[The impact of BMI on the course of the acute SARS-COV-2 infection and the risks that emerge during the first year after the hospital discharge. Subanalysis evidence of the AKTIV and AKTIV 2 registries].

BACKGROUND: There is enough evidence of the negative impact of excess weight on the formation and progression of res piratory pathology. Given the continuing SARS-CoV-2 pandemic, it is relevant to determine the relationship between body mass index (BMI) and the clinical features of the novel coronavirus infection (NCI). AIM: To study the effect of BMI on the course of the acute SARS-COV-2 infection and the post-covid period. MATERIALS AND METHODS: AKTIV and AKTIV 2 are multicenter non-interventional real-world registers. The АКТИВ registry (n=6396) includes non-overlapping outpatient and inpatient arms with 6 visits in each. The АКТИВ 2 registry (n=2968) collected  the  data  of  hospitalized  patients  and  included  3  visits.  All  subjects  were  divided  into  3  groups:  not  overweight  (n=2139), overweight (n=2931) and obese (n=2666). RESULTS: A higher BMI was significantly associated with a more severe course of the infection in the form of acute kidney injury (p=0.018), cytokine storm (p<0.001), serum C-reactive protein over 100 mg/l (p<0.001), and the need for targeted therapy (p<0.001) in the hospitalized patients. Obesity increased the odds of myocarditis by 1,84 times (95% confidence interval [CI]: 1,13-3,00) and the need for anticytokine therapy by 1,7 times (95% CI: 1,30-2,30).The  patients  with  the  1st  and  2nd  degree  obesity,  undergoing  the  inpatient  treatment,  tended  to  have  a  higher  probability  of  a  mortality  rate.  While  in  case  of  morbid  obesity  patients  this  tendency  is  the  most  significant  (odds  ratio  -  1,78; 95% CI: 1,13-2,70). At the same time, the patients whose chronical diseases first appeared after the convalescence period, and those who had certain complaints missing before SARS-CoV-2 infection, more often had BMI of more than 30 kg/m2 (p<0,001).Additionally, the odds of death increased by 2,23 times (95% CI: 1,05-4,72) within 3 months after recovery in obese people over the age of 60 yearsCONCLUSION.  Overweight  and/or  obesity  is  a  significant  risk  factor  for severe  course  of  the  new  coronavirus  infection  and  the associated cardiovascular and kidney damage Overweight people and patients with the 1st and 2nd degree obesity tend to have a high risk of death of SARS-CoV-2 infection in both acute and post-covid periods. On top of that, in case of morbid obesity patients this tendency is statistically significant. Normalization of body weight is a strategic objective of modern medicine and can contribute to prevention of respiratory conditions, severe course and complications of the new coronavirus infection.

CLINICAL AND MORPHOLOGICAL FEATURES OF KIDNEY DAMAGE IN PATIENTS WITH ARTERIAL HYPERTENSION DIED OF SARSCOV- 2 INFECTION

Objective: To assess clinical and pathomorphological features of kidney damage in patients with arterial hypertension (AH) who died of the new coronavirus infection COVID-19. Design and method: A complex analysis of 268 kidney autopsies was carried out, including the study of macro- and microscopic changes reflected in the protocols of pathological and anatomical autopsies and identified during the histological examination. In 224 patients (83.6%) with AH, the diagnosis was confirmed by isolating the SARS-CoV-2 RNA using the polymerase chain reaction;in 44 (16.4%) - through computed tomography of the lungs. The causes of deaths were the following: in 31 patients (11.6%) acute myocardial infarction;in 40 (14.9%) cerebrovascular accident;in 11 (4.1%) pulmonary embolism;222 patients (83%) had acute respiratory distress syndrome. The analysis included 130 men aged 36 to 92 (72.6 years old on average) and 138 women aged 40 to 106 (77.1 years old on average). Results: In the kidneys we detected ischemic changes caused by disturbances in the microvasculature. These are stases, sludges, erythrocyte and fibrin thrombi predominantly in the medulla. In the glomeruli diapedesis hemorrhages, mesangial cells proliferation, basement membrane thickening and fibrinoid necrosis of the capillary wall were observed. In the epithelium of the convoluted tubules, a granular, hyaline-drop dystrophy and a necrosis as the extreme degree of the damage were noted. In the kidneys, a pronounced lymphoid and leukocyte infiltration was detected. These changes were accompanied by inflammation and renal failure symptoms. In particular, the level of C-reactive protein was 140.6 ± 7.42 mg/l;blood ferritin 1258.0 ± 110.1 mcg/l;blood leukocytes 15.0 ± 0.67 10

RISK FACTORS FOR POST-COVID-19 SYNDROME DEVELOPMENT IN PATIENTS WITH ARTERIAL HYPERTENSION

Objective: To determine risk factors for post-COVID-19 syndrome development in patients with arterial hypertension (AH). Design and method: A total of 81 patients with AH were examined 3-6 months after COVID-19. 48 people (group 1: 27 women, 21 men) suffered from SARSCoV- 2 pneumonia with lungs lesion from 15% to 74%. The patients' age was 18-87 years old (65 years old on average). In 38 patients chronic ischemic heart disease (IHD) was diagnosed;in 18 - myocardial infarction (MI);in 10 - permanent atrial fibrillation (AF);in 12 - AF paroxysms. 33 people (group 2: 18 women, 15 men) suffered from COVID-19 in the form of an acute respiratory illness without pneumonia. These patients were aged from 41 to 74 (56.9 years old on average). 25 patients had coronary artery disease;2 - MI;2 - permanent AF;4 - AF paroxysms. Results: Comparing to group 2, in group 1 the patients had higher blood pressure;higher left atrial volume index (LAVI) (35.1 ± 3.3 ml/m2 vs. 29.6 ± 3.2 ml/m2;p < 0.05);higher left ventricular (LV) end-diastolic volume index (EDVI) (76.1 ± 8.8 ml/m2 vs. 62.6 ± 10.3 ml/m2;p < 0.05);lower LV ejection fraction (EF) (56.1 ± 8.1% vs. 63.2 ± 3.9%;p < 0.05). In 7 group 1 patients, an increase in the frequency of AF attacks was detected. In group 1 symptoms of inflammation persisted for a long time: higher levels of C-reactive protein (15 ± 4.9 mg/l vs. 5.5 ± 3.8 mg/l), of blood ferritin (275 ± 106.3 mcg/l vs. 155.6 ± 85.8 mcg/l;p < 0.05), of D-dimer (919.3 ± 77.1 ng/ml vs. 609 ± 87.4 ng/ml;p < 0.05) as well as of total cholesterol (5.8 ± 1.2 mmol/l vs. 4.9 ± 1.1 mmol/l;p < 0.05) and of LDL (4.1 ± 1.1 mmol/l vs. 3.2 ± 1.3 mmol/l;p < 0.05). Conclusions: The revealed risk factors were high blood pressure, an increase in LAVI and LV EDVI, a decrease in LVEF, an increase in LDL, previous MI, and an increase in the frequency of AF paroxysms.

Thrombosis of pulmonary vasculature despite anticoagulation and thrombolysis: the findings from seven autopsies

Background Venous thromboembolism (VTE) with the prevalence of pulmonary microcirculatory thrombosis is considered a common complication of novel coronavirus disease (COVID-19) that develops despite anticoagulation. Methods The clinical course of the disease and the autopsy findings of seven deceased patients with verified COVID-19 were analyzed. The chest computed tomography (CT) scan was routinely performed while CT pulmonary angiography and a duplex ultrasound scan (DUS) of the lower limbs were used in cases of suspected VTE. The VTE prophylaxis was administered to all patients with intermediate or therapeutic doses of low-molecular-weight heparin. The histological examination of the lung tissue and other organs was performed with particular attention paid to the pulmonary vasculature. Results Venous thromboembolism, including deep vein thrombosis in one patient and pulmonary artery thrombosis in two patients, was confirmed by imaging tests despite anticoagulation. Systemic thrombolysis was performed in two patients with putative and confirmed pulmonary embolism. An autopsy revealed the signs of acute respiratory distress syndrome in all seven patients. Abnormalities of lung vessels were found in all cases and were represented by dystrophy and necrosis in the endothelium and muscle fibers, and by infiltration by plasmatic cells, neutrophils, and lymphocytes. Multiple clots of variable maturity were observed. All those changes developed despite anticoagulation and were preserved after systemic thrombolysis. Conclusion Inflammatory and prothrombotic changes in the arterial wall in parallel with the lack of lung perfusion may cause diffuse arterial thrombosis in the lungs. This background may be responsible for the low response to systemic anticoagulation and thrombolysis in severe forms of COVID-19.

Interim guidelines: "Diseases of the digestive organs in the context of a new coronavirus infection pandemic (COVID-19)"

Consensus of experts of the Interregional Public Organization "Society of Gastroenterologists and Hepatologists "North-West", Russian Society for Prevention of Noncommunicable Diseases and the Profile Commission on Therapy and General Medical Practice of the Russian Ministry of Health. Консенсус экспертов Межрегиональной общественной организации «Общество гастроэнтерологов и гепатологов «Северо-Запад», Российского общества профилактики неинфекционных заболеваний и Профильной комиссии по терапии и общей врачебной практике Минздрава России.