Original communication

Myocarditis: A classification of 1402 cases

Medical examiners/coroners typically investigate a large number of natural deaths each year. These include sudden, unexpected deaths due to heart disease, pulmonary thromboemboli, seizures, complications of chronic alcohol use, diabetes, asthma, dementia, among many others. This chapter provides pearls and tips regarding various natural deaths that are commonly, and sometimes rarely, seen by the FP. For example, beyond an arrhythmogenic mechanism, there are several ways that hypertensive cardiovascular disease can cause death. These include ruptured aortic dissections, hypertensive strokes, and ruptured saccular (berry) aneurysms. Sudden death in athletes and in hostile situations also is explored. The workup and interpretation of pulmonary thromboemboli are reviewed.

Fungal infections of the heart occur significantly less frequently than bacterial infections, but they carry an excessively high mortality rate. Fungal endocarditis has an estimate mortality rate of ~50% while bacterial causes result in an ~18% in-hospital mortality (Murdoch et al., 2009). This article covers the cardiac involvement, particularly endocarditis and myocarditis, of common invasive fungi pathogens.

Eosinophilic myocarditis is a type of inflammatory cardiomyopathy characterized by eosinophilic infiltration into myocardial tissue. The accurate myocarditis incidence rate is difficult to determine because of the clinical limitations of an endomyocardial biopsy. The primary pathogenesis of eosinophilic myocarditis is the release of related substances by eosinophils, leading to cell membrane damage and cell destruction. However, evidence suggests that specific genes play a role in myocarditis development.As CMR imaging availability increases, the diagnosis rate of eosinophilic myocarditis will increase. The diagnosis of myocarditis mainly depends on an endocardial biopsy. Glucocorticoids can relieve patients’ symptoms, but the early use of steroids may prevent intermediate disease stage development (i.e., thrombonecrosis and fibrosis with wall thrombosis). Anticoagulant therapy may also affect disease development. In addition to routine follow-up, a regular myocardial biopsy should be considered for discharged patients, if possible.

Viral myocarditis has an incidence rate of 10 to 22 per 100,000 individuals. The presentation pattern of viral myocarditis can range from nonspecific symptoms of fatigue and shortness of breath to more aggressive symptoms that mimic acute coronary syndrome. After the initial acute phase presentation of viral myocarditis, the virus may be cleared, resulting in full clinical recovery; the viral infection may persist; or the viral infection may lead to a persistent autoimmune-mediated inflammatory process with continuing symptoms of heart failure. As a result of these 3 possibilities, the diagnosis, prognosis, and treatment of viral myocarditis can be extremely unpredictable and challenging for the clinician. Herein, the incidence, etiology, definition and classification, clinical manifestation, diagnosis, pathogenesis, prognosis, and treatment of viral myocarditis are reviewed, and how acute clinical care teams might differentiate between viral myocarditis and other acute cardiac conditions is discussed.