Kazakov Yu. M., Chekalina N. I., Mamontova T. V., Vesnina L. E., Nakaznenko N. V., Kocur G. V.

CLINICAL AND EXPERIMENTAL MEDICINE

Scentific article

The urgency of the problem is in the progressive increase in the incidence of CHD in Ukraine and around the world, the effect of AIT on the course of coronary heart disease in combination of the specified pathology, which requires a detailed study of the pathogenetic mechanisms of CHD development under conditions of autoimmune inflammation and the search for new effective methods of diagnosis and treatment. Recognition of the leading role of chronic systemic inflammation in the pathogenesis of both pathological conditions allowed to conduct the scientific research in this direction. Purpose: to study and compare the indices of systemic inflammation and central hemodynamics in patients with stable coronary heart disease (CHD) and in conditions of its combination with autoimmune thyroiditis (AIT). Object and methods. In a single-stage open clinical study, 230 patients with IHD took part: stable angina pectoris, II FC, CH-0, and 50 patients with stable ischemic heart disease in combination with AIT in the stage of euthyroidism. Patients underwent laboratory studies to determine the levels of pro- and anti-inflammatory cytokines (interleukin 1β, interleukin 10 and tumor necrosis factor alpha in the blood and Echocardiography to detect violations of central hemodynamics. Results. The study showed an increased in the level of proinflammatory cytokines with a moderate predominance in patients with the combination of IHD with AIT – more high level of tumor necrosis factor alpha in the blood, a negative effect of the inflammation on the systolic and diastolic functions of the left ventricle, with a predominance of diastolic dysfunction in patients with IHD in combination with AIT. When comparing the data of patients with stable IHD and IHD in combination with AIT, differences were noted with respect to the time of early diastolic filling of left ventricular (DT), which was significantly higher in patients with AIT (p <0,05), as well as in the phase of early diastolic filling of left ventricular, the maximum rate of which (E) in patients with AIT was significantly lower (p <0,05). The prevalence of severity of violations of the diastolic function of the left ventricle in patients with AIT may indicate significant changes in the myocardium under the conditions of the autoimmune process, as well as a greater degree of inflammatory activation of the endothelium with a violation of endothelial-dependent functions under chronic inflammatory conditions. Conclusions. The results obtained define chronic systemic inflammation as a leading factor in the development and progression of IHD in combination with AIT and an important target for the development of pathogenetically valid approaches to treatment in conditions of comorbidity.

ischemic heart disease, autoimmune thyroiditis, chronic systemic inflammation, central hemodynamics

1. Montalescot G, Sechtem U, Achenbach S, Andreotti F, Arden C, Budaj A, et al. 2013 ESC guidelines on the management of stable coronary artery disease. Eur Heart J. 2013;34:2949-3003.
2. Kovalenko VM, Kornatsky VM. Stres i hvoroby sistemy krovoobigu. Kiev: SI NSC Institute of Cardiology named after Acad. MD Strazhesko; 2015. 354 s. [in Ukrainian].
3. Vanderpump MPJ. The epidemiology of thyroid disease. Br Med Bull. 2011;99(1):39-51.
4. Karachentsov YU. Chotirnadtsyatі Danilevskі chitannya. Materiali konferentsiyi z mizhnarodnoyu uchastyu: dosyagnennya ta perspektivi eksperimentalnoyi ta klinichnoyi endokrinologiyi. Kharkiv 2015;104-72. [in Ukrainian].
5. Churilov LP, Stroev YuI. K stoletiyu dvuh velikih vzaimosvyazannyih patofiziologicheskih otkryitiy. Tavricheskiy mediko-biologicheskiy vestnik. 2012;15(3,ch.2):276-81. [in Russiаn].
6. Brunetti ND, Correale M, Pellegrino PL, Munno I, Cuculo A, De Gennaro L, et al. Early inflammatory cytokine response: A direct comparison between spontaneous coronary plaque destabilization vs angioplasty induced. Atherosclerosis. 2014 Oct;236(2):456-60.
7. Ganesh BB, Bhattacharya P, Gopisetty A, Prabhakar BS. Role of cytokines in the pathogenesis and suppression of thyroid autoimmunity. J Interferon Cytokine Res. 2011;31(10):721-31.
8. Egorov AM, Osipov AP, Dzantiyev BB, Gavrilova EM. Teorija i praktika immunofermentnogo analіza. Moscow: The higher school; 1991. 288 s. [in Russiаn].
9. Evangelista A, Flachskampf F, Lancellotti P, BadanoRio L, Aguilar R, Monaghan AM, et al. European Association of Echocardiography recommendations for standardization of performance, digital storage and reporting of echocardiographic studies. Eur J Echocardiogr. 2008;9:438-48.
10. Petri A, Sabine K. Nagljadnaja medicinskaja statistika. Moscow: GEOTAR-MED; 2010. s. 43-68. [in Russiаn].
11. Monaco C, Andreakos E, Kiriakidis S, Mauri C, Bicknell C, Foxwell B, et al. Canonical pathway of nuclear factor kappa B activation selectively regulates proinflammatory and prothrombotic responses in human atherosclerosis. Proc. Natl. Acad. Sci. 2004;101(15):5634-9.
12. Mazziotti G, Sorvillo F, Naclerio C, Farzati A, Cioffi M, Perna R, et al. Type-1 response in peripheral CD4+ and CD8+ T cells from patients with Hashimoto’s thyroiditis. Eur J of Endocrinol. 2003;148(4):383-8.
13. Kaidashev IP. Aktivaciya yadernogo faktora kB kak molekulyarnoj osnovy patogeneza metabolicheskogo syndroma. Pathol Physiol and Experim Ther. 2013;(3):65-72. [in Russiаn].
14. Tousoulis D, Oikonomou E, Economou EK, Crea F, Kaski JC. Inflammatory cytokines in atherosclerosis: current therapeutic approaches. Eur Heart J. 2016 Jun 7;37(22):1723-32.
15. Groux H, Cottrez FJ. The complex role of interleukin-10 in autoimmunity. Autoimmunity. 2003;20(4):281-5.
16. Karin M. The regulation of AP-1 activity by mitogen-activated protein kinases. J Biol Chem. 1995 Jul;270(28):16483-6.
17. Urazova OI, Kravets EB, Novitskiy VV, Rogaleva AV, Budkina TE, Sinyukova OA, i dr. Apoptoz limfotsitov krovi u bolnyih autoimmunnyimi tireopatiyami. Med immunol. 2008;10(2-3):187-92. [in Russiаn].
18. Сopie X, Hnatkova К, Staunton A, Fei L, Camm J, Malik M. Comparison of the predictiv power of increased heart rate wich that of depressed left ventricular ejection fraction and heart rate variability for risk stratification after myocardial infarction results of a 2-year follow-up study. Am Coll Cardiol. 1996;27:270-6.
19. Hallstrem A, Pratt CM, Greene HL, Huther M, Gottlieb S, DeMaria A, et al. Relationship between heart failure, ejection fraction, arrhythmia suppression and mortality: analysis of the cardiac arrhythmia suppression trial. JACC. 1995;13(1):1250-7.
20. Bagmat LF, Nikonova VV, Nelina IN. Vzaimosvyaz’ mezhdu faktorami sistemnogo vospaleniya i tipami diastolicheskoj disfunkcii u podrostkov s patologiej miokarda. Mezhdunar Zhurn Pediatr Akush i ginek. 2015;8(1):15. [in Russiаn].
21. Chervonopis’ka OM. Dіagnostika sercevoi nedostatnostі ta suchasna koncepcіya remodelyuvannya lіvogo shlunochka: rol’ ul’trazvukovogo doslіdzhennya sercya. Ukr. kardіol. zhurn. 2007;2:92-9. [in Ukrainian].
22. Vatutin NT, Kalinkin NV, Eshchenko EV, Kravchenko IN. Reperfuzionnoe povrezhdenie mіokarda. Kardіohі ta Іntervenc Kardіol. 2013;1:15-22. [in Russiаn].
23. Gavras H, Brunner HR. Role of angiotensin and its inhibition in hypertension, ischemic heart disease, and heart failure. Hypertension. 2001;37:342-5.
24. Galenko-Iaroshevsky PA, Sukoyan GV, Ionov DI, Zelenskaya AV, Khvitia NG. Possibility of inhibition of TNF-α/NF-kB signalling pathway activation in myocardium and reverse cardiac hemodynamics in chronic ischemic heart disease. J Clin Exp Pathol. 2017;7(3). Available from: https://pdfs. semanticscholar.org/…/35c55e030206f280ef385 DOI: 10.4172/2161-0681.1000310 25. Frangogiannis NG. The inflammatory response in myocardial injury, repair and remodelin. Nat Rev Cardiol. 2014;11(5):255-65.
25. Chekalіna NІ. Pokazniki endotelіal’noі disfunkcіі u hvorih na autoіmunnij tireoіdit u spoluchennі z іshemіchnoyu hvoroboyu sercya. Zhurn Klіn ta Eksperim Med Doslіd. 2016;4(2):293-302. [in Ukrainian].

«Bulletin of problems biology and medicine» Issue 3 (145), 2018 year, 113-118 pages, index UDK 616.12-008.46+616.441-002.2

10.29254/2077-4214-2018-3-1-145-113-118