Serkova V. K., Lilevskaya A. A., Romanova V. A.

CLINICAL AND EXPERIMENTAL MEDICINE

Scentific article

A number of studies have established that the leading cause of mortality in patients with chronic obstructive pulmonary disease (COPD) is not respiratory failure, but cardiovascular events, including coronary artery disease (CAD). A significant role in the development of coronary atherosclerosis, as the morphological basis of CAD, is played by dyslipoproteinemia (DLP). However, it is quite common for patients with coronary artery disease to have normal lipid profile. It has been shown that even after reaching the target level cholesterol of low density lipoprotein, there remains a significant risk for which other less studied factors, in particular, lipoprotein (a) – LP (a), may be responsible. Although the role of DLP in the development of coronary artery disease is quite a lot of research, works on the study of blood lipid composition in patients with combined cardiorespiratory pathology are rare and ambiguous. Aim of the research: to evaluate the significance of various parameters of blood lipid composition, as a criterion for the development of coronary atherosclerosis and coronary artery disease in patients with COPD. The object and methods of research. 87 patients with COPD were examined, including 48 patients with COPD combined with stable coronary artery disease, and 28 patients with stable coronary artery disease. The study complied with the requirements for clinical trials by the Helsinki Declaration of Human Rights. The verification of the diagnosis of COPD was carried out on the basis of the recommendations of WHO experts – GOLD-2018, the diagnosis of stable coronary artery disease was established in accordance with the European recommendations of 2013. The control group consisted of 30 individuals with no signs of cardiorespiratory pathology. Lipidograms and the level of LP (a) (ELISA) were determined in all examined patients. Statistical processing of the results was performed using the «Statistica» v. 10.0. and Microsoft Office Excel 2010. The results of the study and their discussion. In the group of patients with COPD without CHD, only a moderate increase in the atherogenic index (AI) was observed; the level of LP (a) did not differ from the reference values (p> 0.05). In patients with coronary artery disease and with comorbid pathology, along with a significant increase in IA, there was a decrease in the level of cholesterol high density lipoprotein. The level of LP (a) was significantly increased both in the group of patients with CHD and in its combination with COPD. In patients with COPD without coronary artery disease, moderately proatherogenic changes in lipidogram parameters increased with an increase in the degree of pulmonary ventilation disorder. When combined with COPD and IHD, the effect of the degree of impaired pulmonary ventilation on lipid profile and LP (a) was less pronounced. Conclusion. Analysis of changes in blood lipids indicates the possibility of using more than 3.51 units of AI as predictors of the development of coronary atherosclerosis in patients with COPD and the Lp (a) level is more than 18 mg/dl. With a stable course of coronary artery disease, both in the group with monopathology and in combination with COPD, an elevated level of LP (a) is associated with more severe forms of CHD – III functional class. Increasing the level of LP (a) has the greatest prognostic value for patients with comorbid cardiorespiratory pathology, indicating a hereditary predisposition to early development of atherosclerosis. Introduction to clinical practice of determining the level of LP (a) in the serum of patients with COPD will contribute not only to early diagnosis of coronary artery disease in this group of patients, but also timely treatment and preventive measures aimed at preventing the development and progression of atherosclerosis and atherothrombotic complications.

blood lipids, lipoprotein (a), coronary atherosclerosis, coronary heart disease, COPD, cardiorespiratory comorbidity

1. Oganov RG, Maslennikova GYa. Dostizheniya i neudachi v profilaktike serdechno-sosudistyih zabolevaniy. Kardiovaskulyarnaya terapiya i profilaktika. 2014;13(1):4-7. [in Russian].
2. Chuchalin AG, Aysanov ZR, Avdeev SN, Belevskiy AS, Leschenko IV, Mescheryakova NN, i dr. Federalnyie klinicheskie rekomendatsii po diagnostike i lecheniyu hronicheskoy obstruktivnoy bolezni legkih. Pulmonologiya. 2014;3:15-36. [in Russian].
3. Nichols M, Townsend N, Scarborough P, Rayner M. Cardiovascular disease in Europe 2014: epidemiological update. European Heart Journal. 2014;35(42):2950-9.
4. Roth GA, Forouzanfar MH, Moran AE, Barber R, Nguyen G, Feigin VL, et al. Demographic and Epidemiologic Drivers of Global Cardiovascular Mortality. New England Journal of Medicine. 2015;372(14):1333-41.
5. Naumova LA, Osipova ON. Komorbidnost: mehanizmyi patogeneza, klinicheskoe znachenie. Sovremennyie problemyi nauki i obrazovaniya. 2016;5. [in Russian].
6. Budnevskiy AV, Malyish EYu. Hronicheskaya obstruktivnaya bolezn legkih kak faktor riska razvitiya serdechno-sosudistyih zabolevaniy. Kardiovaskulyarnaya terapiya i profilaktika. 2016;15(3):69-73. [in Russian].
7.  Gubkina VA, Trofimov VI, Tsvetkova LN, Pogoda TE, Mumortsev YuI, Suntsov DA. Hronicheskaya obstruktivnaya bolezn legkih i hronicheskaya serdechnaya nedostatochnost u pozhilyih. Uchenyie zapiski SPbGMU im IP Pavlova. 2016;26(2):11-5. [in Russian].
8. Grigoreva NYu, Mayorova MV, Korolyova ME, Samolyuk MO. Osobennosti formirovaniya i razvitiya serdechno-sosudistyih zabolevaniy u bolnyih hronicheskoy obstruktivnoy boleznyu legkih. Terapevticheskiy arhiv. 2019;91(1):16-47. [in Russian].
9. Cooney M, Dudina A, Bacquer D, Wilhelmsen L, Sans S, Menotti A, et al. HDL cholesterol protects against cardiovascular disease in both genders, at all ages and at all levels of risk. Atherosclerosis. 2009;206(2):611-6.
10. Cholesterol Treatment Trialists’ (CTT) Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170 000 participants in 26 randomised trials. The Lancet. 2010;376(9753):1670-81.
11. Catapano AL, Graham I, Backer GD, Wiklund O, Chapman MJ, Drexel H, et al. 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. European Heart Journal. 2016;37(39):2999-3058.
12. Malaguarnera M, Vacante M, Russo C, Malaguarnera G, Antic T, Malaguarnera L, et al. Lipoprotein (a) in Cardiovascular Diseases. BioMed Research International. 2013;2013:1-9.
13. Nordestgaard BG, Chapman MJ, Ray K, Borén J, Andreotti F, Watts GF, et al. Lipoprotein (a) as a cardiovascular risk factor: current status. European Heart Journal. 2010;31(23):2844-53.
14. Cai A, Li L, Zhang Y, Mo Y, Mai W, Zhou Y. Lipoprotein (a): A Promising Marker for Residual Cardiovascular Risk Assessment. Disease Markers. 2013;35:551-9.
15. Vestbo J, Hurd SS, Agustí AG, Jones PW, Vogelmeier C, Anzueto A, et al. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. American Journal of Respiratory and Critical Care Medicine. 2018;187(4):347-65.
16.  2013 ESC guidelines on the management of stable coronary artery disease. European Heart Journal. 2013;34(38):2949-3003.
17. Tseluyko VI, Mischuk NE. Klinicheskoe i prognosticheskoe znachenie lipoproteina (a). Liki Ukrayini. 2015;1(186):32-8. [in Ukrainian].

«Bulletin of problems biology and medicine» Issue 2 Part 1 (150), 2019 year, 196-199 pages, index UDK 616.24:616.13-004.6:577.115:612.1

10.29254/2077-4214-2019-2-1-150-196-199