Clinical Presentations of Myocarditis

Abstract

Although, myocarditis usually is caused by a viral or postviral autoimmune response, it may result from virtually any infectious agent (rickettsia, bacteria, spirochetes, fungus, and protozoa), drugs and chemicals, physical agents, or as part of an underlying inflammatory or autoimmune process. All the infectious etiologies are characterized by inflammation of the myocardium in response to a systemic dissemination of the offending infectious agent. Patients with viral or postviral autoimmune myocarditis rarely display signs or symptoms of active viral infection, making recognition of this entity more difficult. Most viruses enter through the upper respiratory or gastrointestinal system. Once the virus is released from the local immune barriers it disseminates to the remainder of the body. From 3.5% to 5% of individuals who have infections from cardiotropic viruses will replicate virus in their heart with associated death of myocytes (myocytolysis). Initially, a nonspecific macrophage and IgM antibody reaction results in myocardial inflammation and further myocyte loss. By 14 days an IgG-specific antibody response promotes death of the virus and healing of the inflammatory cardiac reaction. Animal models have demonstrated that viral myocarditis is not associated with a uniform presentation but is influenced by the offending viral agent, the immune response to the virus, and the ability to eliminate viral pathogen from the heart. Patients who have viral myocarditis have similar variations in their symptoms, physical findings, and ‘‘natural history.’’ After the viral illness, there is a variable delay followed by cardiac symptoms in those who have myocarditis, including congestive heart failure, arrhythmia, embolic events, or acute ischemia. Unfortunately, the symptoms of myocarditis are usually nonspecific and include fatigue and weakness as a result of low cardiac output, dyspnea or othopnea caused by elevated filling pressures, chest pain from pericarditis or acute ischemia, and palpitations from arrhythmia. Physical findings are also nondescript but often include a heart rate greater than expected for a given level of activity, the development of gallop rhythms, rubs caused by pericardial irritation, murmurs related to ventricular remodeling, and decreased intensity in the first heart sound. This article concentrates on the clinical presentations of myocarditis, including arrhythmias, acute myocardial infarction, cardiovascular collapse, rapidly progressive cardiomyopathy or arrhythmias, and restrictive cardiomyopathy. Clues to the identification of myocarditis in other systemic illnesses and subacute cardiomyopathy development (perhaps leading to dilated cardiomyopathy) also are discussed.