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Lipid profile and risks of cardiovascular diseases in conditions of rheumatoid arthritis


Authors: Ľudmila Pašková
Published in: Čes. slov. Farm., 2019; 68, 219-228
Category: Review Articles

Overview

Cardiovascular diseases (CVD) belong to the leading causes of mortality worldwide. Elevated levels of total cholesterol and LDL cholesterol are associated with increased incidence of CVD in the population. Reversely, reduction of lipoprotein levels in plasma results in a positive impact on CVD prevention. Patients with rheumatoid arthritis (RA), a chronic inflammatory disease, have markedly increased mortality risk due to CVD, despite lower lipoprotein levels in comparison with common population. This is known as the “lipid paradox”. RA itself represents an independent CVD risk factor acting as an inflammatory component. Inflammation, manifested by systemic elevated concentrations of pro-inflammatory cytokines, mainly interleukin 6 (IL-6), interleukin 1β (IL-1β) and the tumour necrosis factor α (TNF-α) in RA, is considered to be the main contributor of atherogenesis via its impact on lipoprotein metabolism and on the biology of the arterial wall. Atherosclerosis, a complex process including a number of mechanisms, is not only regarded as dysregulation of lipid metabolism, but also as a chronic inflammatory disease. This review summarizes the newest findings about the qualitative and quantitative alterations of lipids and lipoproteins affected by low-grade inflammation triggered by RA and their consequences on atherosclerosis.

Keywords:

Atherosclerosis – rheumatoid arthritis – inflammation – lipid metabolism – HDL


Sources

1. Radovits B. J., Fransen J., Al Shamma S., Eijsbouts A. M., van Riel P. L., Laan R. F. Excess mortality emerges after 10 years in an inception cohort of early rheumatoid arthritis. Arthritis Care Res. (Hoboken) 2010; 62, 362–370.

2. Holmqvist M. E., Wedrén S., Jacobsson L. T., Klareskog L., Nyberg F., Rantapää-Dahlqvist S., Alfredsson L., Askling J. Rapid increase in myocardial infarction risk following diagnosis of rheumatoid arthritis amongst patients diagnosed between 1995 and 2006. J. Intern. Med. 2010; 268, 578–585.

3. Bergholm R., Leirisalo-Repo M., Vehkavaara S., Mäkimattila S., Taskinen M. R., Yki-Järvinen H. Impaired responsiveness to NO in newly diagnosed patients with rheumatoid arthritis. Arterioscler. Thromb. Vasc. Biol. 2002; 22, 1637–1641.

4. Gisterå A., Hansson G. K. The immunology of atherosclerosis. Nat. Rev. Nephrol. 2017; 13, 368–380.

5. Pincus T., Callahan L. F. Taking mortality in rheumatoid arthritis seriously--predictive markers, socioeconomic status and comorbidity. J. Rheumatol. 1986; 13, 841–845.

6. Dessein P. H., Joffe B. I., Veller M. G., Stevens B. A., Tobias M., Reddi K., Stanwix A. E. Traditional and nontraditional cardiovascular risk factors are associated with atherosclerosis in rheumatoid arthritis. J. Rheumatol. 2005; 32, 435–442.

7. Goodson N. J., Solomon D. H. The cardiovascular manifestations of rheumatic diseases. Curr. Opin. Rheumatol. 2006; 18, 135–140.

8. Maradit-Kremers H., Nicola P. J., Crowson C. S., Ballman K. V., Gabriel S. E. Cardiovascular death in rheumatoid arthritis: a population-based study. Arthritis Rheum. 2005; 52, 722–732.

9. González-Gay M. A., González-Juanatey C. Inflammation and lipid profile in rheumatoid arthritis: bridging an apparent paradox. Ann. Rheum. Dis. 2014; 73, 1281–1283.

10. Asanuma Y., Kawai S., Aoshima H., Kaburaki J., Mizushima Y. Serum lipoprotein(a) and apolipoprotein(a) phenotypes in patients with rheumatoid arthritis. Arthritis Rheum. 1999; 42, 443–447.

11. Steiner G., Urowitz M. B. Lipid profiles in patients with rheumatoid arthritis: mechanisms and the impact of treatment. Semin. Arthritis Rheum. 2009; 38, 372–381.

12. Bergheanu S. C., Bodde M. C., Jukema J. W. Pathophysiology and treatment of atherosclerosis : Current view and future perspective on lipoprotein modification treatment. Neth. Heart J. 2017; 25, 231–242.

13. Yang X., Li Y., Ren X., Zhang X., Hu D., Gao Y., Xing Y., Shang H. Oxidative Stress-Mediated Atherosclerosis: Mechanisms and Therapies. Front. Physiol. 2017; 8, 600.

14. Ungurianu A., Margină D., Grădinaru D., Băcanu C., Ilie M., Tsitsimpikou C., Tsarouhas K., Spandidos D. A., Tsatsakis A. M. Lipoprotein redox status evaluation as a marker of cardiovascular disease risk in patients with inflammatory disease. Mol. Med. Rep. 2017; 15, 256–262.

15. Smallwood M. J., Nissim A., Knight A. R., Whiteman M., Haigh R., Winyard P. G. Oxidative stress in autoimmune rheumatic diseases. Free Radic. Biol. Med. 2018; 125, 3–14.

16. Arida A., Protogerou A. D., Kitas G. D., Sfikakis P. P. Systemic inflammatory response and atherosclerosis: The paradigm of chronic inflammatory rheumatic diseases. Int. J. Mol. Sci. 2018; 19.

17. Sproston N. R., Ashworth J. J. Role of C-Reactive Protein at Sites of Inflammation and Infection. Front. Immunol. 2018; 9, 754.

18. Robbins C. S., Hilgendorf I., Weber G. F., Theurl I., Iwamoto Y., Figueiredo J. L., Gorbatov R., Sukhova G. K., Gerhardt L. M., Smyth D., Zavitz C. C., Shikatani E. A., Parsons M., van Rooijen N., Lin H. Y., Husain M., Libby P., Nahrendorf M., Weissleder R., Swirski F. K. Local proliferation dominates lesional macrophage accumulation in atherosclerosis. Nat. Med. 2013; 19, 1166–1172.

19. Hansson G. K., Libby P. The immune response in atherosclerosis: a double-edged sword. Nat. Rev. Immunol. 2006; 6, 508–519.

20. Bäck M., Hansson G. K. Anti-inflammatory therapies for atherosclerosis. Nat. Rev. Cardiol. 2015; 12, 199–211.

21. Plutzky J., Liao K. P. Lipids in RA: Is less not necessarily more? Curr. Rheumatol. Rep. 2018; 20, 8.

22. Säemann M. D., Poglitsch M., Kopecky C., Haidinger M., Hörl W. H., Weichhart T. The versatility of HDL: a crucial anti-inflammatory regulator. Eur. J. Clin. Invest. 2010; 40, 1131–1143.

23. Kerekes G., Soltész P., Dér H., Veres K., Szabó Z., Végvári A., Shoenfeld Y., Szekanecz Z. Effects of biologics on vascular function and atherosclerosis associated with rheumatoid arthritis. Ann. N. Y. Acad. Sci. 2009; 1173, 814–821.

24. Kampoli A. M., Tousoulis D., Antoniades C., Siasos G., Stefanadis C. Biomarkers of premature atherosclerosis. Trends Mol. Med. 2009; 15, 323–332.

25. Derić M., Stokić E., Kojić-Damjanov S., Cabarkapa V., Eremić N. Biochemical markers of atherosclerotic disease. Med. Pregl. 2009; 62(Suppl 3), 15–23.

26. Khovidhunkit W., Kim M. S., Memon R. A., Shigenaga J. K., Moser A. H., Feingold K. R., Grunfeld C. Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. J. Lipid Res. 2004; 45, 1169–1196.

27. Petrov I., Dumitrescu A., Snejdrlova M., Zafrir B., Wożakowska-Kapłon B., Fabryova L., Pintarić H., Bridges I., Petkova R. Clinical Management of High and Very High Risk Patients with Hyperlipidaemia in Central and Eastern Europe: An Observational Study. Adv. Ther. 2019; 36, 608–620.

28. Sharrett A. R., Heiss G., Chambless L. E., Boerwinkle E., Coady S. A., Folsom A. R., Patsch W. Metabolic and lifestyle determinants of postprandial lipemia differ from those of fasting triglycerides: The Atherosclerosis Risk In Communities (ARIC) study. Arterioscler. Thromb. Vasc. Biol. 2001; 21, 275–281.

29. Ye J. Mechanisms of insulin resistance in obesity. Front. Med. 2013; 7, 14–24.

30. Manders R. J., van Dijk J. W., van Loon L. J. Low-intensity exercise reduces the prevalence of hyperglycemia in type 2 diabetes. Med. Sci. Sports Exerc. 2010; 42, 219–225.

31. Henderson G. C., Fattor J. A., Horning M. A., Faghihnia N., Johnson M. L., Mau T. L., Luke-Zeitoun M., Brooks G. A. Lipolysis and fatty acid metabolism in men and women during the postexercise recovery period. J. Physiol. 2007; 584, 963–981.

32. Plaisance, E. P., Fisher, G. Exercise and dietary-mediated reductions in postprandial lipemia. J. Nutr. Metab. 2014; 902065.

33. Kim M. S., Shigenaga J., Moser A., Feingold K., Grunfeld C. Repression of farnesoid X receptor during the acute phase response. J. Biol. Chem. 2003; 278, 8988–8995.

34. Hotamisligil G. S., Shargill N. S., Spiegelman B. M. Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Science 1993; 259, 87–91.

35. Hartman J., Frishman W. H. Inflammation and atherosclerosis: a review of the role of interleukin-6 in the development of atherosclerosis and the potential for targeted drug therapy. Cardiol. Rev. 2014; 22, 147–151.

36. Fatkhullina A. R., Peshkova I. O., Koltsova E. K. The role of cytokines in the development of atherosclerosis. Biochemistry (Mosc) 2016; 81, 1358–1370.

37. Vasanthi P., Nalini G., Rajasekhar G. Role of tumor necrosis factor‐alpha in rheumatoid arthritis: a review. APLAR Journal of Rheumatology 2007.

38. Chen X., Xun K., Chen L., Wang Y. TNF-alpha, a potent lipid metabolism regulator. Cell Biochem. Funct. 2009; 27, 407–416.

39. Bensinger S. J., Bradley M. N., Joseph S. B., Zelcer N., Janssen E. M., Hausner M. A., Shih R., Parks J. S., Edwards P. A., Jamieson B. D., Tontonoz P. LXR signaling couples sterol metabolism to proliferation in the acquired immune response. Cell 2008; 134, 97–111.

40. Reiss A. B., Siegart N. M., de Leon J. Interleukin-6 in atherosclerosis: atherogenic or atheroprotective? Clinical Lipidology 2017; 12, 14–23.

41. Libby P. Role of inflammation in atherosclerosis associated with rheumatoid arthritis. Am. J. Med. 2008; 121, 21–31.

42. Szalai A. J. The biological functions of C-reactive protein. Vascul. Pharmacol. 2002; 39, 105–107.

43. Ridker P. M. High-sensitivity C-reactive protein and cardiovascular risk: rationale for screening and primary prevention. Am. J. Cardiol. 2003; 92, 17K–22K.

44. Ridker P. M. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation 2003; 107, 363–369.

45. Sproston N. R., El Mohtadi M., Slevin M., Gilmore W., Ashworth J. J. The Effect of C-Reactive Protein Isoforms on Nitric Oxide Production by U937 Monocytes/Macrophages. Front. Immunol. 2018; 9, 1500.

46. Zouridakis E., Avanzas P., Arroyo-Espliguero R., Fredericks S., Kaski J. C. Markers of inflammation and rapid coronary artery disease progression in patients with stable angina pectoris. Circulation 2004; 110, 1747–1753.

47. Tölle M., Huang T., Schuchardt M., Jankowski V., Prüfer N., Jankowski J., Tietge U. J., Zidek W., van der Giet M. High-density lipoprotein loses its anti-inflammatory capacity by accumulation of pro-inflammatory-serum amyloid A. Cardiovasc. Res. 2012; 94, 154–162.

48. Watanabe J., Charles-Schoeman C., Miao Y., Elashoff D., Lee Y. Y., Katselis G., Lee T. D., Reddy S. T. Proteomic profiling following immunoaffinity capture of high-density lipoprotein: association of acute-phase proteins and complement factors with proinflammatory high-density lipoprotein in rheumatoid arthritis. Arthritis Rheum. 2012; 64, 1828–1837.

49. Navab M., van Lenten B. J., Reddy S. T., Fogelman A. M. High-density lipoprotein and the dynamics of atherosclerotic lesions. Circulation 2001; 104, 2386–2387.

50. van Lenten B. J., Navab M., Shih D., Fogelman A. M., Lusis A. J. The role of high-density lipoproteins in oxidation and inflammation. Trends Cardiovasc. Med. 2001; 11, 155–161.

51. Litvinov D., Mahini H., Garelnabi M. Antioxidant and anti-inflammatory role of paraoxonase 1: implication in arteriosclerosis diseases. N. Am. J. Med. Sci. 2012; 4, 523–532.

52. Navab M., Berliner J. A., Subbanagounder G., Hama S., Lusis A. J., Castellani L. W., Reddy S., Shih D., Shi W., Watson A. D., van Lenten B. J., Vora D., Fogelman A. M. HDL and the inflammatory response induced by LDL-derived oxidized phospholipids. Arterioscler. Thromb. Vasc. Biol. 2001; 21, 481–488.

53. Bowry V. W., Stanley K. K., Stocker R. High density lipoprotein is the major carrier of lipid hydroperoxides in human blood plasma from fasting donors. Proc. Natl. Acad. Sci. USA 1992; 89, 10316–10320.

54. Besler C., Heinrich K., Rohrer L., Doerries C., Riwanto M., Shih D. M., Chroni A., Yonekawa K., Stein S., Schaefer N., Mueller M., Akhmedov A., Daniil G., Manes C., Templin C., Wyss C., Maier W., Tanner F. C., Matter C. M., Corti R., Furlong C., Lusis A. J., von Eckardstein A., Fogelman A. M., Lüscher T. F., Landmesser U. Mechanisms underlying adverse effects of HDL on eNOS-activating pathways in patients with coronary artery disease. J. Clin. Invest. 2011; 121, 2693–2708.

55. Charles-Schoeman C., Watanabe J., Lee Y. Y., Furst D. E., Amjadi S., Elashoff D., Park G., McMahon M., Paulus H. E., Fogelman A. M., Reddy S. T. Abnormal function of high-density lipoprotein is associated with poor disease control and an altered protein cargo in rheumatoid arthritis. Arthritis Rheum. 2009; 60, 2870–2879.

56. Rosenson R. S., Brewer H. B., Ansell B. J., Barter P., Chapman M. J., Heinecke J. W., Kontush A., Tall A. R., Webb N. R. Dysfunctional HDL and atherosclerotic cardiovascular disease. Nat. Rev. Cardiol. 2016; 13, 48–60.

57. Scott D. L., Wolfe F., Huizinga T. W. Rheumatoid arthritis. Lancet 2010; 376, 1094–1108.

58. Kay J., Calabrese L. The role of interleukin-1 in the pathogenesis of rheumatoid arthritis. Rheumatology (Oxford) 2004; 43(Suppl 3), 32–39.

59. Cavagna L., Boffini N., Cagnotto G., Inverardi F., Grosso V., Caporali R. Atherosclerosis and rheumatoid arthritis: more than a simple association. Mediators Inflamm. 2012; 2012, 147354.

60. Arias de la Rosa I., Escudero-Contreras A., Rodríguez-Cuenca S., Ruiz-Ponce M., Jiménez-Gómez Y., Ruiz-Limón P., Pérez-Sánchez C., Ábalos-Aguilera M. C., Cecchi I., Ortega R., Calvo J., Guzmán-Ruiz R., Malagón M. M., Collantes-Estevez E., Vidal-Puig A., López-Pedrera C., Barbarroja N. Defective glucose and lipid metabolism in rheumatoid arthritis is determined by chronic inflammation in metabolic tissues. J. Intern. Med. 2018; 284, 61–77.

61. Skeoch S., Bruce I. N. Atherosclerosis in rheumatoid arthritis: is it all about inflammation? Nat. Rev. Rheumatol. 2015; 11, 390–400.

62. Vasanthi P., Nalini G., Rajasekhar G. Status of oxidative stress in rheumatoid arthritis. Int. J. Rheum. Dis. 2009; 12, 29–33.

63. Roubenoff R., Dellaripa P., Nadeau M. R., Abad L. W., Muldoon B. A., Selhub J., Rosenberg I. H. Abnormal homocysteine metabolism in rheumatoid arthritis. Arthritis Rheum. 1997; 40, 718–722.

64. Stühlinger M. C., Tsao P. S., Her J. H., Kimoto M., Balint R. F., Cooke J. P. Homocysteine impairs the nitric oxide synthase pathway: role of asymmetric dimethylarginine. Circulation 2001; 104, 2569–2575.

65. McGrath C. M., Young S. P. Lipid and Metabolic Changes in Rheumatoid Arthritis. Curr. Rheumatol. Rep. 2015; 17, 57.

66. Erum U., Ahsan T., Khowaja D. Lipid abnormalities in patients with Rheumatoid Arthritis. Pak. J. Med. Sci. 2017; 33, 227–230.

67. Myasoedova E., Crowson C. S., Kremers H. M., Fitz-Gibbon P. D., Therneau T. M., Gabriel S. E. Total cholesterol and LDL levels decrease before rheumatoid arthritis. Ann. Rheum. Dis. 2010; 69, 1310–1314.

68. Nurmohamed M. T. Atherogenic lipid profiles and its management in patients with rheumatoid arthritis. Vasc. Health Risk Manag. 2007; 3, 845–852.

69. White D., Fayez S., Doube A. Atherogenic lipid profiles in rheumatoid arthritis. N. Z. Med. J. 2006; 119, U2125.

70. Choy E., Ganeshalingam K., Semb A. G., Szekanecz Z., Nurmohamed M. Cardiovascular risk in rheumatoid arthritis: recent advances in the understanding of the pivotal role of inflammation, risk predictors and the impact of treatment. Rheumatology (Oxford) 2014; 53, 2143–2154.

71. AbouAssi H., Connelly M. A., Bateman L. A., Tune K. N., Huebner J. L., Kraus V. B., Winegar D. A., Otvos J. D., Kraus W. E., Huffman K. M. Does a lack of physical activity explain the rheumatoid arthritis lipid profile? Lipids Health Dis. 2017; 16, 39.

72. Walsmith J., Roubenoff R. Cachexia in rheumatoid arthritis. Int. J. Cardiol. 2002; 85, 89–99.

73. Roubenoff R., Roubenoff R. A., Cannon J. G., Kehayias J. J., Zhuang H., Dawson-Hughes B., Dinarello C. A., Rosenberg I. H. Rheumatoid cachexia: cytokine-driven hypermetabolism accompanying reduced body cell mass in chronic inflammation. J. Clin. Invest. 1994; 93, 2379–2386.

74. Jin X., Yao T., Zhou Z., Zhu J., Zhang S., Hu W., Shen C. Advanced Glycation End Products Enhance Macrophages Polarization into M1 Phenotype through Activating RAGE/NF-κB Pathway. Biomed. Res. Int. 2015; 2015, 732450.

75. Klafke J. Z., Porto F. G., Batista R., Bochi G. V., Moresco R. N., da Luz P. L., Viecili P. R. Association between hypertriglyceridemia and protein oxidation and proinflammatory markers in normocholesterolemic and hypercholesterolemic individuals. Clin. Chim. Acta 2015; 448, 50–57.

76. Charles-Schoeman C., Lee Y. Y., Grijalva V., Amjadi S., FitzGerald J., Ranganath V. K., Taylor M., McMahon M., Paulus H. E., Reddy S. T. Cholesterol efflux by high density lipoproteins is impaired in patients with active rheumatoid arthritis. Ann. Rheum. Dis. 2012; 71, 1157–1162.

77. Tanimoto N., Kumon Y., Suehiro T., Ohkubo S., Ikeda Y., Nishiya K., Hashimoto K. Serum paraoxonase activity decreases in rheumatoid arthritis. Life Sci. 2003; 72, 2877–2885.

78. Başkol M., Başkol G., Deniz K., Ozbakir O., Yücesoy M. A new marker for lipid peroxidation: serum paraoxonase activity in non-alcoholic steatohepatitis. Turk. J. Gastroenterol. 2005; 16, 119–123.

79. Walker B. R. Glucocorticoids and cardiovascular disease. Eur. J. Endocrinol. 2007; 157, 545–559.

80. Verhoeven F., Prati C., Maguin-Gaté K., Wendling D., Demougeot C. Glucocorticoids and endothelial function in inflammatory diseases: focus on rheumatoid arthritis. Arthritis Res. Ther. 2016; 18, 258.

81. Cooper C., Bardin T., Brandi M. L., Cacoub P., Caminis J., Civitelli R., Cutolo M., Dere W., Devogelaer J. P., Diez-Perez A., Einhorn T. A., Emonts P., Ethgen O., Kanis J. A., Kaufman J. M., Kvien T. K., Lems W. F., McCloskey E., Miossec P., Reiter S., Ringe J., Rizzoli R., Saag K., Reginster J. Y. Balancing benefits and risks of glucocorticoids in rheumatic diseases and other inflammatory joint disorders: new insights from emerging data. An expert consensus paper from the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO). Aging Clin. Exp. Res. 2016; 28, 1–16.

82. Smolen J. S., Steiner G. Therapeutic strategies for rheumatoid arthritis. Nat. Rev. Drug. Discov. 2003; 2, 473–488.

83. Jacobsson L. T., Turesson C., Gülfe A., Kapetanovic M. C., Petersson I. F., Saxne T., Geborek P. Treatment with tumor necrosis factor blockers is associated with a lower incidence of first cardiovascular events in patients with rheumatoid arthritis. J. Rheumatol. 2005; 32, 1213–1218.

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