Myocarditis, paraparesia and ARDS associated to COVID-19 infection
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ABSTRACT:
SUBMITTER: Jeantin L
PROVIDER: S-EPMC7571901 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:We present the case of a 20-year-old male patient without previous history of cardiovascular disease who was admitted to our hospital with a new onset febrile sensation and chest pain. Chest computed tomography revealed a subpleural consolidation with a halo of ground-glass opacification. Blood tests revealed elevated levels of markers of myocyte necrosis (troponin I and creatine kinase-MB). Nasopharyngeal swab was positive for COVID-19. Cardiac MRI showed myocardial edema and late gadolinium enhancement compatible with myocarditis associated with COVID-19 infection. This case showed that acute myocarditis can be the initial presentation of patients with COVID-19 infection.
| S-EPMC7265842 | biostudies-literature
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| S-BSST563 | biostudies-other
Project description:Introduction and importanceSince COVID 19 was described for the first time in December 2019, we have not stopped discovering its different clinical manifestations. Despite the respiratory complication which is the most common symptomatology, multi-organ dysfunction and multiple cardiovascular complications were described such as acute myocarditis, heart failure and even arrhythmias.Cases presentationTwo patients aged 26 and 56 year-old, developed acute myocarditis related to Covid-19 infection but with different symptomatology.Case 1Presented to the emergency room with digestive symptomatology, Covid-19 infection was confirmed by a positive chest CT scan and positive COVID-19 serology testing. Clinical, biological, radiological findings allowed making the diagnosis of a Covid-19 infection with a bacterial superinfection complicated by a fulminant myocarditis.Case 2Presented to the emergency department with a chest pain, dyspnoea, paroxistic cough, myalgia and fever. A Covid-19 infection was confirmed. The electrocardiogram showed a diffuse ST elevation, echocardiography showed normal systolic function and the high-sensitivity cardiac troponin I level was high. Invasive coronary angiography was performed, revealing angiographically normal coronary arteries.Clinical discussionOur 2 cases were treated differently, case 1 received antibiotherapy because of the bacterial superinfection and inotropic support for the septic and cardiogenic choc. Contrarily to case 2 who received inotropic support, immunoglobulin and corticosteroid. With a total recovery for both patients.ConclusionThis article can help in considering cardiac affection due to SARS-CoV2, even with poor respiratory symptomatology, and to insist on the importance of the cardiac evaluation for young patients with a sever Covid-19 infection.
| S-EPMC8152366 | biostudies-literature
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| S-EPMC8453875 | biostudies-literature
Project description:SARS-CoV-2 is a novel coronavirus that causes acute respiratory distress syndrome (ARDS), death and long-term sequelae. Innate immune cells are critical for host defense but are also the primary drivers of ARDS. The relationships between innate cellular responses in ARDS resulting from COVID-19 compared to other causes of ARDS, such as bacterial sepsis is unclear. Moreover, the beneficial effects of dexamethasone therapy during severe COVID-19 remain speculative, but understanding the mechanistic effects could improve evidence-based therapeutic interventions. To interrogate these relationships, we developed an scRNAseq atlas that is freely accessible (biernaskielab.ca/COVID_neutrophil). We discovered that compared to bacterial ARDS, COVID-19 was associated with distinct neutrophil polarization characterized by either interferon (IFN) or prostaglandin (PG) active states. Neutrophils from bacterial ARDS had higher expression of antibacterial molecules such as PLAC8 and CD83. Dexamethasone therapy in COVID patients rapidly altered the IFNactive state, downregulated interferon responsive genes, and activated IL1R2+ve neutrophils. Dexamethasone also induced the emergence of immature neutrophils expressing immunosuppressive molecules ARG1 and ANXA1, which were not present in healthy controls. Moreover, dexamethasone remodeled global cellular interactions by changing neutrophils from information receivers into information providers. Importantly, male patients had higher proportions of IFNactive neutrophils and a greater degree of steroid-induced immature neutrophil expansion. Indeed, the highest proportion of IFNactive neutrophils was associated with mortality. These results define neutrophil states unique to COVID-19 when contextualized to other life-threatening infections, thereby enhancing the relevance of our findings at the bedside. Furthermore, the molecular benefits of dexamethasone therapy are also defined. The identified molecular pathways can now be targeted to develop improved therapeutics.
2021-10-05 | PXD028429 | Pride
Project description:BackgroundIn late 2019, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which is responsible for coronavirus disease (COVID-19), was identified as the new pathogen to lead pneumonia in Wuhan, China, which has spread all over the world and developed into a pandemic. Despite the over 1 year of pandemic, due to the lack of an effective treatment plan, the morbidity and mortality of COVID-19 remains high. Efforts are underway to find the optimal management for this viral disease.Main bodySARS-CoV-2 could simultaneously affect multiple organs with variable degrees of severity, from mild to critical disease. Overproduction of pro-inflammatory mediators, exacerbated cellular and humoral immune responses, and coagulopathy such as Pulmonary Intravascular Coagulopathy (PIC) contributes to cell injuries. Considering the pathophysiology of the disease and multiple microthrombi developments in COVID-19, thrombolytic medications seem to play a role in the management of the disease. Beyond the anticoagulation, the exact role of thrombolytic medications in the management of patients with COVID-19-associated acute respiratory distress syndrome (ARDS) is not explicit. This review focuses on current progress in underlying mechanisms of COVID-19-associated pulmonary intravascular coagulopathy, the historical use of thrombolytic drugs in the management of ARDS, and pharmacotherapy considerations of thrombolytic therapy, their possible benefits, and pitfalls in COVID-19-associated ARDS.ConclusionsInhaled or intravenous administration of thrombolytics appears to be a salvage therapy for severe ARDS associated with COVID-19 by prompt attenuation of lung injury. Considering the pathogenesis of COVID-19-related ARDS and mechanism of action of thrombolytic agents, thrombolytics appear attractive options in stable patients without contraindications.
| S-EPMC9338522 | biostudies-literature
Project description:The coronavirus disease 2019 (COVID-19) vaccination frequently leads to minor side-effects, that may be more intense after the second dose, but more serious side effects have been reported. We report a case of a 24-year-old man who presented to the hospital with acute substernal chest pain, 4 days after his second COVID-19 Moderna vaccination. Laboratory studies revealed elevated troponins and negative viral serologies. Cardiac magnetic resonance imaging (cMRI) demonstrated edema and delayed gadolinium enhancement of the left ventricle in a midmyocardial and epicardial distribution. The patient was diagnosed with myocarditis following Moderna vaccination. Our case report raises concern that myocarditis is a rare side effect of COVID-19 vaccine. Despite our report, it appears that there is a significantly higher risk of cardiac involvement from COVID-19 infection compared to COVID-19 vaccination.
| S-EPMC8130498 | biostudies-literature
Project description:The SARS-CoV-2 Delta (B.1.617.2) variant is capable of infecting vaccinated persons. An open question remains as to whether deficiencies in specific vaccine-elicited immune responses result in susceptibility to vaccine breakthrough infection. We investigated 55 vaccine breakthrough infection cases (mostly Delta) in Singapore, comparing them against 86 vaccinated close contacts who did not contract infection. Vaccine breakthrough cases showed lower memory B cell frequencies against SARS-CoV-2 receptor binding domain (RBD). Compared to plasma antibodies, antibodies secreted by memory B cells retained a higher fraction of neutralizing properties against the Delta variant. Inflammatory cytokines including IL-1β and TNF were lower in vaccine breakthrough infections than primary infection of similar disease severity, underscoring the usefulness of vaccination in preventing inflammation. This report highlights the importance of memory B cells against vaccine breakthrough, and suggests that lower memory B cell levels may be a correlate of risk for Delta vaccine breakthrough infection.
| S-SCDT-EMM-2021-15227 | biostudies-other
Project description:Various clinical presentations of the 2019 coronavirus disease (COVID-19) have been described, including post-infectious acute and fulminant myocarditis. Here, we describe the case of a young patient admitted for COVID-19-associated post-infectious fulminant myocarditis. Despite optimal pharmacologic management, haemodynamic status worsened requiring support by veno-arterial extracorporeal membrane oxygenation. Emergent heart transplantation was required at Day 11 given the absence of cardiac function improvement. The diagnosis of post-infectious COVID-19-associated myocarditis was made from both pathologic examination of the explanted heart and positive SARS-CoV-2 serology.
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Project description: Not available
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