Officially announced by the World Health Organization (WHO) in March 2020, the coronavirus disease 2019 (COVID-19) pandemic is terrifying with the unimaginable rate of spreading and the large number of deaths. More than 171 million COVID-19 cases including more than 3,6 million deaths have been confirmed worldwide since the start of the pandemic. The high incidence of venous thromboembolic events and non-ARDS (acute respiratory distress syndrome) associated death of patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, despite prophylactic antithrombotic therapy, may indicate the need for a more intensified personalized regime of preventive measures. Respiratory viruses such as influenza A H1N1, SARS-CoV, MERS-CoV and SARS-CoV-2 are known for their affinity for lung tissue and the ability to lead to viral pneumonia and acute respiratory distress syndrome (ARDS). The analyzed data bring up to the hypothesis that microvascular thrombosis, rather than decreased lung compliance, provides oxygenation impairment in COVID-19 patients. The accumulated experience in the management of patients with SARS-CoV-2 indicates that the pathophysiology of systemic microthrombosis associated with COVID-19 may differ from that in sepsis-induced disseminated intravascular coagulation (DIC). In contrast to sepsis-induced coagulopathy consumption of platelets, clotting factors, fibrinogen, and bleeding are rare in patients with severe SARS-CoV-2, suggesting that DIC is not a common complication of COVID-19. The development of micro- and macrovascular thrombosis of the venous and arterial bed in patients with SARS-CoV-2 makes it possible to consider COVID-19 as a systemic “thromboinflammatory” syndrome. According to the international analytical studies, the proportion of thrombosis and thromboembolic complications ranges from 0.9% to 6.5 in patients with a moderate COVID-19, and from 8% to 69% in patients treated in intensive care unit, the proportion of acute arterial obstruction in SARS-CoV-2 patients ranges 0.39% to 11.1%. The team of authors carried out a retrospective analysis of the medical records of 7607 patients hospitalized in 2020 in the infectious disease departments of the 4th city clinical hospital named after N.E. Savchenko. The proportion of patients with pulmonary embolism (PE) in the final diagnosis was 2.1% (n=163), the proportion of patients with deep vein thrombosis (DVT) was 0.9% (n=68), in the structure of patients with DVT the complication of PE was 58.8% (n=40). The variation in the data of national and foreign studies may apparently be related to different diagnostic tactics in verifying the diagnosis of VTE and DVT: the use of duplex ultrasound vascular examination and/or computed tomographic angiography (CTA) of the lungs as screening techniques, the inclusion of different clinical points (symptomatic and/or asymptomatic VTE) by authors in publications, the lack of uniform approaches to thromboprophylaxis, and population differences in the patient samples. There is an urgent need for more in-depth studies of the pathogenesis and molecular basis of thrombosis in patients with COVID-19 to establish the prognostic value of changes in the hemostasis system associated with SARS-CoV-2. Considering unknown long-term results in COVID-19 convalescents, many studies signaling the presence of disabling consequences and the need for subsequent full medical and non-medical rehabilitation, the search for new biomarkers, such as of coagulation, fibrinolysis, activation of endothelium, that are associated with the course, early outcomes and delayed complications in patients with coronavirus infection (SARS-CoV-2) remains relevant.
Cardiac manifestations in COVID-19, including myocardial injury with elevated troponin levels, are common. Myocarditis has been reported as a possible complication in coronavirus patients, but direct evidence for SARS-CoV-2 myocarditis remains limited. The described series of histopathological confirmations of myocarditis in COVID-19 differ in severity and interpretation Clinical manifestations of non-ischemic myocardial injury are nonspecific, dif- ferential diagnosis is even more difficult due to the complications after viral pneumonia. Cardiac Magnetic Resonance Imaging (CMRI) is a powerful tool for studying structural and functional changes in myocardial injury. New pulse sequences of parametric mapping with determination of the T1 and T2 relaxation times of the myocardium are a unique method for quantitative assessment of the myocardium tissue. Within 6 months in 2021, we retrospectively analyzed the CMRI results of 45 patients with COVID-19 at the Republican Scientific and Practical Center “Cardiology”. The percentage of patients with positive criteria for Lake Louise myocarditis was 18% (n = 8). The elevated reference values of T2 ≥ 2σ up to 33% was the most frequent pathological change in myocardial tissue characteristics. There is significant variability in the published data collection as to the prevalence of myocarditis associated with different research methodologies in studies and discrepancies in the interpretation of MRI-mapping data. This brief review is aimed at revising and summari- zing current knowledge on myocarditis in COVID-19 patients and highlight the problems of CMRI diagnostics.
Всемирная организация здравоохранения (ВОЗ) официально объявила о начале пандемии COVID-19 в марте 2020 года. На данный момент, по официальным данным ВОЗ, во всем мире более 195 млн человек были инфицированы коронавирусной инфекцией, а число умерших превысило 4,1 млн. В начале пандемии основное внимание медицинского сообщества было сосредоточено на тропизме вируса к легким, однако накопленные данные отечественных и зарубежных исследований демонстрируют мультиорганность поражения, вызываемого SARSCoV-2, включая ассоциированные с атеротромбозом болезни системы кровообращения (БСК). По имеющимся данным, пациенты с COVID-19 и сопутствующими сердечно-сосудистыми заболеваниями, а также с развившимися сердечно-сосудистыми событиями (ССС) имеют повышенный риск неблагоприятного исхода. ССС у лиц, инфицированных SARS-CoV-2, включают в себя острое повреждение миокарда, острый инфаркт миокарда, миокардит, нарушения ритма, сердечную недостаточность, тромбоэмболические осложнения. Проведен анализ медицинских карт 10 908 стационарных пациентов в возрасте от 18 до 90 лет, находившихся на лечении с01 июня 2020 г. по 31 мая 2021 г. в инфекционных отделениях учреждения здравоохранения «4-я городская клиническая больница им. Н.Е. Савченко», развернутых для пациентов с COVID-19. Наибольший удельный вес в исследуемой когорте имели лица с нарушениями ритма - 13,38% (n=1460), частота выявления миокардита и острого инфаркта миокарда, развившихся на фоне инфекции SARS-CoV-2, составила 0,29% (n=32) и 2,80% (n=305) соответственно, удельный вес пациентов с COVID-19 и тромбоэмболическими событиями - 5,97% (n=651). SARS-CoV-2 может приводить к развитию неблагоприятных ССС либо декомпенсации сопутствующих БСК через прямые или опосредованные механизмы, включающие прямую вирусную токсичность, чрезмерный системный воспалительный ответ, дисрегуляцию ренин-ангиотензин-альдостероновой системы (РААС), эндотелиальную дисфункцию и тромбовоспаление, вентиляционно-перфузионную недостаточность, нарушения электролитного баланса. Проводимая терапия COVID-19 потенциально может обладать кардиотоксическими эффектами. Рассмотрены предполагаемые патофизиологические механизмы и факторы, приводящие к развитию ССС, их влияние на течение и исходы COVID-19. Понимание потенциальных механизмов, лежащих в основе патофизиологии воздействия SARS-CoV-2 на сердечно-сосудистую систему, необходимо для оказания комплексной медицинской помощи пациентам с БСК и COVID-19. TheWorld Health Organization (WHO) officially announced the beginning of the COVID-19 pandemic in March 2020. So far, according to official WHO data, more than 195 million people worldwide have been infected with coronavirus infection, and the number of deaths has exceeded 4.1 million. At the beginning of the pandemic, the focus of the medical community was predominantly on the tropism of the virus to respiratory system, but the data accumulated today from national and foreign studies demonstrate the multiorgan nature of lesions in SARS-CoV-2, including atherothrombosis- associated cardiovascular diseases (CVDs). Patients with COVID-19 and concomitant cardiovascular disease and those who had cardiovascular events (CVE) are reported to have an increased risk of adverse outcomes. CVE in individuals infected with SARS-CoV-2 primarily consists of acute myocardial injury, acute myocardial infarction, myocarditis, rhythm disorders, heart failure, and thromboembolic events. The team of authors analyzed electronic medical records of 10 908 patients aged from 18 to 90 years, who were treated from June 01, 2020 to May 31, 2021 at the infectious disease departments of the 4th City Clinical Hospital named after N.E. Savchenko for patients with coronavirus infection (SARS-CoV-2). Individuals with rhythm disorders prevailed in this analysis - 13.38% (n=1460). The prevalence of persons with myocarditis and acute myocardial infarction developed on the background of SARS- CoV-2 infection was 0.29% (n=32) and 2.80% (n=305), respectively. The prevalence of patients with COVID-19 and thromboembolic events was 5.97% (n=651). SARS-CoV-2 can lead to CVE or decompensation of concomitant CVDs through direct or mediated mechanisms, including direct viral toxicity, excessive systemic inflammatory response, dysregulation of the renin-angiotensin- aldosterone system (RAAS), endothelial dysfunction and thrombosis, ventilation-perfusion failure, electrolyte imbalance, as well as on the background of ongoing therapy, which may potentially have cardiotoxic effects.The published article reviews the main proposed pathophysiological mechanisms and factors that lead to development of CVEs and provides the data on the contribution of CVEs to the course and outcomes in patients with COVID-19. Understanding the potential mechanisms underlying the pathophysiology of SARS-CoV-2 effects on the cardiovascular system is essential for providing comprehensive medical care for patients with CVDs and COVID-19.
Background. At the present time more than 185 million people are infected with the new coronavirus infection (CVI) SARS-CoV-2, which caused COVID-19 pandemic according to WHO. The issue of increased risk of pulmonary embolism (PE) and associated severe course of the disease in persons with abdominal obesity (AO) is actively discussed in national and foreign publications. Objective of the study. To determine the clinical and laboratory features of PE in patients with abdominal obesity infected with SARS-CoV-2 Material and Methods. An analysis of 11.056 medical records of inpatients treated in the infectious disease departments for patients with COVID-19 of the 4th City Clinical Hospital named after N.E. Savchenko of Minsk during the period from April 1, 2020 to May 31, 2021 was performed. AO in subjects included in the retrospective analysis was determined according to WHO criteria as a body mass index greater than or equal to 30 kg/m2, waist circumference greater than 94 cm in men and 80 cm in women, respectively. To determine clinical and laboratory features of PE, as well as the effect of AO on the severity of this complication, inclusion/exclusion/exclusion criteria were developed and a sample of medical records of patients with COVID-19 (n=33), whose diagnosis of PE was verified by computed tomographic angiography of the chest (CTA chest) was formed. Clinical and instrumental parameters and laboratory characteristics were analyzed in the studied groups at the moment of admission to the hospital and at the time of PE development. Results. According to the results of a retrospective analysis of 11 056 medical records, the proportion of patients in whom the final diagnosis of PE was present was 3.68% (n=407), among whom AO was observed in 22.11% (n=90) of patients. The prevalence of subjects with impaired lipid metabolism among those included in the analysis was 11.38% (n=1259). PE developed in 90 patients with CVI and AO (0.81%) and in 317 patients without AO (2.87%). The prevalence of patients with PE (n=90) in the CVI and AO group (n=1259) was 7.15%; among those with CVI without AO (n=9797) - 3.24% (n=317). In the formed group with AO, C-reactive protein (CRP) and fibrinogen levels at hospitalization were higher than in the group of patients without AO: 116.64 (80.38-134.08) mg/L versus 30.21 (15.11-57.21) mg/L (U=36.04; p<0.01) and 6.97 (6.11 to 8.03) g/L versus 4.71 (4.02 to 5.59) g/L (U=12.0, p<0.01) respectively. On the day of suspected PE, CRP levels were higher in the group of patients with AO and COVID-19 than in the group of patients without AO: 71.01 (50.59-105.06) mg/L versus 34.01 (18.85-60.81) mg/L (U=49.00; p<0.05). In patients with CVI and PE, there was a moderate positive relationship between the presence of AO and the severe course of COVID-19 (r=0.41; p<0.05), AO and elevated fibrinogen levels on admission to the hospital (r=0.58 p <0.05), a strong positive relationship between the presence of AO and increased serum CRP level at the time of hospitalization (r = 0.76; p < 0.01), a moderate positive relationship between AO and CRP level determined at the time of development of PE (r = 0.51; p < 0.01). Conclusion. Among the patients with COVID-19 and AO complicated by the development of PE in comparison with patients without AR was determined a higher prevalence of individuals with a severe course of CVI (χ2=5,18; p<0.05), lower oxygen saturation values at admission and at the time of PE development (U =46.5; p<0.05) and (U=49.5; p<0.05), respectively, higher fibrinogen and CRP levels at the time of hospitalization (U=12.0; p<0.01) and (U=36.04; p<0.01), respectively, higher CRP values at the manifestation of PE (U=49.00; p<0.05). The obtained data indicates in favor of the fact that AO can be considered as a risk factor for the severe course of COVID-19. The pathophysiological basis of the development, course and prognosis of thromboembolic complications in patients with COVID-19 and AO requires further clarification during prospective follow-up of this category of patients.
The publication provides a brief overview of the most significant pathogenetic and pathophysiological mechanisms that will explain the phenomenon of comorbidity of chronic obstructive pulmonary disease (COPD) and cardiovascular pathology (CVD). Moreover, in this review is considered the potential impact of the recommended treatment of COPD on the risks and course of cardiovascular diseases from the perspective of evidence-based medicine. It has been shown that COPD and cardiovascular diseases share single risk factors, common pathogenetic mechanisms, unidirectional pathophysiological processes, similar clinical symptoms and effects synergistically with respect to adverse events and outcomes, which allows us to attribute this combination to category of comorbid pathology. The presented results of randomized clinical trials and meta-analyzes demonstrate that currently no COPD guidelines contain detailed clinical recommendations for assessing cardiovascular risk in this category of patients, nor are there enough guidelines for the treatment of COPD in patients with cardiovascular disease or vice versa. In terms of international experience, it is substantiated that the comorbid pathology of COPD and CVD should not be considered isolated from each other.
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