Further investigation did not identify any precipitant of her myocarditis. She was treated with a slow steroid taper. Mechanical support was able to be discontinued after 6 days, when an echocardiogram showed recovered biventricular function. As an outpatient, she continued on standard heart failure medications and steroid taper without recurrence of her heart failure. Fulminant eosinophilic myocarditis is a very rare myocarditis mostly reported in adolescents and young adults.
It can present as cardiogenic shock, conduction disease, or acute myocardial infarction. Still other cases remain idiopathic or undefined. The characteristic histopathology of eosinophilic myocarditis is of a mixed inflammatory cell infiltrate containing prominent numbers of eosinophils without giant cells Fig ure 4.
Myocarditis - Wikipedia
Treatment is focused on timely identification of the disease, treatment of underlying etiologies or withdrawal of any causative agents, and supportive care. While recognition of eosinophilic myocarditis is improving, data regarding its recurrence, risk of future ventricular arrhythmias, and development of post-inflammatory dilated cardiomyopathy are still lacking. The differences between the three types of fulminant myocarditis are summarized in Table 1. Survival in fulminant myocarditis depends on timely identification and implementation of advanced circulatory support.
Biventricular dysfunction remains the main predictor of death or need for transplantation. Endomyocardial biopsy can be considered for those with eosinophilia and recent-onset heart failure with potential allergic reaction class IIa recommendation. Immunosuppression has a potential therapeutic role but requires further investigation before a standardized approach can be recommended. Clinicians should be suspicious for fulminant myocarditis in any patient presenting with new-onset malignant arrhythmias, conduction disease, or sudden cardiovascular collapse.
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Heart failure caused by an infection
Fulminant myocarditis, lymphocytic, giant cell, eosinophilic. The authors have no conflict of interest to declare. Received date. Accepted date.
Open in new tab Open ppt Open in new tab Open ppt Open in new tab Open ppt Small adult studies do suggest some clinical benefit from combination immunosuppression therapy, such as azathioprine in combination with steroids. Open in new tab Open ppt Fulminant eosinophilic myocarditis is a very rare myocarditis mostly reported in adolescents and young adults. Management of fulminant myocarditis: a diagnosis in search of its etiology but with therapeutic options. Curr Heart Fail Rep ; 11 — A histopathologic definition and classification. Am J Cardiovasc Pathol ; 1 :3— Diagnosis of myocarditis: Current state and future perspectives.
Int J Cardiol ; —9.
Myocarditis - pediatric
Fulminant and acute lymphocytic myocarditis: the prognostic value of clinicopathological classification. Eur Heart J ; 22 — The epidemiology of infectious myocarditis, lymphocytic myocarditis and dilated cardiomyopathy. Eur Heart J ; 16 Suppl O — Fulminant HHV-6 myocarditis in an immunocompetent adult: role of cardiac MR in a multidisciplinary approach. A fatal case of Human Herpesvirus 6 chronic myocarditis in an immunocompetent adult. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis.
Viral persistence in the myocardium is associated with progressive cardiac dysfunction. Human herpes virus 6 causing myocarditis in a fetus: an infectious cause to a congenital heart defect. As was the case in our athlete described above, myocarditis is frequently confused for a myocardial infarction based on symptoms, ECG findings and cardiac enzyme release. In this scenario, there should be a low threshold to perform a CMR to confirm the diagnosis of myocarditis. Though not as prevalent as other cardiac diseases, approximately 0. For instance, one of the earliest retrospective studies was done in Swedish orienteers who experienced SCD.
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Of the 15 men and one woman studied, myocarditis was the most common histopathological diagnosis after autopsy and most of the cases were associated with exercise. Of the total number of deaths, were related to exercise and 64 due to cardiac causes.
Exercise also seems to be associated with an increased incidence of SCD in patients with myocarditis. Clearly this is of particular concern to athletes where exercise and competitive sport is a major component of their lifestyle. The natural history of viral myocarditis appears to be characterized by an acute phase of viral replication followed by a sub-acute immune response phase and finally a chronic phase.
The chronic phase ranges from complete recovery to fulminant heart failure. It is unclear, from the available data, whether most SCDs in athletes occur early acute and sub-acute phases or late chronic phase in the disease course. As established in animal models, the mechanism of increased SCD with exercise in the early stage of disease is thought to be a result of an accelerated and progressive inflammatory response leading to an unstable myocardial substrate. This process allows for more necrosis, fibrosis, and subsequently a pro-arrhythmic myocardium. Even in models that studied non-infectious myocarditis, exercise was associated with a pronounced inflammatory response that led to structural changes in the heart.
Current guidelines in the United States recommend that athletes with a probable or definite diagnosis of recent myocarditis should not participate in competitive sports while active inflammation is present regardless of age, gender or left ventricular function Class III, LOE C.
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The duration of inflammation is variable and can take months for resolution. Athletes should undergo clinical testing with an exercise ECG, echocardiogram and Holter monitoring no less than 3 to 6 months after the initial illness class 1 LOE C. European guidelines give similar recommendations on prohibiting competitive activity for athletes; however, they mandate a 6-month restriction before the disease process should be evaluated for resolution.