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Cardiac consequences of Covid-19 infection have been mentioned in various studies as a serious risk factor for in-hospital mortality. However, the existence of residual cardiac dysfunction after the acute phase is seldom investigated especially in people without a history of specific medical disease. One hundred health care workers with positive reverse transcription-polymerase chain reaction test underwent comprehensive 2D and 3D echocardiography six to eight weeks after infection. Patients were classified into Mild, Moderate, and Severe groups based on their clinical characteristics of covid-19 infection, and all echocardiographic parameters were compared between the three groups. Left ventricular (LV) stroke volume index was reduced in all groups compared to normal ranges and was more prominent in the severe group (P-value < 0.05). 3D-derived LV global longitudinal strain (GLS) was significantly lower in the severe group in comparison to the mild group (- 19.3 ± 1 Vs. - 22.2 ± 2, P-value < 0.001) and correlated with highly sensitive CRP level at the acute phase. Left atrial (LA) strains, including LA peak strain, LA contraction strain, and LA reservoir strain, were considerably higher and LA volume index was significantly lower in the clinically severe covid patients. Analysis based on the extent of lung involvement showed significantly increased 3D-derived right ventricular volumes in patients who experienced severe pneumonia despite normalized strains. Conclusion: subclinical LV dysfunction as reduced stroke volume index and GLS exists in the early recovery phase of normal individuals with severe course of covid-19. LA function indicated by LA strains paradoxically increases in severe covid-19 infection in this phase.
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Introduction: After solid organ transplantation, patients require lifelong immunosuppressive medication, increasing susceptibility to COVID-19. We evaluated the clinical outcomes of heart transplant recipients in patients with COVID-19. Methods: We enrolled twenty-two COVID-19 cases of adult heart transplantation from February 2020 to September 2021. Results: The most common symptoms in patients were fever and myalgia. The death occurred in 3 (13.6 %). Conclusion: Although heart transplantation mortality may increase in the acute rejection phase concomitant with COVID-19, immunosuppressive dose reduction may not be necessary for all heart transplant patients with COVID-19.
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It has been shown that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), by coronavirus disease 2019 (COVID-19), can lead to multi-organ impairment including cardiac involvement and immunological problems. Acute myocarditis is one of serious and fatal complications of COVID-19. In this case report, we present a 46-year-old lady with a history of lichen planus dermatitis who has developed a rapidly progressive heart failure after an episode of COVID-19. The pathologic examination of her endomyocardial biopsy specimens was compatible with GCM, and she was successfully treated with a combined immunosuppressive therapy regimen.
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Different cardiovascular presentations of coronavirus disease 2019 can be seen because of the systemic involvement. Considering its new presentations, there is need for further studies regarding the mechanistic pathways involved.
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The novel coronavirus disease 2019 (COVID-19) pandemic has spread worldwide, and finding a safe therapeutic strategy and effective vaccine is critical to overcoming severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Therefore, elucidation of pathogenesis mechanisms, especially entry routes of SARS-CoV-2 may help propose antiviral drugs and novel vaccines. Several receptors have been demonstrated for the interaction of spike (S) protein of SARS-CoV-2 with host cells, including angiotensin-converting enzyme (ACE2), ephrin ligands and Eph receptors, neuropilin 1 (NRP-1), P2X7, and CD147. The expression of these entry receptors in the central nervous system (CNS) may make the CNS prone to SARS-CoV-2 invasion, leading to neurodegenerative diseases. The present review provides potential pathological mechanisms of SARS-CoV-2 infection in the CNS, including entry receptors and cytokines involved in neuroinflammatory conditions. Moreover, it explains several neurodegenerative disorders associated with COVID-19. Finally, we suggest inflammasome and JaK inhibitors as potential therapeutic strategies for neurodegenerative diseases.
Assuntos
Tratamento Farmacológico da COVID-19 , Sistema Nervoso Central/efeitos dos fármacos , Inflamassomos/efeitos dos fármacos , Doenças Neurodegenerativas/tratamento farmacológico , Receptores Virais/genética , SARS-CoV-2/efeitos dos fármacos , Internalização do Vírus/efeitos dos fármacos , Enzima de Conversão de Angiotensina 2/genética , Enzima de Conversão de Angiotensina 2/metabolismo , Antivirais/uso terapêutico , Basigina/genética , Basigina/metabolismo , COVID-19/genética , COVID-19/metabolismo , COVID-19/virologia , Sistema Nervoso Central/metabolismo , Sistema Nervoso Central/virologia , Efrinas/genética , Efrinas/metabolismo , Regulação da Expressão Gênica , Interações Hospedeiro-Patógeno/efeitos dos fármacos , Interações Hospedeiro-Patógeno/genética , Humanos , Fatores Imunológicos/uso terapêutico , Inflamassomos/genética , Inflamassomos/metabolismo , Inibidores de Janus Quinases/uso terapêutico , Janus Quinases/antagonistas & inibidores , Janus Quinases/genética , Janus Quinases/metabolismo , Doenças Neurodegenerativas/genética , Doenças Neurodegenerativas/metabolismo , Doenças Neurodegenerativas/virologia , Neuropilina-1/genética , Neuropilina-1/metabolismo , Receptores Purinérgicos P2X7/genética , Receptores Purinérgicos P2X7/metabolismo , Receptores Virais/antagonistas & inibidores , Receptores Virais/metabolismo , SARS-CoV-2/genética , SARS-CoV-2/metabolismo , SARS-CoV-2/patogenicidade , Transdução de SinaisRESUMO
Detection of viruses like HHV-6 in endomyocardial biopsy or serum serology of patients with myocarditis or heart failure features unresponsive to conventional heart failure therapies could be a potential targeted treatment especially in refractory cases.
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After the advent of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the outbreak of coronavirus disease 2019 (COVID-19) commenced across the world. Understanding the Immunopathogenesis of COVID-19 is essential for interrupting viral infectivity and preventing aberrant immune responses before a vaccine can be developed. In this review, we provide the latest insights into the roles of angiotensin-converting enzyme II (ACE2) and Ang II receptor-1 (AT1-R) in this disease. Novel therapeutic strategies, including recombinant ACE2, ACE inhibitors, AT1-R blockers, and Ang 1-7 peptides, may prevent or reduce viruses-induced pulmonary, cardiac, and renal injuries. However, more studies are needed to clarify the efficacy of these therapeutics. Furthermore, considering the common role of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway in AT1-R expressed on peripheral tissues and cytokine receptors on the surface of immune cells, potential targeting of this pathway using JAK inhibitors (JAKinibs) is suggested as a promising approach in patients with COVID-19 who are admitted to hospitals. In addition to antiviral therapy, potential ACE2- and AT1-R-inhibiting strategies, and other supportive care, we suggest other potential JAKinibs and novel anti-inflammatory combination therapies that affect the JAK-STAT pathway in patients with COVID-19. Since the combination of MTX and baricitinib leads to outstanding clinical outcomes, the addition of baricitinib to MTX might be a potential strategy.
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Angiotensina I/uso terapêutico , Inibidores da Enzima Conversora de Angiotensina/uso terapêutico , Antivirais/uso terapêutico , Azetidinas/uso terapêutico , Infecções por Coronavirus/tratamento farmacológico , Janus Quinases/genética , Metotrexato/uso terapêutico , Pandemias , Fragmentos de Peptídeos/uso terapêutico , Pneumonia Viral/tratamento farmacológico , Sulfonamidas/uso terapêutico , Enzima de Conversão de Angiotensina 2 , Betacoronavirus/efeitos dos fármacos , Betacoronavirus/imunologia , Betacoronavirus/patogenicidade , COVID-19 , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/virologia , Progressão da Doença , Regulação da Expressão Gênica , Interações Hospedeiro-Patógeno/genética , Interações Hospedeiro-Patógeno/imunologia , Humanos , Janus Quinases/antagonistas & inibidores , Janus Quinases/imunologia , Terapia de Alvo Molecular/métodos , Peptidil Dipeptidase A/genética , Peptidil Dipeptidase A/imunologia , Pneumonia Viral/epidemiologia , Pneumonia Viral/imunologia , Pneumonia Viral/virologia , Purinas , Pirazóis , Receptor Tipo 1 de Angiotensina/genética , Receptor Tipo 1 de Angiotensina/imunologia , SARS-CoV-2 , Fatores de Transcrição STAT/antagonistas & inibidores , Fatores de Transcrição STAT/genética , Fatores de Transcrição STAT/imunologia , Transdução de Sinais/genética , Transdução de Sinais/imunologiaRESUMO
Corona virus disease 2019(COVID-19) pandemic has caused a significant burden on the global health system. Considerable cardiovascular involvement has been reported among COVID-19 patients with higher ICU admission and mortality rates among patients with cardiovascular comorbidities. Consequently, diagnostic cardiovascular evaluations such as echocardiography are a crucial part of the disease management. On the other hand, providing safety for the patients and the healthcare personnel is a matter of great concern in the pandemic state. In this document, we have provided recommendations on performing echocardiography in hospital echocardiography labs and outpatient echocardiography clinics during the current COVID-19 (Coronavirus disease of 2019) outbreak.