Objective: To study the frequency and conditions for the emergence of atrial fibrillation paroxysms (AFP) in elderly and late-life patients in the postcovid period on the background of comorbid pathology. Design and method: 2 months after SARS-Cov-2-pneumonia, 124 people were examined, 66 of them (41 men and 25 women) aged 68±5.9 years (group 1) and 58 (33 men and 25 women) aged 81±4.3 years (group 2). According to computed tomography (CT) performed during SARS-CoV-2-pneumonia, in group 1, 12 patients (18.2%) had lung lesion volume < 25% (CT1); 34 patients (51.5%) 25-49% (CT2); 18 patients (27.3%) 50-74% (CT3); 2 patients (3%) > 75% (CT4). In group 2, 14 patients (24.1%) had CT1; 18 patients (31.1%) CT2; 21 patients (36.2%) CT3; 5 patients (8.6%) CT4. All patients had arterial hypertension (AH) and coronary heart disease (CHD) on the background of atherogenic dyslipidemia; 59 had type 2 diabetes mellitus (DM), 13 had chronic kidney disease (CKD). Holter monitoring (HM) was performed for all. The content of ferritin, D-dimer, and CRP in the blood plasma was measured for all. Results: According to the HM, in 13 of 66 (19.7%) group 1 patients, AFP were registered, of which 7 patients had 30-40 minutes seizures, 3 patients – about 2 minutes seizures. 3 patients were hospitalized, their sinus rhythm was restored by cardioversion. In 16 of 58 (27.6%) group 2 patients, HM revealed AFP, 2 of them were hospitalized due to the deterioration of their condition, the sinus rhythm was restored by cardioversion. In 7 patients, AFP did not exceed 30 minutes; in another 7 patients, AFP were short, no more than 2-3 minutes. Blood ferritin in group 1 was 175±66.2 ng/ml; in group 2 212±40.2 ng/ml (p = 0.012); D-dimer 501±50.3 ng/ml and 835±53.8 ng/ml, respectively (p = 0.0002); CRP 4.3±2.1 mg/l and 8±3.3 mg/l, respectively (p = 0.0009). Conclusions: 2 months after SARS-CoV-2-pneumonia with a large area of lung damage, elderly and late-life patients with a very high cardiovascular risk have signs of inflammation, and a tendency to increased thrombosis, which probably causes the AFP emergence.

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 SARS-CoV-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.

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 10^9/l; blood lymphocytes 1.54 ± 0.29 10^9/l; procalcitonin 1.350 ± 0.51 ng/ml. The development of hemorrhagic syndrome was observed in 93 (35%) cases. The level of D-dimer was 4326.4 ± 696.1 ng/ml; fibrinogen 18.2 ± 13.04 g/l; platelets 179.0 ± 8.7 10^9/l. Blood creatinine in patients aged 36 to 59 (27 people) was 120.6 ± 12.2 mmol/l; aged 60 to 80 (136 people) 136.6 ± 10.12 mmol/l; aged over 80 (105 people) 139.0 ± 11.7 mmol/l.Conclusions:The study of the kidneys in patients who died from the new coronavirus infection revealed microvasculature vessels damage and development of coagulation disorders amid the renal failure.