[SARS-COV-2 myocarditis. An update].
Ontology highlight
ABSTRACT:
SUBMITTER: Fard D
PROVIDER: S-EPMC7543970 | biostudies-literature | 2020 Oct
REPOSITORIES: biostudies-literature
Publications
[SARS-COV-2 myocarditis. An update].
Fard D D Huguet R R Koutsoukis A A Deguillard C C Tuffreau A-S AS Deux J-F JF Lim P P Teiger E E
Annales de cardiologie et d'angeiologie 20201008 6
The outbreak of the SARS-CoV-2 virus responsible for the COVID-19 disease has given rise to a new disease whose boundaries are still to be discovered. While the first data suggested a purely respiratory infection, the most recent publications highlight a large pleomorphism of the disease, responsible for multiple organ damage, of which cardiac injury seems to be the most represented. This cardiac injury can present as acute myocarditis. Our aim was to discuss the pathophysiological rationale und ...[more]
Similar Datasets
Project description:Acute myocarditis (AM), a recent-onset inflammation of the heart, has heterogeneous clinical presentations, varying from minor symptoms to high-risk cardiac conditions with severe heart failure, refractory arrhythmias, and cardiogenic shock. AM is moving from being a definitive diagnosis based on histological evidence of inflammatory infiltrates on cardiac tissue to a working diagnosis supported by high sensitivity troponin increase in association with specific cardiac magnetic resonance imaging (CMRI) findings. Though experts still diverge between those advocating for histological definition versus those supporting a mainly clinical definition of myocarditis, in the real-world practice the diagnosis of AM has undoubtedly shifted from being mainly biopsy-based to solely CMRI-based in most of clinical scenarios. It is thus important to clearly define selected settings where EMB is a must, as information derived from histology is essential for an optimal management. As in other medical conditions, a risk-based approach should be promoted in order to identify the most severe AM cases requiring appropriate bundles of care, including early recognition, transfer to tertiary centers, aggressive circulatory supports with inotropes and mechanical devices, histologic confirmation and eventual immunosuppressive therapy. Despite improvements in recognition and treatment of AM, including a broader use of promising mechanical circulatory supports, severe forms of AM are still burdened by dismal outcomes. This review is focused on recent clinical studies and registries that shed new insights on AM. Attention will be paid to contemporary outcomes and predictors of prognosis, the emerging entity of immune checkpoint inhibitors-associated myocarditis, updated CMRI diagnostic criteria, new data on the use of temporary mechanical circulatory supports in fulminant myocarditis. The role of viruses as etiologic agents will be reviewed and a brief update on pediatric AM is also provided. Finally, we summarize a risk-based approach to AM, based on available evidence and clinical experience.
| S-EPMC7263216 | biostudies-literature
Project description: Not available
| S-BSST379 | biostudies-other
Project description:Myocarditis has been described previously as a rare side effect of both influenza and smallpox vaccines. In this report, we present a case of acute perimyocarditis in a young, healthy man after vaccination with the mRNA-1273 severe acute respiratory syndrome coronavirus -2 (SARS-CoV-2; Moderna) vaccine. He presented with chest pain and decompensated heart failure 3 days after administration of his second dose, and his symptoms resolved by 9 days post-inoculation. This case highlights a rare but potentially serious side effect of this mRNA vaccine that primary care physicians and cardiologists should be aware of in order to identify and appropriately manage these patients.
| S-EPMC8278869 | biostudies-literature
Project description:BackgroundWith limited vaccine supplies, an informed position on the status of SARS-CoV-2 infection in people can assist the prioritization of vaccine deployment.ObjectivesWe performed a systematic review and meta-analysis to estimate the global and regional SARS-CoV-2 seroprevalences around the world.Data sourcesWe systematically searched peer-reviewed databases (PubMed, Embase and Scopus), and preprint servers (medRxiv, bioRxiv and SSRN) for articles published between 1 January 2020 and 30 March 2021.Study eligibility criteriaPopulation-based studies reporting the SARS-CoV-2 seroprevalence in the general population were included.ParticipantsPeople of different age groups, occupations, educational levels, ethnic backgrounds and socio-economic status from the general population.InterventionsThere were no interventions.MethodsWe used the random-effects meta-analyses and empirical Bayesian method to estimate the pooled seroprevalence and conducted subgroup and meta-regression analyses to explore potential sources of heterogeneity as well as the relationship between seroprevalence and socio-demographics.ResultsWe identified 241 eligible studies involving 6.3 million individuals from 60 countries. The global pooled seroprevalence was 9.47% (95% CI 8.99-9.95%), although the heterogeneity among studies was significant (I2 = 99.9%). We estimated that ∼738 million people had been infected with SARS-CoV-2 (as of December 2020). Highest and lowest seroprevalences were recorded in Central and Southern Asia (22.91%, 19.11-26.72%) and Eastern and South-eastern Asia (1.62%, 1.31-1.95%), respectively. Seroprevalence estimates were higher in males, persons aged 20-50 years, in minority ethnic groups living in countries or regions with low income and human development indices.ConclusionsThe present study indicates that the majority of the world's human population was still highly susceptible to SARS-CoV-2 infection in mid-2021, emphasizing the need for vaccine deployment to vulnerable groups of people, particularly in developing countries, and for the implementation of enhanced preventive measures until 'herd immunity' to SARS-CoV-2 has developed.
| S-EPMC8548624 | biostudies-literature
Project description:Coronaviruses (CoVs) are a group of RNA viruses that are associated with different diseases in animals, birds, and humans. Human CoVs (HCoVs) have long been known to be the causative agents of mild respiratory illnesses. However, two HCoVs associated with severe respiratory diseases are Severe Acute Respiratory Syndrome-CoV (SARS-CoV) and Middle East Respiratory Syndrome-CoV (MERS-CoV). Both viruses resulted in hundreds of deaths after spreading to several countries. Most recently, SARS-CoV-2 has emerged as the third HCoV causing severe respiratory distress syndrome and viral pneumonia (known as COVID-19) in patients from Wuhan, China, in December 2019. Soon after its discovery, SARS-CoV-2 spread to all countries, resulting in millions of cases and thousands of deaths. Since the emergence of SARS-CoV, many research groups have dedicated their resources to discovering effective antivirals that can treat such life-threatening infections. The rapid spread and high fatality rate of SARS-CoV-2 necessitate the quick discovery of effective antivirals to control this outbreak. Since SARS-CoV-2 shares 79% sequence identity with SARS-CoV, several anti-SARS-CoV drugs have shown promise in limiting SARS-CoV-2 replication in vitro and in vivo. In this review, we discuss antivirals described for SARS-CoV and provide an update on therapeutic strategies and antivirals against SARS-CoV-2. The control of the current outbreak will strongly depend on the discovery of effective and safe anti-SARS-CoV-2 drugs.
| S-EPMC7350231 | biostudies-literature
Project description:ObjectiveTo investigate the association between SARS-CoV-2 vaccination and myocarditis or myopericarditis.DesignPopulation based cohort study.SettingDenmark.Participants4 931 775 individuals aged 12 years or older, followed from 1 October 2020 to 5 October 2021.Main outcome measuresThe primary outcome, myocarditis or myopericarditis, was defined as a combination of a hospital diagnosis of myocarditis or pericarditis, increased troponin levels, and a hospital stay lasting more than 24 hours. Follow-up time before vaccination was compared with follow-up time 0-28 days from the day of vaccination for both first and second doses, using Cox proportional hazards regression with age as an underlying timescale to estimate hazard ratios adjusted for sex, comorbidities, and other potential confounders.ResultsDuring follow-up, 269 participants developed myocarditis or myopericarditis, of whom 108 (40%) were 12-39 years old and 196 (73%) were male. Of 3 482 295 individuals vaccinated with BNT162b2 (Pfizer-BioNTech), 48 developed myocarditis or myopericarditis within 28 days from the vaccination date compared with unvaccinated individuals (adjusted hazard ratio 1.34 (95% confidence interval 0.90 to 2.00); absolute rate 1.4 per 100 000 vaccinated individuals within 28 days of vaccination (95% confidence interval 1.0 to 1.8)). Adjusted hazard ratios among female participants only and male participants only were 3.73 (1.82 to 7.65) and 0.82 (0.50 to 1.34), respectively, with corresponding absolute rates of 1.3 (0.8 to 1.9) and 1.5 (1.0 to 2.2) per 100 000 vaccinated individuals within 28 days of vaccination, respectively. The adjusted hazard ratio among 12-39 year olds was 1.48 (0.74 to 2.98) and the absolute rate was 1.6 (1.0 to 2.6) per 100 000 vaccinated individuals within 28 days of vaccination. Among 498 814 individuals vaccinated with mRNA-1273 (Moderna), 21 developed myocarditis or myopericarditis within 28 days from vaccination date (adjusted hazard ratio 3.92 (2.30 to 6.68); absolute rate 4.2 per 100 000 vaccinated individuals within 28 days of vaccination (2.6 to 6.4)). Adjusted hazard ratios among women only and men only were 6.33 (2.11 to 18.96) and 3.22 (1.75 to 5.93), respectively, with corresponding absolute rates of 2.0 (0.7 to 4.8) and 6.3 (3.6 to 10.2) per 100 000 vaccinated individuals within 28 days of vaccination, respectively. The adjusted hazard ratio among 12-39 year olds was 5.24 (2.47 to 11.12) and the absolute rate was 5.7 (3.3 to 9.3) per 100 000 vaccinated individuals within 28 days of vaccination.ConclusionsVaccination with mRNA-1273 was associated with a significantly increased risk of myocarditis or myopericarditis in the Danish population, primarily driven by an increased risk among individuals aged 12-39 years, while BNT162b2 vaccination was only associated with a significantly increased risk among women. However, the absolute rate of myocarditis or myopericarditis after SARS-CoV-2 mRNA vaccination was low, even in younger age groups. The benefits of SARS-CoV-2 mRNA vaccination should be taken into account when interpreting these findings. Larger multinational studies are needed to further investigate the risks of myocarditis or myopericarditis after vaccination within smaller subgroups.
| S-EPMC8683843 | biostudies-literature
Project description:BackgroundSince the start of the COVID-19 pandemic, many case reports have been presented describing different cardiac symptoms due to the SARS-CoV-2 infection. However, severe cardiac failure due to COVID-19 seems to be rare.Case summaryA 30-year-old woman presented with COVID-19 and cardiogenic shock due to a lymphocytic myocarditis. Since she deteriorated under treatment with inotropes, she was referred to our centre, and veno-arterial extracorporeal life support was started. Subsequently, the aortic valve only opened sporadically, and spontaneous contrast appeared in the left ventricle (LV), pointing towards difficulties with unloading LV. Therefore, an Impella for venting the LV was implanted. After 6 days of mechanical circulatory support, her heart function recovered. All support could be weaned, and 2 months later, she had made a full recovery.DiscussionWe presented a patient with severe cardiogenic shock due to an acute virus-negative lymphocytic myocarditis associated with a SARS-CoV-2 infection. Since the precise aetiology of SARS-CoV-2-related myocarditis remains to be elucidated and no virus could be detected in the heart, a causal relationship remains speculative.
| S-EPMC10198703 | biostudies-literature
Project description:Cases of myocarditis, diagnosed clinically by laboratory tests and imaging have been described in the context of mRNA-based anti-SARS-CoV-2 vaccination. Autopsy-based description of detailed histological features of vaccine-induced myocarditis is lacking. We describe the autopsy findings and common characteristics of myocarditis in untreated persons who received anti-SARS-CoV-2 vaccination. Standardized autopsies were performed on 25 persons who had died unexpectedly and within 20 days after anti-SARS-CoV-2 vaccination. In four patients who received a mRNA vaccination, we identified acute (epi-)myocarditis without detection of another significant disease or health constellation that may have caused an unexpected death. Histology showed patchy interstitial myocardial T-lymphocytic infiltration, predominantly of the CD4 positive subset, associated with mild myocyte damage. Overall, autopsy findings indicated death due to acute arrhythmogenic cardiac failure. Thus, myocarditis can be a potentially lethal complication following mRNA-based anti-SARS-CoV-2 vaccination. Our findings may aid in adequately diagnosing unclear cases after vaccination and in establishing a timely diagnosis in vivo, thus, providing the framework for adequate monitoring and early treatment of severe clinical cases.
| S-EPMC9702955 | biostudies-literature
Project description:ObjectivesOur objective was to examine coronary endothelial and myocardial programming in patients with severe COVID-19 utilizing digital spatial transcriptomics.BackgroundSevere acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has well-established links to thrombotic and cardiovascular events. Endothelial cell infection was initially proposed to initiate vascular events; however, this paradigm has sparked growing controversy. The significance of myocardial infection also remains unclear.MethodsAutopsy-derived cardiac tissue from control (n = 4) and COVID-19 (n = 8) patients underwent spatial transcriptomic profiling to assess differential expression patterns in myocardial and coronary vascular tissue. Our approach enabled transcriptional profiling in situ with preserved anatomy and unaltered local SARS-CoV-2 expression. In so doing, we examined the paracrine effect of SARS-CoV-2 infection in cardiac tissue.ResultsWe observed heterogeneous myocardial infection that tended to colocalize with CD31 positive cells within coronary capillaries. Despite these differences, COVID-19 patients displayed a uniform and unique myocardial transcriptional profile independent of local viral burden. Segmentation of tissues directly infected with SARS-CoV-2 showed unique, pro-inflammatory expression profiles including upregulated mediators of viral antigen presentation and immune regulation. Infected cell types appeared to primarily be capillary endothelial cells as differentially expressed genes included endothelial cell markers. However, there was limited differential expression within the endothelium of larger coronary vessels.ConclusionOur results highlight altered myocardial programming during severe COVID-19 that may in part be associated with capillary endothelial cells. However, similar patterns were not observed in larger vessels, diminishing endotheliitis, and endothelial activation as key drivers of cardiovascular events during COVID-19.
| S-EPMC10034160 | biostudies-literature
Project description:Dysregulated immune responses contribute to the excessive and uncontrolled inflammation observed in severe COVID-19. However, how immunity to SARS-CoV-2 is induced and regulated remains unclear. Here we uncover a role of the complement system in the induction of innate and adaptive immunity to SARS-CoV-2. Complement rapidly opsonizes SARS-CoV-2 particles via the lectin pathway. Complement-opsonized SARS-CoV-2 efficiently induces type-I interferon and pro-inflammatory cytokine responses via activation of dendritic cells, which are inhibited by antibodies against the complement receptors (CR) 3 and 4. Serum from COVID-19 patients, or monoclonal antibodies against SARS-CoV-2, attenuate innate and adaptive immunity induced by complement-opsonized SARS-CoV-2. Blocking of CD32, the FcγRII antibody receptor of dendritic cells, restores complement-induced immunity. These results suggest that opsonization of SARS-CoV-2 by complement is involved in the induction of innate and adaptive immunity to SARS-CoV-2 in the acute phase of infection. Subsequent antibody responses limit inflammation and restore immune homeostasis. These findings suggest that dysregulation of the complement system and FcγRII signaling may contribute to severe COVID-19.
| S-SCDT-10_1038-S44318-024-00061-0 | biostudies-other