Type 2 myocardial infarction in patients with coronavirus disease 2019

Talanas, Giuseppe; Dossi, Filippo; Parodi, Guido

doi:10.2459/jcm.0000000000001136

Cited by 13 publications

(11 citation statements)

References 12 publications

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“…Еще одним механизмом повреждения миокарда является ишемия. Повышенное потребление кислорода миокардом из-за системной инфекции в сочетании с нарастающей гипоксией из-за дыхательной недостаточности приводит к ишемизации миокарда, наиболее заметной при наличии предшествующих хронических сердечно-сосудистых заболеваний, таких как ишемическая болезнь сердца и сердечная недостаточность [23]. Кроме того, потенциальной кардиотоксичностью обладают и использующиеся для лечения COVID-19 лекарственные препараты, такие как лопинавир или дексаметазон [24].…”

Section: Discussionunclassified

“…С начала пандемии исследования предоставили значительный объем данных о поражении сердечнососудистой системы, в том числе в отношении (1) венозного и артериального тромбоза, (2) явлений тромбоэмболии, (3) острого ишемического повреждения миокарда, включая инфаркт миокарда, и (4) активного и пограничного миокардита [14,25,29,30] Поражения сердца при COVID-19 можно разделить по клинико-морфологическим проявлениям на ишемические и воспалительные изменения. Первый тип поражения может возникать в результате повреждения микрососудов и тромбоза вследствие коагулопатии в ответ на вирусную инфекцию, системного воспаления [35], системной гипоксии и несоответствия потребности миокарда в кислороде [23]. Что касается воспалительных изменений, они могут быть связаны с проявлением системной воспалительной реакции и цитокинового шторма либо быть опосредованы прямым вирусным поражением миокарда.…”

Section: Discussionunclassified

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Myocardial lesions in patients with COVID-19. Autopsy case series

Ермола¹,

Galyshevskaya²,

Davydova³

et al. 2022

Clin. Exp. Morphology

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Introduction. Morphological data on SARS-CoV-2-associated heart damage and its mechanisms are rather limited. However, clinical and morphological features of myocardial lesions in COVID-19 patients have been described and include myocardial ischemia, acute coronary syndrome, and acute myocarditis. The prevailing features of myocardial lesions and their consequences are still controversial. The aim of our research was to evaluate the morphological features of myocardial lesions in patients with severe COVID-19, using routine histological examination and immunohistochemistry (CD45) to confirm myocardial inflam-matory infiltration. Materials and methods. We analyzed samples of the left ventricular myocardium obtained during autopsy examination of 48 patients with severe COVID-19 who died from SARS-CoV-2-associated pneumonia. We used histological description and immunohistochemical methods. Results. The results revealed several histopathological features of COVID-19-associated myocardial lesions, including acute ischemia (25% of cases) and mild inflammatory changes termed borderline myocarditis (18.75% of cases). Other significant findings in the myocardium included microcirculatory vessel thrombosis. Conclusion. The study confirms the existing data on damage to myocardium in severe COVID-19. However, further studies are warranted. It may contribute to the development of new management strategies for severe COVID-19 patients. Keywords: SARS-CoV-2, heart, ischemia, myocarditis

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Section: Discussionunclassified

Myocardial lesions in patients with COVID-19. Autopsy case series

Ермола¹,

Galyshevskaya²,

Davydova³

et al. 2022

Clin. Exp. Morphology

View full text Add to dashboard Cite

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“…Other studies have analyzed predominantly Type II myocardial infarction in patients with COVID-19 (60). These studies indicate that such cases may be caused by an imbalance between oxygen supply and demand, possibly due to hypoxia, increased heart rate, systemic inflammation and/or decompensated cardiac failure, and are associated with high in-hospital mortality rates.…”

Section: Acute Myocardial Infarction/acute Coronary Syndromementioning

confidence: 99%

Emerging Role of Platelet-Endothelium Interactions in the Pathogenesis of Severe SARS-CoV-2 Infection-Associated Myocardial Injury

et al. 2022

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Cardiovascular dysfunction and disease are common and frequently fatal complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Indeed, from early on during the SARS-CoV-2 virus pandemic it was recognized that cardiac complications may occur, even in patients with no underlying cardiac disorders, as part of the acute infection, and that these were associated with more severe disease and increased morbidity and mortality. The most common cardiac complication is acute cardiac injury, defined by significant elevation of cardiac troponins. The potential mechanisms of cardiovascular complications include direct viral myocardial injury, systemic inflammation induced by the virus, sepsis, arrhythmia, myocardial oxygen supply-demand mismatch, electrolyte abnormalities, and hypercoagulability. This review is focused on the prevalence, risk factors and clinical course of COVID-19-related myocardial injury, as well as on current data with regard to disease pathogenesis, specifically the interaction of platelets with the vascular endothelium. The latter section includes consideration of the role of SARS-CoV-2 proteins in triggering development of a generalized endotheliitis that, in turn, drives intense activation of platelets. Most prominently, SARS-CoV-2–induced endotheliitis involves interaction of the viral spike protein with endothelial angiotensin-converting enzyme 2 (ACE2) together with alternative mechanisms that involve the nucleocapsid and viroporin. In addition, the mechanisms by which activated platelets intensify endothelial activation and dysfunction, seemingly driven by release of the platelet-derived calcium-binding proteins, SA100A8 and SA100A9, are described. These events create a SARS-CoV-2–driven cycle of intravascular inflammation and coagulation, which contributes significantly to a poor clinical outcome in patients with severe disease.

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“…Differences in the frequency of type 2 MI in non-adjudicated studies are likely related to patient selection and less rigor in applying criteria establishing the presence of acute myocardial ischemia. One potential difference is that 42 in COVID-19 patients, oxygen demand-supply imbalance is often secondary to hypoxemia, increased heart rate, inflammatory status and/or decompensated heart failure, whereas in most type 2 MIs, tachyarrhythmias and anemia are often prevalent mechanisms. Conventional treatment strategies appear appropriate but individualized care is warranted given the heterogeneous presentations and mechanisms.…”

Section: Chronic Myocardial Injurymentioning

confidence: 99%