The role of adipokines and epicardial fat tissue thickness in prognostication of acute coronary syndrome outcomes


DOI: https://dx.doi.org/10.18565/therapy.2023.4.38-46

Davydova A.V., Nikiforov V.S., Khalimov Yu.Sh.

1) A.S. Lukashevsky Kamchatka Regional Hospital, Petropavlovsk-Kamchatsky; 2) I.I. Mechnikov North-Western State Medical University of the Ministry of Healthcare of Russia, Saint Petersburg; 3) Academician I.P. Pavlov First Saint Petersburg State Medical University of the Ministry of Healthcare of Russia
Abstract. Epicardial fat, taking into account its anatomical and physiological features, has been considered for many years as an important factor incardiovascular diseases (CVD) pathogenesis.
The aim: to evaluate the possibility of predicting the negative clinical course of stenocardia during the year after hospitalization for acute coronary syndrome. It is based on the thickness of epicardial fat and adipokines concentration in patients with metabolic disorders.
Material and methods. We studied 38 female and 64 male patients with overweight or obesity, median age 62 [55; 67] years hospitalized for unstable stenocardia of medium or high risk according to the Grace 2.0 scale. During their admission, a survey, examination, laboratory testing to determine the level of leptin, adiponectin, tumor necrosis factor-alpha (TNF-α) and interleukin (IL-6) were performed. Stenting of coronary arteries was made on the 1st–3rd day after hospitalization. Echocardiography on days 2–4 according to the standard protocol with epicardial fat thickness (TEF) measurement along the long axis of the left ventricle at the end of systole was performed. Patients were divided into two groups depending on TEF: Group 1 – TEF up to 7,6 mm (n=46); Group 2 – TEF >7,6 mm (n=56). After 12 months, the control visit of patients, as part of the second stage of the study took place. All together 89 persons (87,2%) were examined – 44 from Group 1 and 45 from Group 2.
Results. The dynamics of laboratory parameters in Group 1 was fixed relatively to the level of adiponectin (p=0,001), leptin (p=0,001), IL-6 (p=0,001) and TNF-α (p=0,001), in Group 2 – levels of leptin (p=0,001), TNF-α (p=0,001) and IL-6 (p=0,001). Significant differences in echocardiographic signs over time in Group 1 were identified in indexes of end-diastolic volume (EDV) and end-systolic volume (ESV; p=0,001), in Group 2- in indexes of left ventricular ejection fraction (LVEF); p=0,001), EDV and ESV (p=0,001). The following factors had a statistically significant effect on the probability of worsening stenocardia: leptin level – 1,08 (95% CI: 1,0–1,16; p=0,046), LV EF – 0,66 (95% CI: 0,52–0,84; p=0,001) and TEF – 2,18 (95% CI: 1,21–3,93; p=0,010).
Conclusion. TEF more than 7,6 mm, elevated leptin concentration and reduced LV EF were independent predictors of unfavorable course of stenocardia within 12 months in patients with unstable stenocardia and metabolic disorders.

Literature


1. Барбараш О.Л., Дупляков Д.В., Затейщиков Д.А. с соавт. Острый коронарный синдром без подъема сегмента ST электрокардиограммы. Клинические рекомендации 2020. Российский кардиологический журнал. 2021; 26(4): 149–202. [Barbarash O.L., Duplyakov D.V., Zateischikov D.A. et al. 2020 clinical practice guidelines for acute coronary syndrome without ST segment elevation. Rossiyskiy kardiologicheskiy zhurnal = Russian Journal of Cardiology. 2021; 26(4): 149–202 (In Russ.)].https://dx.doi.org/10.15829/1560-4071-2021-4449. EDN: BSXPMI.


2. Aguero F., Marrugat J., Elosua R. et al. New myocardial infarction definition affects incidence, mortality, hospitalization rates and prognosis. Eur J Prev Cardiol. 2015; 22(10): 1272–80. https://dx.doi.org/10.1177/2047487314546988.


3. Hirata Y., Kurobe H., Akaike M. et al. Enhanced inflammation in epicardial fat in patients with coronary artery disease. Int Heart J. 2011; 52(3): 139–42. https://dx.doi.org/10.1536/ihj.52.139.


4. Iacobellis G. Epicardial adipose tissue in endocrine and metabolic diseases. Endocrine. 2014; 46(1): 8–15.https://dx.doi.org/10.1007/s12020-013-0099-4.


5. Давыдова А.В., Никифоров В.С., Халимов Ю.Ш. Эпикардиальный жир и активность провоспалительных цитокинов и адипокинов у пациентов с нестабильной стенокардией и метаболическими нарушениями. Эндокринология. Новости. Мнения. Обучение. 2022; 11(2): 27–33. [Davydova A.V., Nikiforov V.S., Khalimov Yu.Sh. et al. Epicardial fat and the activity of proinflammatory cytokines and adipokines in individuals with unstable angina and metabolic disorders. Endokrinologiya. Novosti. Mneniya. Obucheniye = Endocrinology. News. Opinions. Education. 2022; 11(2): 27–33 (In Russ.)].https://dx.doi.org/10.33029/2304-9529-2022-11-2-27-33. EDN: UQZMSK.


6. Collet J.P., Thiele H., Barbato E. et al.; ESC Scientific Document Group. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. 2021; 42(14): 1289–367.https://dx.doi.org/10.1093/eurheartj/ehaa575.


7. Кобалава Ж.Д., Конради А.О., Недогода С.В. с соавт. Артериальная гипертензия у взрослых. Клинические рекомендации 2020. Российский кардиологический журнал. 2020; 25(3): 149–218. [Kobalava Zh.D., Konradi A.O., Nedogoda S.V. et al. Arterial hypertension in adults. Clinical guidelines 2020. Rossiyskiy kardiologicheskiy zhurnal = Russian Journal of Cardiology. 2020; 25(3): 149–218 (In Russ.)]. https://dx.doi.org/10.15829/1560-4071-2020-3-3786. EDN: TCRBRB.


8. Williams B., Mancia G., Spiering W. et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. Eur Heart J. 2018; 39(33): 3021–104. https://dx.doi.org/10.1093/eurheartj/ehy339.


9. Neskovic A.N., Skinner H., Price S. et al. Focus cardiac ultrasound core curriculum and core syllabus of the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2018; 19(5): 475–81. https://dx.doi.org/10.1093/ehjci/jey006.


10. Iacobellis G. Epicardial adipose tissue in contemporary cardiology. Nat Rev Cardiol. 2022; 19(9): 593–606.https://dx.doi.org/10.1038/s41569-022-00679-9.


11. Nabati M., Saffar N., Yazdani J., Parsaee M.S. Relationship between epicardial fat measured by echocardiography and coronary atherosclerosis: A single-blind historical cohort study. Echocardiography. 2013; 30(5): 505–11. https://dx.doi.org/10.1111/echo.12083.


12. Villasante Fricke A.C., Iacobellis G. Epicardial adipose tissue: Clinical biomarker of cardio-metabolic risk. Int J Mol Sci. 2019; 20(23): 5989. https://dx.doi.org/10.3390/ijms20235989.


13. Eroglu S. How do we measure epicardial adipose tissue thickness by transthoracic echocardiography? Anatol J Cardiol. 2015; 15(5): 416–19. https://dx.doi.org/10.5152/akd.2015.5991.


14. Jeong J.W., Jeong M.H., Yun K.H. Echocardiographic epicardial fat thickness and coronary artery disease. Circ J. 2007; 71(4): 536–39. https://dx.doi.org/10.1253/circj.71.536.


15. Libby P. The changing landscape of atherosclerosis. 2021; 592(7855): 524–33. https://dx.doi.org/10.1038/s41586-021-03392-8.


16. Geovanini G.R., Libby P. Atherosclerosis and inflammation: Overview and updates. Clin Sci (Lond). 2018; 132(12): 1243–52.https://dx.doi.org/10.1042/CS20180306.


17. Ference B.A., Ginsberg H.N., Graham I. 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. https://dx.doi.org/10.1093/eurheartj/ehx144.


18. Iacobellis G. Local and systemic effects of the multifaceted epicardial adipose tissue depot. Nat Rev Endocrinol. 2015; 11(6): 363–71. https://dx.doi.org/10.1038/nrendo.2015.58.


19. Mazurek T., Zhang L., Zalewski A. et al. Human epicardial adipose tissue is a source of inflammatory. Circulation. 2003; 108(20): 2460–66. https://dx.doi.org/10.1161/01.CIR.0000099542.57313.C5.


20. Iacobellis G., Corradi D., Sharma A.M. Epicardial adipose tissue: Anatomic, biomolecular and clinical relationships with the heart. Nat Clin Pract Cardiovasc Med. 2005; 2(10): 536–43. https://dx.doi.org/10.1038/ncpcardio0319.


About the Autors


Anna V. Davydova, cardiologist at A.S. Lukashevsky Kamchatka Regional Hospital. Address: 630003, Petropavlovsk-Kamchatsky, 112 Leningradskaya Str. E-mail: anna.pustovaya@gmail.com.
ORCID: https://orcid.org/ 0000-0003-4194-6823
Viktor S. Nikiforov, MD, professor, dean of the Faculty of medicine and biology of I.I. Mechnikov North-Western State Medical University of the Ministry of Healthcare of Russia. Address: 191015, Saint Petersburg, 41 Kirochnaya Str. E-mail: viktor.nikiforov@szgmu.ru. ORCID: https://orcid.org/0000-0001-7862-0937
Yuri Sh. Khalimov, MD, professor, professor of the Department of faculty therapy with a course of endocrinology, cardiology with the clinic named after academician G.F. Lang, Academician I.P. Pavlov First Saint Petersburg State Medical University of the Ministry of Healthcare of Russia. Address: 197022, Saint Petersburg, 6/8 Lva Tolstogo Str. E-mail: yushkha@gmail.com. ORCID: https://orcid.org/0000-0002-7755-7275


Similar Articles


Бионика Медиа