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1-2 . 2020

Heterogeneity of atherosclerosis

Abstract

Cardiovascular events associated with atherosclerosis can develop by achieving treatment goals following current clinical guidelines and failure to achieve the set goals, including risk factors such as dyslipidemia, high blood pressure, hyperglycemia, systemic inflammation, and unhealthy lifestyle.

The aim of this literature review is to consider biomarkers that influence the progression of atherosclerosis-associated cardiovascular diseases.

According to modern concepts, atherosclerosis is a chronic disease involving lipid and immune metabolism disorders, innate, acquired immunity, accompanied by inflammation. It is known that the leading role in the emergence and development of atherosclerosis and its complications, causing lipoproteins. The review considers the literature data indicating that atherosclerosis is a complex, multifaceted biochemical process associated with well-known low-density lipoproteins. Following the updated recommendations for more intensive lipid-lowering therapy, increasing attention is paid to assessing the residual risk associated with atherosclerosis. Cholesterol, hyperglycemic, inflammatory, infectious theories of the development of atherosclerosis are considered. Studying the heterogeneity of atherosclerosis can help gain a deeper understanding of the molecular mechanisms of the onset and development of atherosclerosis, which may help develop new targeted therapies.

Keywords:residual risk, low-density lipoprotein cholesterol, infectious theory, apolipoprotein B, lipoprotein (a), hyperglycemia and atherosclerosis

Funding. The study had no sponsor support.

Conflict of interests. The authors declare no conflict of interests.

For citation: Obrezan A.G., Danilova A.V. Heterogeneity of atherosclerosis. Kardiologiya: novosti, mneniya, obuchenie [Cardiology: News, Opinions, Training]. 2020; 8 (1-2): 54-9. DOI: https://doi.org/10.24411/2309-1908-2020-11202 (in Russian)

REFERENCES

1. Lilly L.S. Pathophysiology of the Cardiovascular System. Transl. from Engl. Moscow: BINOM, Laboratoriay znaniy, 2016: 182–218. ISBN 978-5-9963-0726-5. (in Russian)

2. Hermans M.P., et al. Residual microvascular risk in type 2 diabetes in 2014: is it time for a re-think? A perspective from the residual risk reduction initiative (R3i). J Diabetes Metab. 2014; 5: 8. DOI: https://doi.org/10.4172/2155-6156.1000413

3. Ference B.A., Ginsberg H.N., et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017; 38 (32): 2459–72. DOI: https://doi.org/10.1093/eurheartj/ehx144

4. Poznyak A., et al. The diabetes mellitus–atherosclerosis connection: the role of lipid and glucose metabolism and chronic inflammation. Int J Mol Sci. 2020; 21 (5): 1835. DOI: https://doi.org/10.3390/ijms21051835

5. van den Berg M.J., et al. Low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, triglycerides, and apolipoprotein B and cardiovascular risk in patients with manifest arterial disease. Am J Cardiol. 2016; 118 (6): 804–10. DOI: https://doi.org/10.1016/j.amjcard.2016.06.048

6. Sattar N. Comparison of the associations of apolipoprotein B and non-high-density lipoprotein cholesterol with other cardiovascular risk factors in patients with the metabolic syndrome in the Insulin Resistance Atherosclerosis Study. Circulation. 2004; 110: 2687–93. DOI: https://doi.org/10.1161/01.CIR.0000145660.60487.94

7. Bhatt D.L. REDUCE-IT: residual cardiovascular risk in statin-treated patients with elevated triglycerides: now we can REDUCE-IT! Eur Heart J. 2019; 40 (15): 1174–5. DOI: https://doi.org/10.1093/eurheartj/ehz179

8. Langlois M.R., et al. Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM for the European Atherosclerosis Society (EAS) and the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM). Clin Chem Lab Med. 2020; 294: 46–61. DOI: https://doi.org/10.1515/cclm-2019-1253

9. Pencina K.M., et al. Trajectories of non-HDL cholesterol across midlife: implications for cardiovascular prevention. J Am Coll Cardiol. 2019; 74 (1): 70–9. DOI: https://doi.org/10.1016/j.jacc.2019.04.047

10. Carr S.S. Non-HDL-cholesterol and apolipoprotein B compared with LDL-cholesterol in atherosclerotic cardiovascular disease risk assessment. Pathology. 2019; 51 (2): 148–54. DOI: https://doi.org/10.1016/j.pathol.2018.11.006

11. Shapiro M.D., Fazio S. From lipids to inflammation. Circ Res. 2016. 118: 732–49. DOI: https://doi.org/10.1161/CIRCRESAHA.115.306471

12. Tsimikas S., et al. NHLBI working group recommendations to reduce lipoprotein(a)-mediated risk of cardiovascular disease and aortic stenosis. J Am Coll Cardiol. 2018; 71: 177–92. DOI: https://doi.org/10.1016/j.jacc.2017.11.014

13. Burgess S. Association of LPA variants with risk of coronary disease and the implications for lipoprotein (a)-lowering therapies: a Mendelian randomization analysis. JAMA Cardiol. 2018; 3 (7): 619–27. DOI: https://doi.org/10.1001/jamacardio.2018.1470

14. Nordestgaard B.G., et al. Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM. Atherosclerosis. 2020; 294: 46–61. DOI: https://doi.org/10.1016/j.atherosclerosis.2019.12.005

15. Kukharchuk V.V., Ezhov M.V., et al. Diagnostics and correction of lipid metabolism disorders for the prevention and treatment of atherosclerosis. Russian recommendations, VII revision. Ateroskleroz i dislipidemii [Atherosclerosis and Dyslipidemia]. 2020; 1 (38): 7–42. DOI: https://doi.org/10.34687/2219-8202.JAD.2020.01.0002 (in Russian)

16. Stam-Slob M.C. Effect of type 2 diabetes on recurrent major cardiovascular events for patients with symptomatic vascular disease at different locations. Diabetes Care. 2015; 38: 1528–35. DOI: https://doi.org/10.2337/dc14-2900

17. Wan Z., Fan Y., et al. NLRP3 inflammasome promotes diabetes-induced endothelial inflammation and atherosclerosis. Diabetes Metab Syndr Obes. 2019; 12: 1931–42. DOI: https://doi.org/10.2147/DMSO.S222053

18. Feng H., et al. High glucose and lipopolysaccharide prime NLRP3 inflammasome via ROS/TXNIP pathway in mesangial cells. J Diabetes Res. 2016; 2016: 6973175. DOI: https://doi.org/10.1155/2016/6973175

19. Bornfeldt K.E. Does elevated glucose promote atherosclerosis? Pros and Cons. Circ Res. 2016; 119 (2): 190–3. DOI: https://doi.org/10.1161/CIRCRESAHA.116.308873

20. Wolf D., Ley K. Immunity and inflammation in atherosclerosis. Circ Res. 2019; 124: 315–27. DOI: https://doi.org/10.1161/CIRCRESAHA.118.313591

21. Menon V., Kumar A. Impact of baseline glycemic control on residual cardiovascular risk in patients with diabetes mellitus and highrisk vascular disease treated with statin therapy. J Am Heart Assoc. 2020; 9 (1): e014328. DOI: https://doi.org/10.1161/JAHA.119.014328

22. Wolf D., et al. Immunity and Inflammation in atherosclerosis. Circ Res. 2019; 124 (2): 315–27. DOI: https://doi.org/10.1161/CIRCRESAHA.118.313591

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CHIEF EDITOR
CHIEF EDITOR
Andrey G. Obrezan
MD, Professor, Head of the Hospital Therapy Department of the Saint Petersburg State University, Chief Physician of SOGAZ MEDICINE Clinical Group, St. Petersburg, Russian Federation

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