Post-mortem differential diagnosis from COVID-19: A case of fulminant myocarditis HHV-6 related.
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SUBMITTER: Colombo D
PROVIDER: S-EPMC8661597 | biostudies-literature |
REPOSITORIES: biostudies-literature
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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
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| S-EPMC4683890 | biostudies-literature
Project description:Fulminant myocarditis (FM) is a severe disease with a rapidly progressive and life-threatening course caused mainly by viral infection. The symptoms, laboratory findings, and presence of ECG changes resemble acute coronary syndrome. Therefore, coronary angiography is usually helpful in making the appropriate diagnosis. However, failure to obtain complete coronary artery images due to coronary artery anatomic variations poses a challenge for the diagnosis of FM. Here, we report a case of FM preliminarily diagnosed as acute coronary syndrome (ACS) due to the presence of coronary artery anomaly.
| S-EPMC8669105 | biostudies-literature
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.
| S-EPMC8239812 | 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:BACKGROUND:Coronavirus disease 2019 (COVID-19) has been demonstrated to be the cause of pneumonia. Nevertheless, it has not been reported as the cause of acute myocarditis or fulminant myocarditis. CASE PRESENTATION:A 63-year-old male was admitted with pneumonia and cardiac symptoms. He was genetically confirmed as having COVID-19 according to sputum testing on the day of admission. He also had elevated troponin I (Trop I) level (up to 11.37 g/L) and diffuse myocardial dyskinesia along with a decreased left ventricular ejection fraction (LVEF) on echocardiography. The highest level of interleukin-6 was 272.40 pg/ml. Bedside chest radiographs showed typical ground-glass changes indicative of viral pneumonia. Laboratory test results for viruses that cause myocarditis were all negative. The patient conformed to the diagnostic criteria of the Chinese expert consensus statement for fulminant myocarditis. After receiving antiviral therapy and mechanical life support, Trop I was reduced to 0.10 g/L, and interleukin-6 was reduced to 7.63 pg/mL. Moreover, the LVEF of the patient gradually recovered to 68%. The patient died of aggravation of secondary infection on the 33rd day of hospitalization. CONCLUSION:COVID-19 patients may develop severe cardiac complications such as myocarditis and heart failure. This is the first report of COVID-19 complicated with fulminant myocarditis. The mechanism of cardiac pathology caused by COVID-19 needs further study.
| S-EPMC7146072 | biostudies-literature
Project description:Necrotizing eosinophilic myocarditis is a rare but potentially fatal condition that requires prompt recognition and treatment. We describe a case of a young athlete presenting with chest pain and breathlessness, with evidence of rapidly deteriorating cardiac function. The condition was successfully treated with corticosteroids, with no evidence of residual myocardial damage. This is the first reported case to demonstrate the utility of cardiac magnetic resonance imaging for diagnosis and monitoring response to treatment. It also highlights the value of endomyocardial biopsy in establishing a tissue diagnosis in cases of fulminant myocarditis, in order to direct treatment appropriately.
| S-EPMC5695162 | biostudies-other
Project description:BackgroundWhilst myocarditis or myocardial injury due to severe acute respiratory syndrome coronavirus 2 infection is commonly reported, profound primary cardiac dysfunction requiring mechanical circulatory support, with the development of fulminant myocarditis prior to respiratory failure, is rarely described. The endomyocardial biopsy (EMB) findings in these patients is seldom reported, the findings are varied, and effective treatment unknown.Case summaryA 39-year-old female with no significant past medical history and confirmed Delta variant coronavirus disease 2019 (COVID-19) infection (Day 3), presented with a 1 day history of diarrhoea, vomiting, and abdominal pain. The patient denied respiratory symptoms and chest X-ray was clear. Lactate level was 6.3, initial troponin T 118 ng/L. Despite resuscitation, the patient significantly deteriorated in the emergency department, resulting in pulseless electrical activity arrest requiring veno-arterial extra-corporeal membrane oxygenation cardiopulmonary resuscitation. Over the following 36 h, cardiac function deteriorated to near-complete left ventricular (LV) standstill. Coronary angiography revealed normal coronary arteries with slow flow. Endomyocardial biopsy showed diffuse interstitial macrophage infiltrate and small vessel thromboses. Left ventricular function did not improve over the following 7 days, and despite treatment with tocilizumab, high-dose steroids, and intravenous immunoglobulin, she eventually died due to disease-related complications.DiscussionPrimary cardiac dysfunction secondary to COVID-19 infection is rarely reported. Little is known about the incidence, natural history, and pathophysiology of fulminant COVID-19 myocarditis. We present the most severe case of cardiac dysfunction due to COVID-19 reported in a young patient without respiratory compromise who never recovered from any cardiac function.
| S-EPMC9037826 | biostudies-literature
Project description:Fulminant myocarditis can present with life threatening arrhythmias, and cardiogenic shock due to ventricular failure. The diagnosis of myocarditis usually requires histological and immunological information, as its aetiology may be infectious (viral or non-viral), autoimmune or drug related. The treatment of fulminant myocarditis depends on the underlying cause but usually includes high dose systemic steroids as well as physiological support. Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) can be used to support patients as a bridge to recovery by supporting biventricular function and decompressing the heart. V-A ECMO carries risks and complications of its own such as thrombus formation or bleeding. Different diagnostic modalities, such as transthoracic (TTE) and transoesophageal (TOE) echocardiography, are central to the monitoring of progression of disease and recovery of heart function. This case highlights the importance of early recognition and early support with VA-ECMO in fulminant myocarditis, as well as the role of repeated echocardiography when weaning from physiological support.
| S-EPMC7424325 | biostudies-literature
Project description:AimsTo investigate cardiac pathology in critically ill patients with coronavirus disease 2019 (COVID-19) and identify associations between pathological changes and clinical characteristics.MethodsThe present autopsy cohort study included hearts from 26 deceased patients hospitalized in intensive care units due to COVID-19, and was conducted at four sites in Wuhan, China. Cases were divided into a neutrophil infiltration group and a no-neutrophil group based on the presence or absence of histopathologically identified neutrophilic infiltrates.ResultsAmong the 26 patients, histopathological examination identified active myocarditis in four patients. All patients with myocarditis exhibited extensive accompanying neutrophil infiltration, and all patients without myocarditis did not. The neutrophil infiltration group exhibited significantly higher rates of detection of interleukin-6 (100 vs. 4.6%) and tumor necrosis factor-alpha (100 vs. 31.8%) than the no-neutrophil group (both p < 0.05). On admission, four patients with neutrophil infiltration in myocardium had significantly higher baseline levels of aspartate aminotransferase, D dimer, and high-sensitivity C reactive protein than the other 22 patients (all p < 0.05). During hospitalization, patients with neutrophil infiltration had significantly higher maximum creatine kinase-MB (median 280.0 IU/L vs. 38.7 IU/L, p = 0.04) and higher troponin I (median 1.112 ng/ml vs. 0.220 ng/ml, p = 0.56) than patients without neutrophil infiltration.ConclusionActive myocarditis was frequently associated with neutrophil infiltration in the hearts of deceased patients with severe COVID-19. Patients with neutrophil-infiltrated myocarditis had a series of severely abnormal laboratory test results on admission, and high maximum creatine kinase-MB during hospitalization. The role of neutrophils in severe heart injury and systemic conditions in patients with COVID-19 should be emphasized.
| S-EPMC9614157 | biostudies-literature