Saklatvala J, Ridley SH et al. Hihg-density lipoproteins differentially modulate cytokine-induced expression of E-selectin and cyclooxygenase-2. Arterioscler Thromb Vasc Biol 1999; 19(4): 910– 917.
Labels
Paediatric cardiology Internal medicine Cardiac surgery CardiologyArticle was published in
Cardiology Review
2019 Issue 3
Most read in this issue
- Cardiovascular effects of recreational drugs (cocaine, marijuana, methamphetamines)
- Sarcoidosis – current view on pathogenesis, diagnosis and treatment
- Epidemiology of tuberculosis
- Amiodarone lung toxicity – ‘amiodarone lung’