Clinical and morphological characteristics of SARS-CoV-2-related myocarditis proven by the presence of viral RNA and proteins in myocardial tissue

Kogan, Evgeniya; Kukleva, Anna; Berezovskiy, Yu S; Благова, О В; Zharkov, N.V.; Айнетдинова, Д. Х.; Demyashkin, Grigory

doi:10.17116/patol2021830415

Cited by 7 publications

(5 citation statements)

References 30 publications

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“…Более того, такая локализация по данным магнитно-резонансной томографии характерна для миокардита [7]. Отечественные исследователи указывают на возможный патогенетический механизм "постковидного" миокардита -прямое повреждение кардиомиоцитов при COVID-19 с последующей воспалительной реакцией, которая может поддерживаться и после элиминации вируса из миокарда [17,18]. Вероятно, диффузное поражение ЛЖ по данным ЭхоКГ с использованием STE (преимущественно базального уровня) через 3 мес.…”

Section: Discussionunclassified

“…Коган Е. А. и др. [17] представили данные морфологического исследования, согласно которому особенностью ассоциированного c SARS-CoV-2 (Severe Acute Respiratory Syndrome CoronaVirus 2) миокардита является его сочетание с коронариитом, в т.ч. мелких веток коронарных артерий.…”

Section: Discussionunclassified

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Relationship between latent left ventricular contractile dysfunction and signs of immune inflammation in patients with COVID-19 pneumonia

Shirokov

Yaroslavskaya

Krinochkin

et al. 2023

Cardiovasc Ther Prev

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Aim. To investigate the relationship between echocardiographic parameters and laboratory immune inflammation signs in patients after coronavirus disease 2019 (COVID-19) pneumonia depending on the left ventricular (LV) involvement according to speckle tracking echocardiography (STE).Material and methods. The study included 216 patients (men, 51,1%, mean age, 50,1±11,1 years). The examination was carried out in patients 3 months after COVID-19 pneumonia. Patients were divided in 3 groups: group I (n=41) — diffuse decrease (≥4 segments the same LV level) of longitudinal strain (LS) according to STE; group II (n=67) — patients with regional decrease (LS reduction ≥3 segments corresponding to systems of the anterior, circumflex or right coronary arteries); group III — patients without visual left ventricle involvement (n=108).Results. There were no significant differences in LV ejection fraction — 68,9±4,1% in group I, 68,5±4,4% in group II and 68,6±4,3 in group III (p=0,934). A decrease in the global longitudinal left ventricle strain was detected significantly more often in groups I and II compared with group III (-17,8±2,0, -18,5±2,0 and -20,8±1,8%, respectively; p<0,001). At the same time, LS depression of LV basal level (-14,9±1,5, -16,8±1,2% and -19,1±1,7%; p<0,001), as well as a decrease in LS of LV inferior-posterior segments in group with diffuse involvement was detected significantly more often than in groups II and III. In addition, we revealed a significant difference in interleukin-6 concentration — 3,1 [2,5;4,0], 3,1 [2,4;3,8] and 2,5 [3,8;1,7] pg/ml, (p=0,033), C-reactive protein — 4,0 [2,2;7,9], 5,7 [3,2;7,9] and 2,4 [1,1;4,7] mg/l, (p<0,001), tumor necrosis factor-a — 5,9±1,9, 6,2±1,9 and 5,2±2,0 pg/ml, (p=0,004) and ferritin — 130,7 [56,5;220,0], 92,2 [26,0;129,4] and 51,0 [23,2;158,9] pg/l, respectively (p=0,025).Conclusion. A relationship was found between diffuse and regional left ventricular involvement according to STE and signs of immune inflammation in patients 3 months after COVID-19 pneumonia.

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Section: Discussionunclassified

Relationship between latent left ventricular contractile dysfunction and signs of immune inflammation in patients with COVID-19 pneumonia

Shirokov

Yaroslavskaya

Krinochkin

et al. 2023

Cardiovasc Ther Prev

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“…This mortality rate of 15% might go as high as 27.3% in the case of Takotsubo cardiomyopathy, which is the actual myocardial pathology in 48% of cases suspected to have SARS-CoV-2-related myocarditis [ 15 ]. The recent identification of SARS-CoV-2 RNA in the myocardial tissue of deceased COVID-19 patients [ 16 ] strongly suggests that the myocardial injury reported in about 7% of patients hospitalized due to COVID-19 [ 17 ] might actually be the result of viral infection, rather than collateral immune-based damage.…”

Section: Myocarditis and Heart Failure In Covid-19mentioning

confidence: 99%

Type 2 alveolar epithelial cell-derived circulating extracellular vesicle-encapsulated surfactant protein C as a mediator of cardiac inflammation in COVID-19

et al. 2022

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Among the countless endeavours made at elucidating the pathogenesis of COVID-19, those aimed at the histopathological alterations of type 2 alveolar epithelial cells (AT2) are of outstanding relevance to the field of lung physiology, as they are the building blocks of the pulmonary alveoli. A merit of high regenerative and proliferative capacity, exocytotic activity resulting in the release of extracellular vesicles (EVs) is particularly high in AT2 cells, especially in those infected with SARS-CoV-2. These AT2 cell-derived EVs, containing the genetic material of the virus, might enter the bloodstream and make their way into the cardiovascular system, where they may infect cardiomyocytes and bring about a series of events leading to heart failure. As surfactant protein C, a marker of AT2 cell activity and a constituent of the lung surfactant complex, occurs abundantly inside the AT2-derived EVs released during the inflammatory stage of COVID-19, it could potentially be used as a biomarker for predicting impending heart failure in those patients with a history of cardiovascular disease.

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“…На сегодня эти данные сами по себе уникальны. Если возможность развития миокардита в рамках острой COVID-19 неоднократно доказана с помощью ЭМБ и исследований аутопсийного материала [1,8], то исследований морфологически верифицированного постковидного миокардита практически нет. Несмотря на широкое обсуждение в литературе последнего года таких понятий, как long-COVID, постковидный синдром [9], частота миокардита как компонента этого синдрома оценивается лишь в единичных работах и на очень низком уровне (0,4% в течение года после болезни, вместе с перикардитом [10]), причем ни о какой морфологической диагностике речи не идет.…”

Section: клиническая и исследовательская медицинаunclassified

Infective and nonbacterial thrombotic endocarditis in patients with post-COVID-19 viral-immune myocarditis

et al. 2022

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The possibility of heart inflammation (both myocardial and endocardial) months after a coronavirus disease 2019 (COVID-19) has not been practically studied, especially since approaches to the treatment of myocarditis in combination with various endocarditis forms have not been developed.Aim. To study the prevalence and mechanisms of SARS-CoV-2-associated endocardial injury in patients with morphologically verified post-COVID-19 myocarditis, as well as to develop approaches to comprehensive therapy.Material and methods. The study included 18 patients with severe morphologically verified post-COVID-19 myocarditis (men, 9; 51,1±9,4 years; 35 to 66 years). Patients with prior verified myocarditis/myocardial infarction, rheumatic heart disease, and systemic immune diseases were excluded. The average time after COVID-19 was 6,5 [3.5; 10] months The diagnosis of myocarditis was confirmed by endomyocardial biopsy (including immunohistochemical examination with antibodies to CD3, CD20, CD45, CD68, and to SARS-CoV-2 antigens; polymerase chain reaction for SARS-CoV-2 RNA, DNA of cardiotropic viruses). The blood level of anticardiac antibodies was determined by indirect immunofluorescence. In addition, echocardiography, magnetic resonance imaging (n=8), cardiac multislice tomography (n=1), and coronary angiography (n=14) were performed.Results. Biopsy revealed active (n=12) and borderline (n=3) lymphocytic myocarditis, eosinophilic (n=2) and giant cell (n=1) myocarditis. In 4 patients, nonbacterial thrombotic endocarditis (NBTE) with parietal and intravascular thrombosis was diagnosed, and in one patient — infective endocarditis (IE) of the bicuspid aortic valve. Myocardial persistence of SARS-CoV-2 was detected in 72% of cases (in 3 patients — with NBTE; in 1 — with IE; in 9 — without endocarditis). Titers of anticardiac antibodies increased by 3-4 times in 94% of patients. Patients with endocarditis were characterized by larger heart chambers, lower ejection fraction (27,5±6,6 vs 36,0±13,4%), more severe pulmonary hypertension, and valvular regurgitation. Intraventricular thrombosis according to echocardiography/magnetic resonance imaging and cardiac embolism was not observed. Treatment in all patients included methylprednisolone at an average dose of 24 mg a day. In 10 patients, the result was monitored for at least 3 months as follows: the ejection fraction was 46,0±12,7% and 44,3±7,3% in patients with and without endocarditis, respectively.Conclusion. Endocarditis in patients with post-COVID-19 myocarditis was detected in 28% (1 patient — IE; 4 — NBTE). The key mechanisms of post-COVID-19 myocarditis and NBTE are long-term (up to 18 months) myocardial persistence of SARS-Cov-2 and the development of an autoimmune reaction. Endocarditis was diagnosed in more severe patients, including those with giant cell and eosinophilic myocarditis. The effectiveness of steroid therapy in combination with anticoagulants in patients with NBTE requires further study. In case of IE, steroids can also be used in the treatment of myocarditis (in combination with antibiotics and immunoglobulin).

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Clinical and morphological characteristics of SARS-CoV-2-related myocarditis proven by the presence of viral RNA and proteins in myocardial tissue

Cited by 7 publications

References 30 publications

Relationship between latent left ventricular contractile dysfunction and signs of immune inflammation in patients with COVID-19 pneumonia

Relationship between latent left ventricular contractile dysfunction and signs of immune inflammation in patients with COVID-19 pneumonia

Type 2 alveolar epithelial cell-derived circulating extracellular vesicle-encapsulated surfactant protein C as a mediator of cardiac inflammation in COVID-19

Infective and nonbacterial thrombotic endocarditis in patients with post-COVID-19 viral-immune myocarditis

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