The clinical presentation of acute myocarditis is highly variable, ranging from asymptomatic, to subtle to cardiogenic shock and even sudden cardiac death. There are no pathognomonic clinical features. The classic presentation is similar to that of heart failure with symptoms of dyspnea, orthopnea, and leg swelling. Palpitations and syncope may also occur. In one study of clinically suspected cases, about a quarter of patients had reduced LVEF, sustained ventricular arrhythmias, or symptoms of low cardiac output [10]. When the pericardium is involved, as in myopericarditis, chest pain with features similar to pericarditis will arise. As the most common cause of myocarditis is viral, a viral prodrome (fever, arthralgia, fatigue), usually 1 to 2 weeks before the onset of heart failure symptoms, may be described by the patient. The 2013 European Society of Cardiology position statement on myocarditis breaks the presentation down to three distinct but overlapping clinical profiles: acute coronary syndrome-like (chest pain not explained by evidence supporting CAD), new-onset or worsening heart failure (in the absence of known HF or CAD), and life-threatening conditions (arrhythmia, cardiogenic shock, severely impaired LV function) [11]. Other manifestations of an infectious agent, such as dysphagia in patients with Chagas disease (caused by Trypanosoma cruzi) or neurological symptoms in patients infected with diphtheria, also may occur. In addition, patients with a non-infectious etiology often will have manifestations of their underlying systemic disease, such as skin or kidney involvement in patients with connective tissue disease. 

There are no specific physical exam findings associated with myocarditis. Physical examination may range from normal to features similar to that of heart failure, including S3 gallop, jugular venous distention, peripheral edema, and tachycardia. In addition, patients with ventricular dilatation may have a mitral regurgitation murmur, which is classically described as an apical pansystolic murmur. A pericardial friction rub may be appreciated, especially if there is concurrent pericarditis. Additional findings may suggest an underlying disease in non-infectious etiologies. Also, patients with eosinophilic myocarditis will have a pruritic maculopapular rash. When the pericardium is involved, a friction rub also may be heard on cardiac auscultation.

Diagnosis of acute myocarditis is challenging because other clinical entities may mimic the diagnosis. This is further complicated by the variable clinical presentation of acute myocarditis. Acute myocarditis should be suspected in patients with clinical signs and symptoms concerning the illness regardless of workup, especially in young patients (age 25-50) with no history of cardiac disease. Clues related to underlying etiology may support the diagnosis, such as viral prodrome or signs of connective tissue disease. [12][13][14]

Initial evaluation for acute myocarditis should include an EKG, echocardiogram, serum troponin, and BNP. Troponin elevation, which is usually dramatic, is present in more than half of the patients. BNP is useful to assess for evidence of heart failure and ventricular stretch, which may suggest myocarditis in the right clinical picture. EKG often shows nonspecific ST changes; however, it also may show sinus tachycardia or ventricular arrhythmias (40% of patients). Also, changes consistent with pericarditis, including diffuse ST elevation, may be present in those with pericardial involvement. An echocardiogram is useful in assessing the degree of cardiac dysfunction and in helping rule out other causes, including valvular disease.

A chest radiograph is neither sensitive nor specific for myocarditis but may show an enlarged heart size, pulmonary vascular congestion, or pleural effusion. CT angiography to evaluate for other causes of chest pain may be indicated. Percutaneous coronary angiography is indicated in patients at high risk for coronary artery disease to help rule out an ischemic cause of cardiac dysfunction in the right setting. Cardiac magnetic resonance imaging seems to be promising and may help differentiate ischemic from non-ischemic etiologies of dilated cardiomyopathy. In addition, a complete blood count with differential showing eosinophilia may hint to eosinophilic myocarditis. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are usually elevated but nonspecific. Viral antibody testing can be done in the right setting; however, specificity is low and often can result in a delay in diagnosis without any change in management.

Endomyocardial biopsy, though rarely done due to its invasive nature, is the gold standard for diagnosis of myocarditis. According to the Heart Failure Society of America, biopsy should be reserved for patients with acute deterioration of the cardiac function of unknown etiology that is failing the usual medical therapy. The classic histological findings include lymphocytic infiltrates with myocyte necrosis, as described by the Dallas criteria.

Management is primarily supportive but also includes treating any identifiable cause. Patients with heart failure should receive standard treatment including beta-blockers, angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, and diuretics if needed. Immunosuppressive therapy has not shown clinical benefit and, therefore, should not be used routinely except in patients who have underlying systemic autoimmune or granulomatous inflammatory diseases. Although viral etiology is the most commonly identified cause, the efficacy of antiviral therapy is unknown, and routine antiviral therapy is not recommended. Non-steroid anti-inflammatory agents should be avoided in the acute setting as they may impair the healing of the myocardium. In severe cases, mechanical support devices such as an intra-aortic pump or left ventricular assist devices also can be used, with consideration of heart transplant as well. In these instances, it is important to consider a transfer to tertiary care centers for surgical support if needed. Patients may develop dysrhythmias or left atrial or ventricular thrombus requiring anticoagulation. Finally, patients should be counseled on limiting exercise and avoiding alcohol, especially in the acute phase, as it may increase viral replication. Long-term follow-up with serial echocardiography is recommended.[15][16]

• Acute coronary syndrome
• Coronary artery disease
• Coronary vasospasm
• Myocardial ischemia/infarction
• Pulmonary edema
• Unstable angina
• Congestive heart failure
• Pericarditis
• Pericardial effusion

Complications of acute myocarditis result from the damage to the cardiac muscle and include heart failure, arrhythmia, myocardial infarction, and sudden cardiac arrest.

Acute myocarditis has many causes, and its presentation can range from asymptomatic to mild to severe. Most patients need admission due to the risk of rapid progression to life-threatening conditions, including decompensated cardiomyopathy, heart failure, ventricular dysrhythmias, and death. In addition to the attending physician, the nurse and other staff are critical for serial monitoring of these patients. All patients need to be educated on the need for rest and abstaining from alcohol and tobacco. The pharmacist should educate the patient on the need to remain compliant with their medications (beta-blocker or ACE inhibitor). Most of these patients also have mild to moderate dyspnea and hence may benefit from chest physical therapy. Because of fatigue, a physical therapy consult is recommended to help build exercise endurance. Enrollment in a cardiac rehab program is beneficial for most patients. Finally, the patient should be educated on a healthy lifestyle, maintaining healthy body weight, and a low-fat diet.[17][18] (Level V)

Outcomes

The general outcome after viral myocarditis is good. However, recovery can be long and may take 3-7 years. However, some patients may develop left ventricular dilatation and may need ongoing treatment for heart failure and arrhythmias. A few patients may require a heart transplant. Those who exhibit the soluble Fas ligand at presentation generally tend to have a good prognosis, whereas those who have anti-myosin autoantibodies have a worse outcome. Cardiogenic shock can occur but is rare. The mortality for acute myocarditis is about 20% at 12 months, and at four years, there is a 56% survival. Patients who require a ventricular assist device while awaiting a heart transplant generally do not fare well if the wait is more than 1-2 weeks.[15][19] (Level V)