Myocarditis

Myocarditis describes a heterogeneous group of disorders characterized by myocardial inflammation in the absence of predominant acute or chronic ischemia.

May present as fulminant, acute, or chronic myocarditis.

12-lead ECG, chest x-ray, cardiac biomarkers, and two-dimensional echocardiography should be ordered in all patients with suspected myocarditis. Endomyocardial biopsy may be indicated for some patients to confirm the diagnosis, but the potential risks and benefits should be carefully assessed. In children, cardiac magnetic resonance imaging (MRI) is the preferred diagnostic modality because it is noninvasive.

Treatment is usually supportive care and conventional heart failure therapy. More severe presentations may need aggressive pharmacologic treatment with escalation to mechanical circulatory support. Occasionally, certain cases do not respond to conventional therapy and progress to heart transplantation or death.

Prognosis is variable but is related to presentation and underlying etiology. Most cases of viral myocarditis are asymptomatic and spontaneously resolve. Patients who present with mild to moderate heart failure tend to improve or recover but may progress to chronic severe heart failure. Key risk factors for adverse prognosis include symptomatic heart failure, cardiogenic shock, electrical instability, biventricular reduced ejection fraction, late gadolinium enhancement on cardiac MRI, and giant cell myocarditis.

Myocarditis is clinically and pathologically defined as inflammation of the myocardium in the absence of the predominant acute or chronic ischemia characteristic of coronary artery disease. It is a clinical syndrome of nonischemic myocardial inflammation resulting from a heterogeneous group of infectious, immune, and nonimmune diseases. Histopathologically, it is characterized by an inflammatory cellular infiltrate with or without evidence of myocyte injury.[1]Tschöpe C, Ammirati E, Bozkurt B, et al. Myocarditis and inflammatory cardiomyopathy: current evidence and future directions. Nat Rev Cardiol. 2021 Mar;18(3):169-93. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7548534 http://www.ncbi.nlm.nih.gov/pubmed/33046850?tool=bestpractice.com ​​[Figure caption and citation for the preceding image starts]: Histologic findings in a patient with giant cell myocarditis. A: severe myocardial necrosis and fibrotic replacement of the cardiomyocytes with granulation tissue and fibrosis is present in a section from the anterolateral left ventricular wall; B: a sharp demarcating border between vital and necrotic myocardium is seen, confirmed by additional immunohistochemical staining for myoglobin; C: at the inflammatory border, cells consisting of prominent multinucleated giant cells, macrophages, lymphocytes, and eosinophilic granulocytes are seen in close proximity to vital myocardium; D: immunohistochemical staining for complement 4d is positive in all vessels, suggestive of complement cascade activationFrom: Rasmussen TB, Dalager S, Andersen NH, et al. BMJ Case Reports 2009; doi:10.1136/bcr.09.2008.0997 [Citation ends].