SeminarMyocarditis
Introduction
Myocarditis refers to the clinical and histological manifestations of a broad range of pathological immune processes in the heart. Alterations in the number and function of lymphocyte subsets and macrophages and antibody-mediated injury are typically found in patients with acute and chronic myocarditis. The immune reaction in the heart causes structural and functional abnormalities in cardiomyocytes, which in turn leads to regional or global contractile impairment, chamber stiffening, or conduction system disease. Patients with acute myocarditis often present with non-specific symptoms of chest pain, dyspnoea, or palpitations; however, sometimes acute viral myocarditis can cause cardiac damage without symptoms, and the risk of chronic dilated cardiomyopathy (DCM) in this setting is uncertain. Immune-mediated cardiac injury and dysfunction can also occur in chronic myocarditis.
Section snippets
Classification
Myocarditis can be classified by cause, histology, immunohistology, and clinicopathological and clinical criteria (panel, figure 1). From each categorisation, the treating clinician should consider what information will provide unique prognostic and therapeutic information in a given clinical scenario. For example, assessment of left ventricular function in acute myocarditis is useful because more severe ventricular dysfunction is associated with greater risk of death or need for heart
Cause
Myocarditis can result from a wide spectrum of infectious pathogens, including viruses, bacteria, chlamydia, rickettsia, fungi, and protozoans, as well as toxic and hypersensitivity reactions. Viruses are the infectious pathogens most frequently implicated in reports of acute myocarditis. In the 1950s and 1960s, experimental and later seroepidemiological studies linked enteroviruses, particularly group B Coxsackie viruses, to myocarditis.29, 30 In the 1980s, molecular techniques, including PCR,
Pathogenesis
Myocarditis results from the interaction of an external environmental trigger with the host's immune system. The availability of murine enteroviral models of myocarditis has facilitated much of our understanding of the disorder.56, 57 From the pathophysiological point of view, the disease can be conceptually divided into three phases: (1) acute viral, (2) subacute immune, and (3) chronic myopathic.
Diagnosis
When myocarditis is suspected, more common causes of cardiovascular disease, such as atherosclerotic and valvular heart disease, should be excluded according to present American Heart Association (AHA), American College of Cardiology Foundation (ACCF), European Society of Cardiology (ESC), and Heart Failure Society of America (HFSA) guidelines.65, 66, 67
In patients with clinically suspected acute myocarditis, confirmatory testing usually begins with serum biomarkers. Troponin 1 was raised in
Possible subclinical acute myocarditis
The optimum management strategy for patients who have a rise in troponin concentrations or ECG changes suggestive of myocarditis or myopericarditis without cardiovascular symptoms is not known. These patients are often encountered during a medical assessment for non-cardiovascular disorders such as a flu-like illness. The short-term prognosis of possible subclinical acute myocarditis is good, but the long-term consequences are unknown. If ventricular function is normal, a reasonable therapeutic
Summary
The aim of this Seminar was to provide a clinical classification and guidelines for the assessment and treatment of suspected myocarditis in medical environments and epidemiological research where biopsy is unfeasible at present. We have emphasised the strengths and limitations of non-invasive methods such as echocardiography and cardiac MRI. Recently, several clinical scenarios in which EMB results added unique prognostic data or guide therapy have been defined. Therefore, we recommend that
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