SST2 LEVELS IN COVID-19 AND HF PATIENTS

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Relevance: It is known that many 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 the absolute increase in the activity of viral diseases by 5 - 7% is directly related to an increase in the frequency of hospitalizations for heart failure by 24% or more. 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].

Objective: To study sST2 levels in patients with chronic heart failure and  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-CoV -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-CoV-2 patients, without symptoms and signs of HF in the anamnesis (n = 20).  All patients gave verbal voluntary 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-CoV -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-linked immunosorbent blood tests with determination of the level of sST2.

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: During the research, the level of the protein sST2 was determined. So in the second group of patients without symptoms and signs of  CHF, the level of this biomarker was statistically significantly less - 22.97±4.3 4 ng / ml (16.4; 30.2) (p<0.0001) compared with gr. 1 34.47± 11.48 ng /ml. It is worth noting that the level  of sST2 in patients with CHF increased with an increase in FC CHF: I FC (23.7 8±5.21), II FC (3 3.91±7.49), III FC (43.02±14, 07). A higher level of sST2 in patients with CHF with an increase in FC may reflect more pronounced processes of hypertrophy and remodeling of the myocardium and evidence that the induction of sST2 is caused by mechanical overload of cardiomyocytes. Accordingly, an increase in the level of this biomarker may reflect myocardial stress, processes changes in the architectonics of the heart in the development of CHF and fibrosis.  sST2 to

Also, the ratio of the chances of a favorable course of CHF and Covid-19 or death depending on the level of sST2 (threshold value ˃35 n g / ml) was studied.  The resulting OR was 8.14 [95% CI 1.80952; 36.6429]. Therefore, patients with an sST2 below the threshold level were 8.1 4 times lower than patients with a sST2 level of 2˃35 ng/mL.

Discussion: An increase in sST2 levels in CHF patients after covid-19 may indicate an intensification of  the myocardial remodeling process. The data obtained in the study are consistent with the scientific hypothesis of an increase in sST2 production in mechanically overloaded cardiomyocytes, reflecting myocardial stress, remodeling ventricular ingress and fibrosis [4, 5].

Conclusion: Thresholds  for cardiac  biomarker a (sST2) for stratification and isolation of risk groups among patients with Covid-19, CHF and Covid-19 have been determined. In patients with Covid-19 and CHF, a strong association has been found between high levels of cardiac  biomarker (sSt2) and a negative short-term prognosis (ICU transfer/death).  The analysis of sST2 levels allows us to draw conclusions about the prospects of its introduction in the diagnosis and prognosis of the course  in patients with CHF, as a biomarker of myocardial stress, ventricular remodeling and fibrosis.

About the authors

Yuliya O. Glavatskikh

Voronezh State Medical University named after N. N. Burdenko

Author for correspondence.
Email: Yuliyag36@gmail.com
ORCID iD: 0000-0002-2398-5987
SPIN-code: 9762-6156
Russian Federation, 10 Studentskaya str., Voronezh, 394036, Russia

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

Sofia A. Budnevskaya

Voronezh State Medical University named after N. N. Burdenko

Email: yuliyag36@gmail.com
ORCID iD: 0000-0003-3649-5642
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: 0000-0001-6636-6644
SPIN-code: 1262-6060
Russian Federation, 10 Studentskaya str., Voronezh, 394036, Russia

Tatiana A. Chernik

Voronezh State Medical University named after N. N. Burdenko

Email: t.a.chernik@vrngmu.ru
ORCID iD: 0000-0003-1371-0848
SPIN-code: 8102-8569
Russian Federation, 10 Studentskaya str., Voronezh, 394036, Russia

References