PRO-INFLAMMATORY CYTOKINE LEVELS IN PATIENTS WITH HF AND COVID- 19
- Authors: Tokmachev R.E.1, Glavatskikh Y.O.1, Drobysheva V.R.1, Budnevskaya S.A.1
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Affiliations:
- Voronezh State Medical University named after N. N. Burdenko
- Issue: Vol 12 (2023): MATERIALS OF THE XIX INTERNATIONAL BURDENKOVO SCIENTIFIC CONFERENCE APRIL 20-22, 2023
- Pages: 659-661
- Section: Medicine without frontiers
- URL: https://new.vestnik-surgery.com/index.php/2415-7805/article/view/8361
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Abstract
Relevance. Since the beginning of the pandemic, the number of coronavirus infections has reached 662,221,274. These figures are largely due to the decompensation of heart failure as a result of the accession of respiratory infections and other intercurrent diseases. The main systemic effect of Covid-19 is systemic inflammation. At the same time, the underlying mechanisms are quite diverse and have not yet been sufficiently studied.
Objective. To study the level of systemic inflammation indicators (levels of circulating TNF-α, IL-1β, IL-6) in patients with chronic heart failure who have had COVID-19.
Materials and methods. The study included patients aged 40 to 70 years diagnosed with CHF of ischemic genesis hospitalized with SARS-CoV-2(n=60). The control group consisted of patients hospitalized with SARS-CoV-2, without signs of HF( n=20). All patients underwent laboratory methods with the determination of the levels of IL-1β, IL-6,TNF-α.
Results: The analysis of cytokine status indicators demonstrated an increase in the levels of pro-inflammatory cytokines in all the studied subgroups in comparison with their levels in 2021 with a stable course of CHF. At the same time, there were no significant differences in the content of IL-1β, IL-6, TNF-α in the studied groups.
Conclusion: Thus, the course of the new coronavirus infection is accompanied by an aggressive inflammatory reaction with the release of a large number of pro-inflammatory cytokines, which can be considered as potential markers of the prognosis of the course and outcomes of the disease in both patients with CHF and patients without HF.
Full Text
Relevance: The influence of various viral infections on the myocardium is an indisputable fact. Thus, viruses affect the heart, both as a result of direct viral processes and through indirect mechanisms associated with the body's immune response [1]. Analysis of the results of numerous studies leads to the conclusion that an absolute increase in the activity of viral diseases is associated with an increase in the frequency of hospitalizations for heart failure. Since the beginning of the pandemic, the number of coronavirus infections has reached 662,221,274, and the number of deaths has reached 6,701,780 [2]. These indicators are largely associated with the decompensation of heart failure as a result of the accession of respiratory infections and other intercurrent diseases. Increased levels of cardiac biomarkers during coronavirus infection reflect excess inflammation, viral load, cytokine storm, and atherothrombotic process, which can cause direct or indirect heart damage [3]. The main pathogenetic effect of Sars-CoV 2 is systemic inflammation. At the same time, the underlying mechanisms are quite diverse and have not yet been sufficiently studied [4].
Objective: To study the level of systemic inflammation indicators (levels of circulating TNF-α, IL-1β, IL-6) in patients with chronic heart failure who have had COVID-19.
Materials and methods: The study included patients aged 40 to 70 years with a diagnosis of CHF of ischemic genesis (including 33 men and 27 women, mean age 63.7±8.1 years) who underwent a full clinical and laboratory examination confirmed by a diagnosis of Covid-19, with a positive polymerase chain reaction (PCR) smear from the nasopharynx for SARS-C oV infection -2 (n=60). The control group consisted of patients with symptoms and signs associated with Covid-19 and positive polymerase chain reaction (PCR) of a nasopharyngeal swab for SARS-C infection about V-2 patients, without symptoms and signs of HF in the anamnesis (n = 20). All patients gave verbalvoluntary informed consent to participate in the study. All clinical procedures and treatment were carried out in accordance with the current recommendations for the treatment of patients with a new coronavirus infection, as well as in accordance with the current recommendations of the Ministry of Health of Russia for the diagnosis and treatment of CHF (2020).
Clinical-instrumental and laboratory examination was performed on all patients included in the study: group 1 (60 patients with CHF and various LV EF during their hospitalization for novel coronavirus infection), group 2 (control group - 20 hospitalized with symptoms and signs associated with Covid-19 and positive polymerase chain reaction (PCR) nasopharyngeal swab for SARS-C infection about V -2 patients, without symptoms and signs of HF in the anamnesis).
The study did not include patients with bronchopulmonary diseases, chronic kidney disease (stage 3b and above), diabetes mellitus, persistent atrial fibrillation, anemia, diseases of the musculoskeletal system, obesity (2-3 degrees), oncological diseases, with an established diagnosis of chronic pulmonary heart.
All patients with CHF included in the study were observed by us since 2020, and during the entire time of observation of them after discharge from the hospital (hospitalization for Covid-19), they had the opportunity to contact a cardiologist. Within six months, 8 people (6 people with CHF and 2 people with no history of symptoms and signs of HF) dropped out of the study due to the onset of one of the endpoints (death). Laboratory tests were carried out. Laboratory tests were carried out methods: general clinical and enzyme immunoassays of blood with determination of the levelof IL-1β, IL-6, TNF-α.
Statistical analysis was carried out using the Statistica 12 software package. The normality of the data distribution was assessed using a test (Shapira-Wilke). The initial continuous variables were presented as a standard mean deviation and compared using the Student t-criterion, in the form of a median and interquartile range, and compared using the Mann-Whitney and Kruskal-Wallis tests. Categorical ones were compared using the exact the Fisher method. Differences between subgroups were considered statistically significant at a significance level of p<0.05.
Results: The analysis of cytokine status indicators demonstrated an increase in the levels of pro-inflammatory cytokines in all the studied subgroups in comparison with their levels in 2021 with a stable course of CHF. At the same time, there were no significant differences in the content of IL-1β, IL-6, TNF-α in the study groups (in group 1 in 2021). IL-1β 25.4 ± 6.20, in 2022 in this group with Covid-19 - 235.7 ± 48.6; in the control group, the level of IL-1β was 228.8±40.1; in group 1 in 2021 IL-6 40.2 ± 1 4.3 0, in 2022 in this group with Covid-19 - 115.0 ± 40.5; in the control group, the level of IL-6 was 113.1 ± 42.2;The level of TNF-α in group 1 in 2021 was 36.4 ± 14.81, in 2022 in this group with Covid-19 - 192.3 ± 53.4; in the control group, the level The TNF-α was 187.9±46.3).
Discussion: An increase in the level of IL-1β, IL-6, TNF-α at the time of hospitalization of patients for Covid-19 compared with the results of cytokine analysis in these patients in 2021 with a stable course of CHF, on the one hand, may reflect one of the pathophysiological mechanisms of myocardial damage as a result of increased systemic inflammation, which in turn leads to the progression and decompensation of HF, on the other hand [5] . Systemic inflammation leads to activation of ASC, an increase in heart rate with a short period of increased contractility and vasoconstriction through hyperactivation of RAAS [6]. This leads to cardiotoxic effects with induction of cardiomyocyte apoptosis and focal necrosis of the myocardium, which undoubtedly can also be attributed to the mechanisms of progression of heart failure.
Conclusion: Thus, the new coronavirus infection is accompanied by an aggressive inflammatory response with the release of large amounts of pro-inflammatory cytokines, which can be considered as potential markers of the prognosis of the course and outcomes of the disease, both in patients with and without HF.
About the authors
Roman E. Tokmachev
Voronezh State Medical University named after N. N. Burdenko
Email: r-tokmachev@mail.ru
ORCID iD: 0000-0001-6379-4635
SPIN-code: 5922-6679
Russian Federation, 10 Studentskaya str., Voronezh, 394036, Russia
Yuliya O. Glavatskikh
Voronezh State Medical University named after N. N. Burdenko
Email: Yuliyag36@gmail.com
ORCID iD: 0000-0002-2398-5987
SPIN-code: 9762-6156
Russian Federation, 10 Studentskaya str., Voronezh, 394036, Russia
Valeria R. Drobysheva
Voronezh State Medical University named after N. N. Burdenko
Email: drobyshevavr@gmail.com
ORCID iD: 0000-0003-0563-5286
SPIN-code: 1262-6060
Russian Federation, 10 Studentskaya str., Voronezh, 394036, Russia
Sofia A. Budnevskaya
Voronezh State Medical University named after N. N. Burdenko
Author for correspondence.
Email: yuliyag36@gmail.com
ORCID iD: 0000-0001-6636-6644
Russian Federation, 10 Studentskaya str., Voronezh, 394036, Russia
References
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- Tokmachev R, Kravchenko A, Budnevsky A et al. Features of the functional status and cytokine profile of patients with chronic heart failure in combination with chronic obstructive pulmonary disease. International Journal of Biomedicine. 2021;11(1):9–13.
- Tokmachev R.E., Kravchenko A.Y., Budnevsky A.V. et al. POTENTIAL BIOMARKERS FOR HEART FAILURE DIAGNOSTICS AND MANAGEMENT. Pakistan Journal of Medical and Health Sciences. 2021. Т. 14. № 4. С. 1813-1816.
- Tokmachev R.E., Kravchenko A.Ya., Budnevsky A.V. et al. SST2 PROTEIN SERUM LEVELS IN PATIENTS WITH CHRONIC HEART FAILURE International Journal of Biomedicine. 2020. Т. 10. № 4. С. 342-346.
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