Predictors of Coronary Plaque Vulnerability in Patients with Stable Coronary Artery Disease
https://doi.org/10.18087/cardio.2020.10.n1188
Abstract
Aim To identify new predictors for vulnerability of atherosclerotic coronary plaques in patients with stable ischemic heart disease (sIHD).
Material and methods This prospective, single-center study included 58 patients with sIHD. Unstable plaques were detected with virtual histology intravascular ultrasound of proximal and medium segments of a coronary artery without significant lesions according to coronarography data. Indexes of inflammation, dyslipidemia and carbohydrate metabolism were considered as candidate predictors for coronary plaque vulnerability.
Results In 56 coronary arteries, 58 plaques were detected, 12 of which (20.7 %) were unstable. Vulnerable plaques differed morphologically from stable ones by a greater size of the necrotic core (35.1±8.5 % vs. 24.0±13.2 %; р=0.008), calcified nodules (2.0 [1.0; 5.0] % vs. 1.0 [0; 2.0] %; р=0.006), and a lower content of fibrous components (54.9±10.2 % vs. 66.4±15.8 %; р=0.02). In addition, vulnerable plaques more frequently narrowed the arterial lumen by >70 % of the lumen area (33.3 % vs. 2.2 %; р=0.0006). Correlation analysis showed a negative correlation between the level of high-density lipoproteins (HDL) and calcium volume (r= –0.4104; р=0.023); a positive correlation between the blood glucose level as determined by the oral glucose tolerance test and the lipid component (r=0.48198; р=0.033); and a negative correlation between the apolipoprotein A level and the calcium volume (r= –0.4297; р=0.008).
Conclusion The study demonstrated a high prevalence of vulnerable plaques in nontarget coronary arteries in patients with sIHD. In this process, dyslipidemia indexes (LDL, apolipoproteins A) correlate with the calcium volume whereas blood glucose, as measured in the oral glucose tolerance test, correlates with the lipid component of coronary plaque.
Keywords
About the Authors
N. A. KocherginRussian Federation
PhD, researcher
A. M. Kochergina
Russian Federation
PhD, researcher
V. I. Ganyukov
Russian Federation
PhD, department head
O. L. Barbarash
Russian Federation
PhD, director of Institution
References
1. Roth GA, Johnson C, Abajobir A, Abd-Allah F, Abera SF, Abyu G et al. Global, Regional, and National Burden of Cardiovascular Diseases for 10 Causes, 1990 to 2015. Journal of the American College of Cardiology. 2017;70(1):1—25. DOI: 10.1016/j.jacc.2017.04.052
2. Yonetsu T, Jang I-K. Advances in Intravascular Imaging: New Insights into the Vulnerable Plaque from Imaging Studies. Korean Circulation Journal. 2018;48(1):1–15. DOI: 10.4070/kcj.2017.0182
3. Costopoulos C, Huang Y, Brown AJ, Calvert PA, Hoole SP, West NEJ et al. Plaque Rupture in Coronary Atherosclerosis Is Associated With Increased Plaque Structural Stress. JACC: Cardiovascular Imaging. 2017;10(12):1472–83. DOI: 10.1016/j.jcmg.2017.04.017
4. Tagieva N.R., Shakhnovich R.M., Mironov V.M., Ezhov M.V., Matchin Yu.G., Mitroshkin M.G. et al. Comparison of Atherosclerotic Lesions in Patients With Acute Myocardial Infarction and Stable Angina Pectoris Using Intravascular Ultrasound. Kardiologiia. 2015;55(7):5–13.
5. Stone GW, Maehara A, Lansky AJ, de Bruyne B, Cristea E, Mintz GS et al. A Prospective Natural-History Study of Coronary Atherosclerosis. New England Journal of Medicine. 2011;364(3):226–35. DOI: 10.1056/NEJMoa1002358
6. Laimoud M, Faris F, Elghawaby H. Coronary Atherosclerotic Plaque Vulnerability Rather than Stenosis Predisposes to Non-ST Elevation Acute Coronary Syndromes. Cardiology Research and Practice. 2019;2019:1–7. DOI: 10.1155/2019/2642740
7. Theodorou K, Boon RA. Endothelial Cell Metabolism in Atherosclerosis. Frontiers in Cell and Developmental Biology. 2018;6:82. DOI: 10.3389/fcell.2018.00082
8. Kochergin N.A., Kochergina A.M., Ganjukov V.I., Barbarash O.L. Vulnerable atherosclerotic plaques of coronary arteries in patients with stable coronary artery disease. Complex Issues of Cardiovascular Diseases. 2018;7(3):65–71. DOI: 10.17802/2306-1278-2018-7-3-65-71
9. Stefanadis C, Antoniou C, Tsiachris D, Pietri P. Coronary Atherosclerotic Vulnerable Plaque: Current Perspectives. Journal of the American Heart Association. 2017;6(3):e005543. DOI: 10.1161/JAHA.117.005543
10. Tong DC, Whitbourn R, MacIsaac A, Wilson A, Burns A, Palmer S et al. High-Sensitivity C-Reactive Protein Is a Predictor of Coronary Microvascular Dysfunction in Patients with Ischemic Heart Disease. Frontiers in Cardiovascular Medicine. 2018;4:81. DOI: 10.3389/fcvm.2017.00081
11. Liu H-H, Cao Y-X, Sun D, Jin J-L, Zhang H-W, Guo Y-L et al. Highsensitivity C-reactive protein and hypertension: combined effects on coronary severity and cardiovascular outcomes. Hypertension Research. 2019;42(11):1783–93. DOI: 10.1038/s41440-019-0293-8
12. Tsujita K, Sugiyama S, Sumida H, Shimomura H, Yamashita T, Yamanaga K et al. Impact of Dual Lipid-Lowering Strategy With Ezetimibe and Atorvastatin on Coronary Plaque Regression in Patients With Percutaneous Coronary Intervention: The Multicenter Randomized Controlled PRECISE-IVUS Trial. Journal of the American College of Cardiology. 2015;66(5):495–507. DOI: 10.1016/j.jacc.2015.05.065
13. Cheng JM, Oemrawsingh RM, Garcia-Garcia HM, Boersma E, van Geuns R-J, Serruys PW et al. PCSK9 in relation to coronary plaque inflammation: Results of the ATHEROREMO-IVUS study. Atherosclerosis. 2016;248:117–22. DOI: 10.1016/j.atherosclerosis.2016.03.010
14. Androulakis E, Zacharia E, Papageorgiou N, Lioudaki E, Bertsias D, Charakida M et al. High-density Lipoprotein and Low-density Lipoprotein Therapeutic Approaches in Acute Coronary Syndromes. Current Cardiology Reviews. 2017;13(3):168–82. DOI: 10.2174/1573403X13666170209145622
15. Zimetti F, Freitas WM, Campos AM, Daher M, Adorni MP, Bernini F et al. Cholesterol efflux capacity does not associate with coronary calcium, plaque vulnerability, and telomere length in healthy octogenarians. Journal of Lipid Research. 2018;59(4):714–21. DOI: 10.1194/jlr.P079525
16. Desouza CV, Bolli GB, Fonseca V. Hypoglycemia, Diabetes, and Cardiovascular Events. Diabetes Care. 2010;33(6):1389–94. DOI: 10.2337/dc09-2082
17. Su G, Mi S, Tao H, Li Z, Yang H, Zheng H et al. Association of glycemic variability and the presence and severity of coronary artery disease in patients with type 2 diabetes. Cardiovascular Diabetology. 2011;10(1):19. DOI: 10.1186/1475-2840-10-19
18. Kuroda M, Shinke T, Sakaguchi K, Otake H, Takaya T, Hirota Y et al. Effect of Daily Glucose Fluctuation on Coronary Plaque Vulnerability in Patients Pre-Treated With Lipid-Lowering Therapy. JACC: Cardiovascular Interventions. 2015;8(6):800–11. DOI: 10.1016/j.jcin.2014.11.025
19. Kato M, Dote K, Naganuma T, Sasaki S, Ueda K, Okita M et al. Clinical Predictors of Culprit Plaque Rupture Assessed on Intravascular Ultrasound in Acute Coronary Syndrome. Circulation Journal. 2010;74(9):1936–42. DOI: 10.1253/circj.CJ-10-0086
20. Cheng JM, Garcia-Garcia HM, de Boer SPM, Kardys I, Heo JH, Akkerhuis KM et al. In vivo detection of high-risk coronary plaques by radiofrequency intravascular ultrasound and cardiovascular outcome: results of the ATHEROREMO-IVUS study. European Heart Journal. 2014;35(10):639–47. DOI: 10.1093/eurheartj/eht484
Review
For citations:
Kochergin N.A., Kochergina A.M., Ganyukov V.I., Barbarash O.L. Predictors of Coronary Plaque Vulnerability in Patients with Stable Coronary Artery Disease. Kardiologiia. 2020;60(10):20-26. https://doi.org/10.18087/cardio.2020.10.n1188