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Aims: Myocardial calcification is an unusual condition in which excess calcium is deposited in the myocardium. Herein, we report two cases of myocardial calcification from our clinical experience. Furthermore, we conduct a systematic review to examine the clinical course and associated pathologies of myocardial calcification. Methods and results: This systematic review was registered in PROSPERO (CRD42023463285). PubMed and Scopus were searched according to the following inclusion criteria: (i) case reports or case series describing patients with myocardial calcification; (ii) diagnosis of myocardial calcification by computed tomography (CT); (iii) adequate description of patients, including their chief complaint, medical history, evaluations, and treatments; and (iv) publication in English. Among the 75 patients, 24 had sepsis, 14 had myocarditis, and 37 had other pathologies. The mortality rate was 33% for patients with sepsis, 14% for patients with myocarditis, and 11% for patients with other pathologies. Follow-up CT findings beyond 2 years were reported in six patients, showing that the CT findings of myocardial calcification persisted but subsided over time. Autopsy was performed in seven patients, and extensive interstitial fibrosis and collection of inflammatory cells were observed in patients with myocarditis, sepsis, and ischaemic heart disease. Conclusion: While various medical conditions can cause myocardial calcification, accompanying conditions commonly reported with myocardial calcification were sepsis and myocarditis. The CT findings of myocardial calcification tend to regress over time if the underlying disease can be treated.
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Immune checkpoint inhibitors (ICIs) improve the outcomes of several types of cancer. However, they are also associated with various immune-related adverse events including myocarditis. ICI-induced myocarditis is a rare, potentially life-threatening adverse event. We herein report two cases of corticosteroid-refractory ICI-induced myocarditis. In both cases, additional immunosuppressive therapies, such as intravenous immunoglobulin and tacrolimus, successfully resolved myocarditis. Given the corticosteroid-refractory nature of these cases, we suggest that prompt addition of other immunosuppressive drugs to corticosteroid therapy should be considered in the treatment of ICI-induced myocarditis.
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Viral myocarditis is a serious complication of viral infections that is known to impact young adults and can result in significant cardiac issues like earlier onset of heart failure, arrhythmia, or structural heart disease if not detected and treated promptly. This is a case report focusing on a 25-year-old woman diagnosed with viral myocarditis highlighting the diagnostic difficulties it can present with due to its diverse symptoms. Following a thorough diagnostic workup and appropriate treatment, including diuretics, antibiotics, and guideline-directed medical therapy, her condition significantly improved. Early suspicion and prompt treatment are important because myocarditis can lead to long-term heart failure. This case shows the nature of the symptoms and the challenges posed by current diagnostic methods. By conducting clinical assessments and using advanced imaging techniques, the diagnosis was confirmed, leading to appropriate treatment for this patient.
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Myocarditis is a rare cardiomyocyte inflammatory process, typically caused by viruses, with potentially devastating cardiac sequalae in both competitive athletes and in the general population. Investigation into myocarditis prevalence in the Coronavirus disease 2019 (COVID-19) era suggests that infection with Severe acute respiratory syndrome coronavirus (SARS-CoV-2) is an independent risk factor for myocarditis, which is confirmed mainly through cardiovascular magnetic resonance imaging. Recent studies indicated that athletes have a decreased risk of myocarditis after recent COVID-19 infection compared to the general population. However, given the unique nature of competitive athletics with their frequent participation in high-intensity exercise, athletes possess distinct factors of susceptibility for the development of myocarditis and its subsequent severe cardiac complications (e.g., sudden cardiac death, fulminant heart failure, etc.). Under this context, this review focuses on comparing myocarditis in athletes versus non-athletes, owing special attention to the distinct clinical presentations and outcomes of myocarditis caused by different viral pathogens such as cytomegalovirus, Epstein-Barr virus, human herpesvirus-6, human immunodeficiency virus, and Parvovirus B19, both before and after the COVID-19 pandemic, as compared with SARS-CoV-2. By illustrating distinct clinical presentations and outcomes of myocarditis in athletes versus non-athletes, we also highlight the critical importance of early detection, vigilant monitoring, and effective management of viral and non-viral myocarditis in athletes and the necessity for further optimization of the return-to-play guidelines for athletes in the COVID-19 era, in order to minimize the risks for the rare but devastating cardiac fatality.
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Background: Takayasu arteritis is a large-vessel vasculitis that affects the aorta and its primary branches. Myocarditis is a rare life-threatening complication and potential diagnostic pitfall in patients with Takayasu arteritis. Case summary: A previously healthy 18-year-old woman presenting with fever, back pain, and dyspnoea was admitted to another hospital for acute hypertension (blood pressure, 230/106 mmHg) and congestive heart failure. Intravenous methylprednisolone pulse with antihypertensive and diuretic medications slightly improved her congestion. However, she developed acute kidney injury and was transferred to our hospital. Transthoracic echocardiography indicated a left ventricular ejection fraction of 45% and diffuse left ventricular hypokinesis. Doppler ultrasound test and magnetic resonance angiography revealed severe bilateral renal artery stenosis. Her diagnosis was Takayasu arteritis, and she received high-dose glucocorticoids. She required temporary haemodialysis, but 2 months after admission, her serum creatinine improved to 1.1 mg/dL without surgical or cardiovascular interventions. Although the pre-discharge test with 1.5 T cardiac magnetic resonance initially failed to diagnose myocarditis, 3 T cardiac magnetic resonance imaging revealed increased native T1 values on T1 mapping (1283-1393 ms), moderate pericardial effusion, and systolic left ventricular wall motion abnormality, indicating active myocarditis. During 6-month subcutaneous tocilizumab treatment (162 mg/week), a left ventricular ejection fraction improved to 55-60% without a relapse. Discussion: This case report highlights the benefits of early multimodal imaging tests including cardiac magnetic resonance imaging for myocarditis and renal artery involvement in Takayasu arteritis. Tocilizumab might be an efficient therapeutic option for severe acute manifestations including myocarditis in young women of reproductive age.
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Coxsackie B virus is primarily associated with fever, pharyngitis, and gastrointestinal symptoms, while myocarditis is rarely reported. We present a rare case of a 47-year-old male with a history of hypertension and obesity, who developed Coxsackie B virus-induced myositis, myocarditis, and polyarthralgia. The patient presented with worsening back pain radiating to his chest, migratory arthralgia, exertional dyspnea, and bilateral shoulder pain with arm weakness. Initial investigations revealed elevated creatinine kinase (CK) levels and troponin I, alongside a high white blood cell (WBC) count and C-reactive protein (CRP) levels. Given the patient's symptoms and uptrending troponin without EKG changes, there was a high concern for non-ST-elevation myocardial infarction (NSTEMI), leading to initial treatment with aspirin and IV heparin. However, further questioning revealed a recent sore throat and contact with an ill family member, prompting investigations for an infectious etiology. A viral panel confirmed Coxsackie B virus infection. The patient made a full recovery with supportive care. This case highlights the importance of considering viral causes, particularly the Coxsackie B virus, in patients presenting with muscle pain, cardiac symptoms, and joint pain. Comprehensive viral testing is crucial for early identification and appropriate management to prevent long-term complications. Understanding the mechanisms of Coxsackie B virus infection is essential for developing effective treatment strategies addressing both the viral infection and the inflammatory response.
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The pathogenesis of chronic active myocarditis remains unclear. A 65-year-old man underwent permanent pacemaker implantation for sick sinus syndrome and pulmonary vein isolation for paroxysmal atrial fibrillation. Four years later, the left ventricular ejection fraction decreased from 51â¯% to 35â¯%, and the apical left ventricular inferior wall developed akinesis. Isolated cardiac sarcoidosis was suspected; however, prednisolone and optimal medical therapy failed to improve the symptoms. Even after cardiac resynchronization therapy followed by atrioventricular junction ablation for untreatable atrial tachycardia, the patient died of heart failure eight years after referral. An autopsy revealed inflammatory cell infiltration accompanied by cardiac myocytolysis in both atria and ventricles. He was diagnosed with chronic active myocarditis based on pathological findings and a persistent increase in the blood high-sensitivity cardiac troponin levels before death. The myocardium around the sinus node showed extensive and severe fibrosis with mild inflammation, suggesting a chronic inflammatory phase. In contrast, the left atrium and both ventricles showed active myocardial inflammation with fibrosis, suggesting a persistently active inflammatory phase. This case demonstrated that atrial inflammation caused intractable atrial arrhythmia, while ventricular inflammation led to biventricular heart failure, and highlighted the presence of spatially and temporally heterogeneous inflammation in chronic active myocarditis. Learning objective: We describe a case of chronic active myocarditis with spatially and temporally heterogeneous lesions throughout the four cardiac chambers. Inflammatory cell infiltration was observed in both atria and ventricles. Extensive fibrosis replaced the myocardium around the sinus node, suggesting a chronic phase. The left atrium and ventricles showed active inflammation, suggesting an active phase. Atrial and ventricular inflammation led to atrial arrhythmia and heart failure, respectively.
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BACKGROUND: Clozapine-induced inflammation, such as myocarditis and pneumonia, can occur during initial titration and can be fatal. Fever is often the first sign of severe inflammation, and early detection and prevention are essential. Few studies have investigated the effects of clozapine titration speed and concomitant medication use on the risk of clozapine-induced inflammation. AIMS: We evaluated the risk factors for clozapine-associated fever, including titration speed, concomitant medication use, gender and obesity, and their impact on the risk of fever and the fever onset date. METHOD: We conducted a case-control study. The medical records of 539 Japanese participants with treatment-resistant schizophrenia at 21 hospitals in Japan who received clozapine for the first time between 2010 and 2022 were retrospectively investigated. Of these, 512 individuals were included in the analysis. Individuals were divided into three groups according to the titration rate recommended by international guidelines for East Asians: the faster titration group, the slower titration group and the ultra-slower titration group. The use of concomitant medications (such as antipsychotics, mood stabilisers, hypnotics and anxiolytics) at clozapine initiation was comprehensively investigated. Logistic regression analysis was performed to identify the explanatory variables for the risk of a fever of 37.5°C or higher lasting at least 2 days. RESULTS: Fever risk significantly increased with faster titration, male gender and concomitant use of valproic acid or quetiapine. No increased fever risk was detected with the use of other concomitant drugs, such as olanzapine, lithium or orexin receptor antagonists. Fever onset occurred significantly earlier with faster titration. Multivariate analysis identified obesity as being a factor that accelerated fever onset. CONCLUSION: A faster titration speed and concomitant treatment with valproic acid and quetiapine at clozapine initiation increased the risk of clozapine-associated fever. Clinicians should titrate clozapine with caution and consider both the titration speed and concomitant medications.
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Background: Immunotherapy with immune checkpoint inhibitors (ICIs) enhances the host immune reaction against tumour cells by inhibiting intrinsic down-regulators of the T cell-mediated immune response. Although the advent of ICIs has dramatically changed oncology, ICIs may also trigger an overactivation of T cells against non-cancerous tissues, leading to off-target immune-related adverse events (irAEs). Case summary: A 64-year-old man with a history of seven courses of atezolizumab, an ICI, for small-cell lung cancer and coronavirus disease 2019 (COVID-19) was admitted to the hospital complaining of acute chest pain. Transthoracic echocardiography showed preserved ejection fraction (EF), but electrocardiography indicated precordial ST-elevations and marked increases in biomarkers for myocardial injury were observed. Emergent cardiac catheterization showed no significant coronary stenosis. On the fifth hospital day, EF decreased to 25% and pericardial effusion occurred. Endomyocardial biopsy was immediately performed, and prednisolone (60 mg/day) was administered. Troponin I level rapidly reduced, ST changed, and EF improved. Histological examinations demonstrated CD8-predominant T lymphocytic infiltration with myocardial cell injury, consistent with irAE-myocarditis. Discussion: In irAEs, myocarditis is the most common and severe cardiac manifestation with a high mortality. Even at 20 weeks after the initial ICI treatment, irAE-myocarditis occurs and the clinical presentation may mimic ST-elevation myocardial infarction. The histopathological findings suggested the high possibility of irAE-myocarditis rather than COVID-19-induced myocarditis, but COVID-19 has possibly played a role in the development of late-onset irAE-myocarditis. This educational case implies the importance of immediate recognition of irAE even after stable ICI treatment.
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This article describes the case of a 40-year-old individual who presented with fulminant myocarditis. Initial ECG displayed sinus tachycardia with a heart rate of 117 bpm, QS complexes in leads V1-V3, ST-segment depression in leads II, III, aVF, V5-V6, and ST-segment elevation >0.2 mV in leads V1 through V3. The initial clinical assessment suggested an acute anteroseptal myocardial infarction. However, subsequent diagnostic evaluation through coronary angiography disclosed that the coronary arteries were normal. Therefore, clinicians should carefully consider the differential diagnosis between these conditions, as their management strategies differ markedly. Two hours after admission, the patient unexpectedly developed syncope. The ECG findings were consistent with the typical characteristics of bidirectional ventricular tachycardia. Our report described the appearance and morphology as well as mechanism of bidirectional ventricular tachycardia in detail. Additionally, we delineate differential diagnoses for disease that can cause bidirectional ventricular tachycardia, such as aconite poisoning, digoxin overdose, immune checkpoint inhibitor (ICI), myocardial ischemia, and hereditary channelopathies, such as catecholaminergic polymorphic ventricular tachycardia (CPVT) and Andersen-Tawil syndrome. Therefore, clinicians should recognize this ECG finding immediately and initiate appropriate treatment promptly as these measures may be vital in saving the patient's life.
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Eletrocardiografia , Humanos , Eletrocardiografia/métodos , Adulto , Diagnóstico Diferencial , Masculino , Taquicardia/diagnóstico , Taquicardia/fisiopatologia , Miocardite/diagnóstico , Miocardite/fisiopatologia , Miocardite/complicações , Taquicardia Ventricular/diagnóstico , Taquicardia Ventricular/fisiopatologiaRESUMO
Immune checkpoint inhibitors have transformed the treatment for multiple cancers and are increasingly used in recent years, but they can cause potentially life-threatening cardiac toxicity. We report a case of a 64-year-old gentleman who presented to the Emergency Department with symptoms of fatigue and breathlessness whilst receiving treatment with an immune checkpoint inhibitor, pembrolizumab, for cholangiocarcinoma. He was found to be in cardiogenic shock with an abnormal electrocardiogram and elevated cardiac troponin at presentation. Echocardiogram demonstrated severely impaired right and left ventricular function. Computed tomography pulmonary angiography and invasive coronary angiography excluded pulmonary embolism and acute myocardial infarction, respectively, and he was diagnosed with immune checkpoint inhibitor associated myocarditis. He was treated with high-dose methylprednisolone and a dobutamine infusion. Within days, his troponin and C-reactive protein levels decreased, and his left ventricular function improved. He was established on heart failure therapies and discharged from hospital 12 days later.
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Drug reaction with eosinophilia and systemic symptoms (DRESS) is a severe drug reaction characterized by skin rash, organ involvement, lymph node swelling, eosinophilia, and atypical lymphocytosis, with myocarditis being a rare but potentially fatal complication. It has been reported that in patients with cardiac involvement due to DRESS, older age and shorter periods between offending drug exposure and symptom onset are associated with mortality. We report a case of fatal DRESS-associated myocarditis in a young woman, occurring one month after drug exposure, despite intensive immunosuppressive therapy. This case report highlights the risk of mortality from DRESS-associated myocarditis even in patients lacking known risk factors.
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BACKGROUND: The association between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mRNA vaccines and myocarditis/pericarditis in the Japanese population has not been systematically investigated. This study was aimed at clarifying the association between SARS-CoV-2 mRNA vaccines (BNT162b2 and mRNA-1273) and myocarditis/pericarditis as well as influencing factors by using the Japanese Adverse Drug Event Report database. METHODS: Reporting odds ratios (RORs) and 95 % confidence intervals (95 % CIs) for the association between the vaccines and myocarditis/pericarditis were calculated using data from the database (April 2004-December 2023). Age, sex, onset time, and outcomes in symptomatic patients were evaluated. RESULTS: The total number of reports was 880,999 (myocarditis: 1846; pericarditis: 761). The adverse events associated with the vaccines included myocarditis (919 cases) and pericarditis (321 cases), with the ROR [95 % CIs] being significant for both (myocarditis: 30.51 [27.82-33.45], pericarditis: 21.99 [19.03-25.40]). Furthermore, the ROR [95 % CIs] of BNT162b2 and mRNA-1273 were 15.64 [14.15-17.28] and 54.23 [48.13-61.10], respectively, for myocarditis, and 15.78 [13.52-18.42] and 27.03 [21.58-33.87], respectively, for pericarditis. Furthermore, most cases were ≤30 years or male. The period from vaccination to onset was ≤8 days, corresponding to early failure type based on analysis using the Weibull distribution. Outcomes were recovery or remission for most cases; however, they were severe or caused death in some cases. CONCLUSION: In the Japanese population, SARS-CoV-2 mRNA vaccination was significantly associated with the onset of myocarditis/pericarditis. The influencing factors included age of ≤30 years and male. Furthermore, although most adverse events occurred early after vaccination, overall outcomes were good.
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BACKGROUND: Detecting ongoing inflammation in myocarditis patients has prognostic relevance, but there are limited data on the detection of chronic myocarditis and its differentiation from healed myocarditis. OBJECTIVES: This study sought to assess the performance of cardiac magnetic resonance (CMR) for the detection of ongoing inflammation and the discrimination of chronic myocarditis from healed myocarditis. METHODS: Consecutive patients with persistent symptoms (>30 days) suggestive of myocarditis were prospectively enrolled from a single tertiary center. All patients underwent a multiparametric 1.5-T CMR protocol including biventricular strain, T1/T2 mapping, and late gadolinium enhancement (LGE). Endomyocardial biopsy was chosen for the reference standard diagnosis. RESULTS: Among 452 consecutive patients, 103 (median age: 50 years; 66 men) had evaluable CMR and cardiopathologic reference diagnosis: 53 (51%) with chronic lymphocytic myocarditis and 50 (49%) with healed myocarditis. T2 mapping as a single parameter showed the best accuracy in detecting chronic myocarditis, if abnormal in ≥3 segments (92%; 95% CI: 85-97), and provided the best discrimination from healed myocarditis, as defined by the area under the receiver-operating characteristic curve (0.87 [95% CI: 0.79-0.93]; P < 0.001), followed by radial peak systolic strain rate of the left ventricle (0.86) and the right ventricle (0.84); T1 mapping (0.64), extracellular volume fraction (0.62), and LGE (0.57). Specificity increased when T2 mapping was combined with elevation of either troponin or C-reactive protein. CONCLUSIONS: A multiparametric CMR protocol allows detection of ongoing myocardial inflammation and discrimination of chronic myocarditis from healed myocarditis, with segmental T2 mapping and biventricular strain analysis showing higher diagnostic accuracy compared with T1 mapping, extracellular volume fraction, and LGE. The use of biomarkers (troponin or C-reactive protein) may improve specificity.
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The management of acute myocarditis (AM) is addressed in multiple clinical guidelines. We systematically reviewed current guidelines developed by national and international medical organizations on the management of AM to aid clinical practice. Publications in MEDLINE, EMBASE and Cochrane were identified between 1 January 2013 and 12 April 2024. Additionally, the websites of relevant organizations and the Guidelines International Network, Guideline Central, and NHS knowledge and library hub were reviewed. Two reviewers independently screened titles and abstracts, two reviewers assessed the rigour of guideline development, and one reviewer extracted the recommendations. Two of the three guidelines identified showed good rigour of development. Those rigorously developed agreed on the definition of AM, sampling serum troponin as part of the workflow for AM, testing for B-type natriuretic peptides in heart failure, key diagnostic imaging in the form of cardiovascular magnetic resonance, coronary angiography to exclude significant coronary disease, indications for endomyocardial biopsy (EMB), and indications for immunosuppression and advanced treatment options. Discrepancies exist in sampling creatine kinase-myocardial bound as a marker of myocardial injury, indications for EMB, and indications for immunosuppression and treatment of uncomplicated AM. Evidence is lacking for the use of 18F-Fluorodeoxyglucose Positron Emission Tomography for myocardial imaging, exercise restriction, follow-up measures and genetic testing, and there are few high-quality randomized trials to support treatment recommendations. Recommendations for management of AM in the guidelines have largely been developed from expert opinion rather than trial data.
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Hypereosinophilic syndrome (HES) is a disorder characterized by elevated levels of eosinophils, which may be associated with multi-organ involvement depending on severity. The recent diagnostic criteria for idiopathic HES require an elevated absolute eosinophil count (AEC) above 1500 cells/mcL with evidence of tissue damage. We present a case of a 37-year-old male firefighter with a purported history of eosinophilic bronchitis who was referred to the hospital with syncopal episodes and a persistent productive cough. The patient showed an AEC of 4500 cells/mcL on admission associated with high inflammatory markers. Cardiac imaging demonstrated acute myocarditis with heart failure and a reduced ejection fraction. Chest imaging was initially suggestive of community-acquired pneumonia. Workup was negative for a malignant etiology; infectious causes similarly were excluded. After a multidisciplinary evaluation, a diagnosis of idiopathic HES was made and steroids were instituted with rapid resolution of symptoms. Our case illustrates the importance of considering hypereosinophilia as a precipitating factor for acute heart failure in an otherwise healthy adult. An expeditious diagnosis can lead to early initiation of steroids to avoid progression toward multi-organ failure.
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BACKGROUND: Immune checkpoint inhibitor (ICI) myocarditis is an uncommon but potentially fatal complication of immunotherapy. Cardiac imaging is essential to make timely diagnoses as there are critical downstream implications for patients. OBJECTIVE: To determine the agreement of cardiac magnetic resonance (CMR) and 18 F-fluorodeoxyglucose Positron Emission Tomography (FDG-PET) in patients with suspected ICI myocarditis. METHODS: Patients with suspected ICI myocarditis, who underwent CMR and 18 F-FDG-PET imaging at a single cardio-oncology service from 2017 to 2023, were enrolled. CMR was performed according to recommended guidelines for assessment of myocarditis. 18 F-FDG-PET imaging was performed following 18 h carbohydrate-free fast. Imaging was analysed by independent reviewers to determine the presence or absence of ICI myocarditis. RESULTS: Twelve patients (mean age 60 ± 15 years old, 7 [58%] male) underwent both CMR and 18 F-FDG-PET imaging. Three (25%) met the 2018 Lake Louise Criteria for CMR diagnosis of myocarditis; 4 (33%) had evidence of myocardial inflammation as determined by 18 F-FDG-PET. Amongst those with positive 18 F-FDG-PET, mean standard uptake value (SUV) was 3.5 ± 1.7. There was agreement between CMR and PET in 7 cases (CMR and PET positive (n = 1), CMR and PET negative (n = 6)) and discordance in 5 cases (CMR positive and PET negative (n = 2), CMR negative and PET positive (n = 3)). CONCLUSION: Both CMR and PET provide complementary clinical information in diagnostic of ICI myocarditis. CMR informs on myocardial oedema, whilst 18 F-FDG-PET provides information on glucose metabolism reflecting monocyte and lymphocytic activity. Future studies should investigate the role of hybrid PET-CMR for the timely diagnosis of ICI myocarditis.
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OBJECTIVES: To investigate the burden of disease of myocarditis in Germany and identify similarities and differences in myocarditis with or without COVID-19. METHODS: All patients hospitalized with myocarditis in Germany were included in this nationwide retrospective analysis. Data were retrieved from the Federal Statistical Office of Germany (DESTATIS) for the years from 2007 to 2022. The primary endpoint was hospital mortality. RESULTS: A total of 88,159 patients hospitalized with myocarditis were analyzed. Annual cases increased from 5100 in 2007 to 6593 in 2022 (p < 0.001 for trend) with higher incidence during winter months. Incidence per 100,000 inhabitants was 6.2 in 2007 rising to 7.8 in 2022 (p < 0.001 for trend). Hospital mortality remained constant at an average of 2.44% (p = 0.164 for trend). From 2020 to 2022, 1547/16,229 (9.53%) patients were hospitalized with both, myocarditis and COVID-19 (incidence 0.62/100,000 inhabitants and 180/100,000 hospitalizations with COVID-19). These patients differed significantly in most patient characteristics and had a higher rate of hospital mortality compared to myocarditis without COVID-19 (12.54% vs. 2.26%, respectively, p < 0.001). CONCLUSIONS: Myocarditis hospitalizations were slowly rising over the past 16 years with hospital mortality remaining unchanged. Incidence of hospitalizations with combined myocarditis and COVID-19 was low, but hospital mortality was high.
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Myocarditis presents with a broad spectrum of clinical severity, ranging from subclinical illness to sudden death. Children with fulminant myocarditis often require inotropic or mechanical circulatory support; however, recurrent acute myocarditis is extremely rare. There is limited evidence to guide the management of recurrent acute myocarditis because the relevant literature is sparse. Here, we present a rare pediatric case of recurrent acute myocarditis. This patient experienced two episodes of fulminant myocarditis and two episodes of suspected myocarditis over an eight-year period; each episode fully resolved with preserved cardiac function. Three episodes were associated with influenza virus infection. During each episode, the electrocardiography, echocardiogram, and laboratory findings improved. Autoimmune and chronic myocarditis were not suspected because of the rapid onset of myocarditis associated with viral infection. Genetic testing by next-generation sequencing was performed; however, no underlying genetic illnesses were identified. Human leukocyte antigen genotyping was performed, and the results determined the genotype to be HLA-DQB1*0302/0303, which reports indicate might be involved in the development of myocarditis in mice or humans. The combination of these genotypes in myocardial cells may be associated with susceptibility to influenza infection or acute myocarditis. Learning objective: There is little evidence regarding susceptibility to myocarditis. We present a pediatric patient who experienced two episodes of fulminant myocarditis and two episodes of suspected myocarditis associated with influenza infection and a specific human leukocyte antigen genotype. This case highlights the importance of understanding myocarditis susceptibility.
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We report the case of a 16-year-old boy who had myopericarditis following the first dose of a selective androgen receptor modulator called Testolone ("RAD-140"). These drugs are widely abused by physically active young adults; however, the drugs' side effects, which can be life-threatening, are not well characterized.