PERICARDIAL INVOLVEMENT ASSOCIATED WITH SARS-COV-2 INFECTION. PROSPECTIVE OBSERVATION IN THE COVID- WARD

Purpose. To identify the occurrence and structure of changes in the pericardium ultrasonography among patients who have undergone COVID-19 and have cardiological symptoms, as well as to compare these changes with the pericarditis aspects and the infection time duration in a prospective cohort observational study. Methods. Inclusion/exclusion criteria: current or transferred COVID-19, new symptoms that occurred during or after infection and forced to consult a cardiologist, the absence of other prerequisites for pericarditis and vaccination against SARS-CoV-2. Echocardiography was performed with an emphasis on the pericardium and an assessment of the echogenicity amplification, the area of the hyperechoic zone, thickness and artifacts, as well as a questionnaire. Results. From 05.2020 to On 10.2020, 335 patients from the covid ward and 284 patients from the out-patient clinic were included. 86% of patients had transient chest discomfort. The peaks of treatment accrued to 4-5 and 10-11 weeks (Me 10[2-36] (1 to 64) weeks) from SARS-CoV-2 infection occurred. Typical ECG changes were registered in 3%, pericardial friction noise – in 7% of patients. In 20% of patients discomfort in the heart area was the first, in 27% – the dominant, in 14% – the only symptom of COVID-19. According to EchoCG data, 96% of the examined patients had ultrasound signs of different changes in the pericardium: slight effusion in 65%, signs of tamponade in 2%, thickening in 12%, local hyperechogenicity in 83%, local adhesion in 8% of patients. The group without pericardial changes was distinguished by the presence of epicardial fat >7 mm. A combination of the echo-cardiography criteria with the second symptom recorded at the visit or earlier was present in 76% of the applicants. Comparison of the recorded ultrasound patterns with the time elapsed since infection allowed us to distinguish ultrasound phases: 1) the phase of damage (pattern of initial edema) occurred at 1 week, 2) the phase of edema /exudation (pattern of visible effusion) – at 3 weeks, 3) fibrosis (pattern of pericardial compaction) – at 11 weeks, 4) regression of inflammatory changes (pattern of local fibrin deposition) – on week 22, 5) residual signs of transferred inflammation may be visualized in patients with symptoms 44 weeks after COVID-19. Conclusions. Consideration of the infectious process triggered by SARS-CoV-2, as a systemic inflammation, allows us to interpret the phenomenon of pericardial involvement as a reactive serositis having ultrasound phases. It was possible to trace some patterns of echocardiography at different stages of the infectious and post-infectious period. Clinical data of 76% of patients can be interpreted as pericarditis, changes in 20% – as an increase in echogenicity of the pericardium. © 2022 Russian Electronic Journal of Radiology. All rights reserved.

PERICARDIAL INVOLVEMENT ASSOCIATED WITH SARS-COV-2 INFECTION. PROSPECTIVE OBSERVATION IN THE COVID- WARD.

Purpose. To identify the occurrence and structure of changes in the pericardium ultrasonography among patients who have undergone COVID-19 and have cardiological symptoms, as well as to compare these changes with the pericarditis aspects and the infection time duration in a prospective cohort observational study. Methods. Inclusion/exclusion criteria: current or transferred COVID-19, new symptoms that occurred during or after infection and forced to consult a cardiologist, the absence of other prerequisites for pericarditis and vaccination against SARS-CoV-2. Echocardiography was performed with an emphasis on the pericardium and an assessment of the echogenicity amplification, the area of the hyperechoic zone, thickness and artifacts, as well as a questionnaire. Results. From 05.2020 to On 10.2020, 335 patients from the covid ward and 284 patients from the out-patient clinic were included. 86% of patients had transient chest discomfort. The peaks of treatment accrued to 4-5 and 10-11 weeks (Me 10[2-36] (1 to 64) weeks) from SARS-CoV-2 infection occurred. Typical ECG changes were registered in 3%, pericardial friction noise - in 7% of patients. In 20% of patients discomfort in the heart area was the first, in 27% - the dominant, in 14% - the only symptom of COVID-19. According to EchoCG data, 96% of the examined patients had ultrasound signs of different changes in the pericardium: slight effusion in 65%, signs of tamponade in 2%, thickening in 12%, local hyperechogenicity in 83%, local adhesion in 8% of patients. The group without pericardial changes was distinguished by the presence of epicardial fat >7 mm. A combination of the echo-cardiography criteria with the second symptom recorded at the visit or earlier was present in 76% of the applicants. Comparison of the recorded ultrasound patterns with the time elapsed since infection allowed us to distinguish ultrasound phases: 1) the phase of damage (pattern of initial edema) occurred at 1 week, 2) the phase of edema /exudation (pattern of visible effusion) - at 3 weeks, 3) fibrosis (pattern of pericardial compaction) - at 11 weeks, 4) regression of inflammatory changes (pattern of local fibrin deposition) - on week 22, 5) residual signs of transferred inflammation may be visualized in patients with symptoms 44 weeks after COVID-19. Conclusions. Consideration of the infectious process triggered by SARS-CoV-2, as a systemic inflammation, allows us to interpret the phenomenon of pericardial involvement as a reactive serositis having ultrasound phases. It was possible to trace some patterns of echocardiography at different stages of the infectious and post-infectious period. Clinical data of 76% of patients can be interpreted as pericarditis, changes in 20% - as an increase in echogenicity of the pericardium.Copyright © 2022 Russian Electronic Journal of Radiology. All rights reserved.

[A new approach in the diagnosis of lung lesions in patients with COVID-19: lung ultrasound protocol versus CT scan].

AIM: To develop a protocol for ultrasound diagnostics of COVID-19 pneumonia and to assess the diagnostic capabilities of the method in comparison with computer tomography (CT). MATERIALS AND METHODS: The study included 59 patients with a new coronavirus infection. In order to identify changes in the lung tissue characteristic of a new coronavirus infection, we used a special protocol for ultrasound of the lungs, which was developed by us in such a way that the data obtained were compared by segment with the results of CT of the lungs. RESULTS: When comparing the results of lung ultrasound with the data of CT diagnostics, according to the new protocol, the percentage of lung tissue damage during ultrasound of the lungs averaged 70.8% in the group [62.5; 87.5], and according to the results of CT 70.0% [60.0; 72.5] (p=0.427). Thus, the ultrasound of the lung lesions was almost completely consistent with the changes revealed by CT. In order to assess the diagnostic value of lung ultrasound in identifying severe lung tissue lesions corresponding to CT 34, ROC analysis was performed, which showed the high diagnostic value of lung ultrasound in identifying severe lung tissue lesions. CONCLUSION: A new protocol was developed for assessing the severity of lung tissue damage according to ultrasound data, which showed a high diagnostic value in detecting COVID-19 pneumonia in comparison with CT. The results obtained give reason to recommend this protocol of ultrasound of the lungs as a highly sensitive method in diagnosing the severity of COVID-19 pneumonia. Its application is very important for dynamic examination of patients, especially in conditions of low availability of CT.

Echocardiographic phenomenon of pericarditis in patients with severe COVID-19 pneumonia. One-year observation

Funding Acknowledgements Type of funding sources: None. Introduction. As seen in practice, such an ultrasound (us) phenomenon as the inflammation of the pericardium caused by COVID-19 is underestimated due to a very tough time pressure in the infection unit, minor effusion and the incorrect interpretation of cardialgia. The study is intended to evaluate the frequency of cases when the pericardium is involved in the COVID- syndrom, describe us-changes and dynamics throughout the year. Methods. We performed TTEchocardiography of pts during the first days of their admission to COVID-centre with pneumonia CT3-4 and during the year following their discharge, once in 4 months. The study was conducted by one observer, one equipment with same brightness settings. Results. 158 of 720 pts returned for a follow-up. 36 pts excluded due to the recurring infection, and 47 ones got vaccinated. Analyzed 75 cases. In the acute phase of infection, circumferential effusion was found in 98% of pts (the max pericardial layer separation by 4[3-6] mm). 2%pts has a thick layer of epicardial fat, which could possibly hide the minor hydropericardium. Furthermore, we captured a moderate increase in the echogenity of pericardium, especially in the inferolateral segments, multiple artifacts like B-lines stretching from pericardium line to the lungs in the basal ventricular segments left and right and around the atria. On 4 months after infection pericardial layer separation by≥3mm was detected in 8% pts (in persisting cases, effusion was 5[3-9] mm). Only the half of the pts had heart failure. The group without effusion demonstrated hyperechogenity of pericardium in the left basal segments, and both atria along perimeter of the free walls, confluent artifacts like the comet tail and the waterfall. In 8 months pericarditis with effusion persevered in 2 pts, with the max pericardial layer separation 5 and 3mm and vertical confluent artifacts. On the other pts, the hyperechogenic area of the pericardium reduced down to the basal inferolateral segments of left ventricle, base of the left atrium in 82% and the base of the right atrium in 18%. In 12 months, 1 pt had the recurring pericarditis, notwithstanding the therapy. The minimum hyperechogenity in the basal inferolateral segments of the left ventricle persisted in 61% of pts. The number of separate, narrow vertical artifacts was not different from the pts without COVID-19 (1-4 per view).  Conclusions Perhaps, the pericardium is a target organ for COVID-19, since it is involved in the acute phase of pneumonia in 98% of cases. Us-signs of the pericarditis persevere throughout many months after the pt’s discharge. Even the minor hydropericardium should be observed, since the clinic may deteriorate in 85% of cases in 4 months after the infection even in those pts who have no heart failure. Pericarditis, as an us-phenomenon, demonstrates the predictable dynamics of visual changes throughout the year. To interpret the changes, vertical artifacts of the pericardium should be evaluated. Figure. 56yo, acute COVID-CT3, effusion, bright   Figure. same pt, 3mo after:effusion, comet-tale

Effusive pericarditis in the pathogenesis of cardiac arrhythmias in COVID19: a case series

A wide variety of nonpulmonary manifestations of a coronavirus disease 2019 (COVID19) has enriched clinical performance of cardiac diseases with atypical symptoms. Two COVID19 cases are presented, where sinus bradycardia and syncope, which are rare in COVID19, were the leading ones after the infection. The patients had no prior cardiovascular diseases, while the examination did not detected neurological pathology and myocarditis. Echocardiography showed relatively small pericardial effusion, which is supposed to be a cause of the symptoms as the diagnosis to exclude. A local buildup of inflammatory fluid around the sinus node and extensive ganglion plexuses around the atria can possibly affect the automatism and chronotropic compensation in addition to the myocardial inflammation. As part of the treatment against the hydropericardium syndrome, the symptoms disappeared, without reoccurring within subsequent 6month followup. The third clinical case regards the pandemic outbreak, when we could not even suspect that the systemic inflammation would persist for many months after COVID19 and radiofrequency ablation can lead to sudden cardiac death. © 2022 Vserossiiskoe Obshchestvo Kardiologov. All rights reserved.