The course of chronic heart failure in patients after COVID-19 against the background of active cytomegalovirus infection

Abstract

Background. A new coronavirus infection may be complicated in the post-COVID period by the development of adverse cardiovascular events associated with chronic heart failure.

Aim. To study the features of the course of chronic heart failure in patients after COVID-19 infection against the background of active cytomegalovirus infection.

Material and methods. The study included 102 patients with chronic heart failure with reduced and intermediate left ventricular ejection fractions, who underwent COVID-19 in mild and moderate forms. The control group consisted of 61 patients with chronic heart failure and no COVID-19. Within 6 months after the infection with COVID-19, the features of the course of chronic heart failure were assessed. Quantitative determination of deoxyribonucleic acid (DNA) of cytomegalovirus in blood plasma was carried out by polymerase chain reaction. To assess the risk of adverse events, the odds ratio (OR) with a 95% confidence interval (95% CI) was calculated. Quantitative data were presented as median and interquartile range (25th and 75th percentiles).

Results. After coronavirus infection, the risk of an unfavorable course of chronic heart failure (OR=6.237; 95% CI=2.911–13.362; p=0.001), hospitalization due to decompensation of chronic heart failure (OR=5.9; 95% CI=1.313–26.504; p=0.033), an increase in the functional class of heart failure by 1 class or more (OR=4.19; 95% CI=1.636–10.736; p=0.009), development of atrial fibrillation paroxysms (OR=3.832; 95% CI=1.385–10.599, p=0.014), significantly increased. The number of copies of cytomegalovirus DNA in patients who underwent COVID-19 was significantly higher in the group of patients with an unfavorable course of chronic heart failure compared to the same group, in which patients did not tolerate COVID-19 — 2238.5 (1888.5; 2647.5) and 1411.5 (1112.5; 1684.5) copies/ml, respectively (p <0.001).

Conclusion. Patients with chronic heart failure after 6 months of COVID-19 infection are at high risk of developing adverse cardiovascular events against the background of active cytomegalovirus infection.

Keywords

COVID-19 / cytomegalovirus / herpes virus / heart failure / prognosis

References

[1] Tufan A, Avanoğlu Güler A, Matucci-Cerinic M. COVID-19, immune system response, hyperinflammation and repurposing antirheumatic drugs. Turk J Med Sci. 2020;50(SI-1):620–632. DOI: 10.3906/sag-2004-168.

[2] Arutyunov AG, Seferovic P, Bakulin IG, Bakulina NV, Batyushin MM, Boldina MV, Krstacic G, Macut D, Salukhov VV, Shimosawa T, Shustov VV, Tarlovskaya EI, Vrtovec B, Wanner C, Aisanov ZR, Arutyunov GP, Avdeev SN, Babin AP, Cattaneo M, Chesnikova AI, Ezhov MV, Kamilova UK, Koziolova NA, Lopatin YuM, Mitkovskaya NP, Morais J, Galstyan GR, Sarybaev ASh, Sugraliev AB, Yavelov IS, Essaian AM, Zolotovskaya IA, Zhangelova ShB, Zyryanov SK, Melnikov ES, Bashkinov RA, Shlyakhto EV. Rehabilitation after COVID-19. Resolution of the International Expert Council of the Eurasian Association of Therapists and the Russian Society of Cardiology. Russian Journal of Cardiology. 2021;26(9):4694. (In Russ.) DOI: 10.15829/1560-4071-2021-4694.

[3] Арутюнов А.Г., Сеферович П., Бакулин И.Г., Бакулина Н.В., Батюшин М.М., Болдина М.В., Кршташич Г., Мацут Дж., Салухов В.В., Шимосава Т., Шустов В.В., Тарловская Е.И., Вртовец Б., Ваннер К., Айсанов З.Р., Арутюнов Г.П., Авдеев С.Н., Бабин А.П., Каттанео М., Чесникова А.И., Ежов М.В., Камилова У.К., Козиолова Н.А., Лопатин Ю.М., Митьковская Н.П., Мораис Ж., Галстян Г.Р., Сарыбаев А.Ш., Сугралиев А.Б., Явелов И.С., Есаян А.М., Золотовская И.А., Жангелова Ш.Б., Зырянов С.К., Мельников Е.С., Башкинов Р.А., Шляхто Е.В. Реабилитация после COVID-19. Резолюция Международного совета экспертов Евразийской ассоциации терапевтов и Российского кардиологического общества. Российский кардиологический журнал. 2021;26(9):4694. DOI: 10.15829/1560-4071-2021-4694.

[4] Al-Aly Z, Xie Y, Bowe B. High-dimensional characterization of post-acute sequelae of COVID-19. Nature. 2021;594:259–264. DOI: 10.1038/s41586-021-03553-9.

[5] Ayoubkhani D, Khunti K, Nafilyan V, Maddox T, Humberstone B, Diamond I, Banerjee A. Post-COVID syndrome in individuals admitted to hospital with COVID-19: Retrospective cohort study. BMJ. 31;372:n693. DOI: 10.1136/bmj.n693.

[6] Jeong SJ, Ku NS, Han SH, Choi JY, Kim CO, Song YG, Kim JM. Anti-cytomegalovirus antibody levels are associated with carotid atherosclerosis and inflammatory cytokine production in elderly Koreans. Clin Chim Acta. 2015;445:65–69. DOI: 10.1016/j.cca.2015.03.015.

[7] Kim HW, de Chantemèle EB, Weintraub NL. Perivascular adipocytes in vascular disease. Arterioscler Thromb Vasc Biol. 2019;39:2220–2227. DOI: 10.1161/ATVBAHA.119.312304.

[8] Kytömaa S, Hegde S, Claggett B, Udell JA, Rosamond W, Temte J, Nichol K, Wright JD, Solomon SD, Vardeny O. Association of influenza-like illness activity with hospitalizations for heart failure: The atherosclerosis risk in communities study. JAMA Cardiol. 2019;4(4):363–369. DOI: 10.1001/jamacardio.2019.0549.

[9] Chatrath N, Kaza N, Pabari PA, Fox K, Mayet J, Barton C, Cole GD, Plymen CM. The effect of concomitant COVID-19 infection on outcomes in patients hospitalized with heart failure. ESC Heart Fail. 2020;7(6):4443–4447. DOI: 10.1002/ehf2.13059.

[10] Lechner-Scott J, Levy M, Hawkes C, Yeh A, Giovannoni G. Long COVID or post COVID-19 syndrome. Mult Scler Relat Disord. 2021;55:103268. DOI: 10.1016/j.msard.2021.103268.

[11] Bieber S, Kraechan A, Hellmuth JC, Muenchhoff M, Scherer C, Schroeder I, Irlbeck M, Kaeaeb S, Massberg S, Hausleiter J, Grabmaier U, Orban M, Weckbach LT. Left and right ventricular dysfunction in patients with COVID-19--associated myocardial injury. Infection. 2021;49(3):491–500. DOI: 10.1007/s15010-020-01572-8.

[12] Fox SE, Vander Heide RS. COVID-19: the heart of the matter-pathological changes and a proposed mechanism. J Cardiovasc Pharmacol Ther. 2021;26:217–224. DOI: 10.1177/1074248421995356.

[13] Vrints CJM, Krychtiuk KA, Van Craenenbroeck EM, Segers VF, Price S, Heidbuchel H. Endothelialitis plays a central role in the pathophysiology of severe COVID-19 and its cardiovascular complications. Acta Cardiol. 2021;76:109–124. DOI: 10.1080/00015385.2020.1846921.

[14] Robinson FA, Mihealsick RP, Wagener BM, Hanna P, Poston MD, Efimov IR, Shivkumar K, Hoover DB. Role of angiotensin-converting enzyme 2 and pericytes in cardiac complications of COVID-19 infection. Am J Physiol Heart Circ Physiol. 2020;319:H1059–H1068. DOI: 10.1152/ajpheart.00681.2020.

[15] Speir E, Modali R, Huang ES, Leon MB, Shawl F, Finkel T, Epstein SE. Potential role of human cytomegalovirus and p53 interaction in coronary restenosis. Science. 1994;265:391–394. DOI: 10.1126/science.8023160.

[16] Rey JR, Caro-Codón J, Rosillo SO, Iniesta ÁM, Castrejón-Castrejón S, Marco-Clement I, Martín-Polo L, Merino-Argos C, Rodríguez-Sotelo L, García-Veas JM, Martínez-Marín LA, Martínez-Cossiani M, Buño A, Gonzalez-Valle L, Herrero A, López-Sendón JL, Merino JL Heart failure in COVID-19 patients: Prevalence, incidence and prognostic implications. Eur J Heart Fail. 2020;22:2205–2215. DOI: 10.1002/ejhf.1990.

RIGHTS & PERMISSIONS

Eco-Vector