Fulminant micro and macroangiopathic sequalae in a patient with COVID-19.
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ABSTRACT:
SUBMITTER: Bhandari SS
PROVIDER: S-EPMC7717199 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundA high proportion of COVID-19 patients were reported to have cardiac involvements. Data pertaining to cardiac sequalae is of urgent importance to define subsequent cardiac surveillance.MethodsWe performed a systematic cardiac screening for 97 consecutive COVID-19 survivors including electrocardiogram (ECG), echocardiography, serum troponin and NT-proBNP assay 1-4 weeks after hospital discharge. Treadmill exercise test and cardiac magnetic resonance imaging (CMR) were performed according to initial screening results.ResultsThe mean age was 46.5 ± 18.6 years; 53.6% were men. All were classified with non-severe disease without overt cardiac manifestations and did not require intensive care. Median hospitalization stay was 17 days and median duration from discharge to screening was 11 days. Cardiac abnormalities were detected in 42.3% including sinus bradycardia (29.9%), newly detected T-wave abnormality (8.2%), elevated troponin level (6.2%), newly detected atrial fibrillation (1.0%), and newly detected left ventricular systolic dysfunction with elevated NT-proBNP level (1.0%). Significant sinus bradycardia with heart rate below 50 bpm was detected in 7.2% COVID-19 survivors, which appeared to be self-limiting and recovered over time. For COVID-19 survivors with persistent elevation of troponin level after discharge or newly detected T wave abnormality, echocardiography and CMR did not reveal any evidence of infarct, myocarditis, or left ventricular systolic dysfunction.ConclusionCardiac abnormality is common amongst COVID-survivors with mild disease, which is mostly self-limiting. Nonetheless, cardiac surveillance in form of ECG and/or serum biomarkers may be advisable to detect more severe cardiac involvement including atrial fibrillation and left ventricular dysfunction.
| S-EPMC7877588 | biostudies-literature
Project description:BackgroundFulminant myocarditis is a catastrophic disease with high mortality and complications. A viral aetiology is frequent and the implication of SARS-CoV-2 is not yet known.Case summaryA 38-year-old woman who recently arrived from Spain presented with palpitations that started suddenly 3 days prior to presentation and were associated with haemodynamic instability, without dyspnoea or chest pain. We found features of myopericarditis on the electrocardiogram and severe systolic dysfunction on the echocardiogram. The chest tomography showed findings which suggested COVID-19 infection, and PCR for SARS-CoV-2 was positive. The cardiac magnetic resonance image showed Lake Louise criteria for myocarditis. The patient was treated with immunomodulatory, steroid, and immunoglobulin therapy, with a favourable clinical response.DiscussionThe importance of this case lies in highlighting the severe cardiac involvement in a young patient, without previous risk factors, positive for COVID-19, and the favourable response to the medical treatment given.
| S-EPMC7454494 | biostudies-literature
Project description:To investigate the role of gene expression in patients with COVID-19. Full article available at DOI: 10.1136/bmjopen-2020-044497.
2023-01-30 | GSE217948 | GEO
Project description:Proteomics analysis of exosomes isolated from four temporal phases of COVID-19
2021-05-19 | PXD026091 | Pride
Project description:BackgroundCoronavirus disease 2019 (COVID-19) spreading from Wuhan, Hubei province in China, is an expanding global pandemic with significant morbidity and mortality. Even though respiratory failure is the cardinal form of severe COVID-19, concomitant cardiac involvement is common. Myocarditis is a challenging diagnosis due to heterogeneity of clinical presentation, ranging from mild symptoms to fatal arrhythmia and cardiogenic shock (CS). The aetiology is often viral and endomyocardial biopsy (EMB) is the gold standard for definite myocarditis. However, the diagnosis is often made on medical history, clinical presentation, magnetic resonance imaging, and blood tests.Case summaryWe present a 43-year-old man with mixed connective tissue disease treated with hydroxychloroquine who rapidly developed CS 4 days from symptom onset with fever and cough, showing positive polymerase chain reaction nasopharyngeal swab for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA. While computed tomography of the thorax was normal, high-sensitivity troponin T was elevated and electrocardiogram showed diffuse ST elevation and low voltage as signs of myocardial oedema. Echocardiography showed severe depression of left ventricular function. The myocardium recovered completely after a week with mechanical circulatory support (MCS). EMB was performed but could neither identify the virus in the cardiomyocytes, nor signs of inflammation. Still the most probable aetiology of CS in this case is myocarditis as a sole symptom of COVID-19.DiscussionCOVID-19 patients in need of hospitalization present commonly with respiratory manifestations. We present the first case of fulminant myocarditis rapidly progressing to CS in a COVID-19 patient without respiratory failure, successfully treated with inotropes and MCS.
| S-EPMC7799209 | biostudies-literature
Project description:Purpose of reviewCOVID-19 impacts multiple organ systems and is associated with high rates of morbidity and mortality. Pathogenesis of viral infection, co-morbidities, medical treatments, and psychosocial factors may contribute to COVID-19 related neuropsychological and psychiatric sequelae. This systematic review aims to synthesize available literature on psychiatric and cognitive characteristics of community-dwelling survivors of COVID-19 infection.Recent findingsThirty-three studies met inclusion/exclusion criteria for review. Emerging findings link COVID-19 to cognitive deficits, particularly attention, executive function, and memory. Psychiatric symptoms occur at high rates in COVID-19 survivors, including anxiety, depression, fatigue, sleep disruption, and to a lesser extent posttraumatic stress. Symptoms appear to endure, and severity of acute illness is not directly predictive of severity of cognitive or mental health issues. The course of cognitive and psychiatric sequelae is limited by lack of longitudinal data at this time. Although heterogeneity of study design and sociocultural differences limit definitive conclusions, emerging risk factors for psychiatric symptoms include female sex, perceived stigma related to COVID-19, infection of a family member, social isolation, and prior psychiatry history.SummaryThe extant literature elucidates treatment targets for cognitive and psychosocial interventions. Research using longitudinal, prospective study designs is needed to characterize cognitive and psychiatric functioning of COVID-19 survivors over the course of illness and across illness severity. Emphasis on delineating the unique contributions of premorbid functioning, viral infection, co-morbidities, treatments, and psychosocial factors to cognitive and psychiatric sequelae of COVID-19 is warranted.
| S-EPMC8183238 | biostudies-literature
Project description:We describe the first case report of fulminant myocarditis and complete heart block which was initially presented by severe systolic dysfunction and tachyarrhythmia, in a patient who recently recovered from covid-19. Continuous close follow-up should be considered for patients infected with COVID-19 after discharge, especially for those with any metabolic and pharmacologic risk factors for the conductive block to recognize these rare complications and reverse CHB early by administering a high dose of corticosteroid or other anti-inflammatory medications. <Learning objective: To illustrate the presentation of COVID-19 fulminant myocarditis by severe systolic dysfunction, tachyarrhythmia, and different degrees of atrioventricular block. To introduce the proper management of fulminant myocarditis in a patient who recently recovered from covid-19.>.
| S-EPMC8057742 | biostudies-literature
Project description:BackgroundAdults who have been infected with SARS-CoV-2 can develop a multisystem inflammatory syndrome (MIS-A), including fulminant myocarditis. Yet, several patients fail to meet MIS-A criteria, suggesting the existence of distinct phenotypes in fulminant COVID-19-related myocarditis.ObjectivesThis study sought to compare the characteristics and clinical outcome between patients with fulminant COVID-19-related myocarditis fulfilling MIS-A criteria (MIS-A+) or not (MIS-A-).MethodsA monocentric retrospective analysis of consecutive fulminant COVID-19-related myocarditis in a 26-bed intensive care unit (ICU).ResultsBetween March 2020 and June 2021, 38 patients required ICU admission (male 66%; mean age 32 ± 15 years) for suspected fulminant COVID-19-related myocarditis. In-ICU treatment for organ failure included dobutamine 79%, norepinephrine 60%, mechanical ventilation 50%, venoarterial extracorporeal membrane oxygenation 42%, and renal replacement therapy 29%. In-hospital mortality was 13%. Twenty-five patients (66%) met the MIS-A criteria. MIS-A- patients compared with MIS-A+ patients were characterized by a shorter delay between COVID-19 symptoms onset and myocarditis, a lower left ventricular ejection fraction, and a higher rate of in-ICU organ failure, and were more likely to require mechanical circulatory support with venoarterial extracorporeal membrane oxygenation (92% vs 16%; P < 0.0001). In-hospital mortality was higher in MIS-A- patients (31% vs 4%). MIS-A+ had higher circulating levels of interleukin (IL)-22, IL-17, and tumor necrosis factor-α (TNF-α), whereas MIS-A- had higher interferon-α2 (IFN-α2) and IL-8 levels. RNA polymerase III autoantibodies were present in 7 of 13 MIS-A- patients (54%) but in none of the MIS-A+ patients.ConclusionMIS-A+ and MIS-A- fulminant COVID-19-related myocarditis patients have 2 distinct phenotypes with different clinical presentations, prognosis, and immunological profiles. Differentiating these 2 phenotypes is relevant for patients' management and further understanding of their pathophysiology.
| S-EPMC9291241 | biostudies-literature
Project description:BackgroundCoronavirus Disease 2019 (COVID-19) can lead to the development of acute respiratory distress syndrome (ARDS). In some patients with non-resolvable (NR) COVID-19, lung injury can progress rapidly to the point that lung transplantation is the only viable option for survival. This fatal progression of lung injury involves a rapid fibroproliferative response and takes on average 15 weeks from initial symptom presentation. Little is known about the mechanisms that lead to this fulminant lung fibrosis (FLF) in NR-COVID-19.MethodsUsing a pre-designed unbiased PCR array for fibrotic markers, we analyzed the fibrotic signature in a subset of NR-COVID-19 lungs. We compared the expression profile against control lungs (donor lungs discarded for transplantation), and explanted tissue from patients with idiopathic pulmonary fibrosis (IPF). Subsequently, RT-qPCR, Western blots and immunohistochemistry were conducted to validate and localize selected pro-fibrotic targets. A total of 23 NR-COVID-19 lungs were used for RT-qPCR validation.FindingsWe revealed a unique fibrotic gene signature in NR-COVID-19 that is dominated by a hyper-expression of pro-fibrotic genes, including collagens and periostin. Our results also show a significantly increased expression of Collagen Triple Helix Repeat Containing 1(CTHRC1) which co-localized in areas rich in alpha smooth muscle expression, denoting myofibroblasts. We also show a significant increase in cytokeratin (KRT) 5 and 8 expressing cells adjacent to fibroblastic areas and in areas of apparent epithelial bronchiolization.InterpretationOur studies may provide insights into potential cellular mechanisms that lead to a fulminant presentation of lung fibrosis in NR-COVID-19.FundingNational Institute of Health (NIH) Grants R01HL154720, R01DK122796, R01DK109574, R01HL133900, and Department of Defense (DoD) Grant W81XWH2110032 to H.K.E. NIH Grants: R01HL138510 and R01HL157100, DoD Grant W81XWH-19-1-0007, and American Heart Association Grant: 18IPA34170220 to H.K.-Q. American Heart Association: 19CDA34660279, American Lung Association: CA-622265, Parker B. Francis Fellowship, 1UL1TR003167-01 and The Center for Clinical and Translational Sciences, McGovern Medical School to X.Y.
| S-EPMC9667270 | biostudies-literature
Project description:The contribution of neurological symptomatology to morbidity and mortality after infection with Severe Acute Respiratory Syndrome-associated Coronavirus (SARS CoV II) is ill-defined. We hereby present a case of a 57-year old male patient, in excellent physical condition, who was admitted to the Intensive Care Unit (ICU), with respiratory distress duo to SARS CoV II-induced bilateral pneumonia. After 2 weeks at the ICU, with respiratory conditions improving, the patient developed lethal cerebral edema. This case advocates regular wake-up calls in Coronavirus disease 2019 patients for neurological (radiological) evaluation to provide rapid diagnosis and a therapeutic window for fulminant central nervous system complications.
| S-EPMC7332918 | biostudies-literature