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Emergency and Acute Medicine – Myocarditis

Myocarditis is an inflammatory disease of the heart muscle characterized by myocyte necrosis and subsequent myocardial destruction. The condition typically results from a direct cytotoxic injury to cardiac myocytes by an infectious or toxic agent, followed by a secondary immune-mediated response that worsens myocardial damage. The true incidence is unknown because many cases are mild or asymptomatic; however, autopsy studies suggest myocarditis is present in 1–7% of the general population and in more than 50% of patients with HIV. It is more common in males than females, with an average age at diagnosis of approximately 42 years, and is a major cause of unexpected sudden death in individuals younger than 40 years.


The etiology of myocarditis is broad and includes infectious, toxic, autoimmune, and hypersensitivity causes. Viral infections are the most common etiology, particularly enteroviruses such as coxsackievirus B, adenovirus, influenza, herpesviruses, hepatitis C, HIV, Epstein–Barr virus, and cytomegalovirus. Bacterial causes include diphtheria, tuberculosis, meningococcus, mycoplasma, and group A streptococcus. Parasitic infections such as Trypanosoma cruzi (Chagas disease) represent the most common global cause of myocarditis and heart failure, especially in Central and South America. Additional causes include fungal, rickettsial, helminthic infections, medications (notably anthracyclines, cocaine, and certain antibiotics), toxins, radiation, autoimmune diseases, and envenomation from insects or snakes.


Clinical presentation is variable and ranges from mild viral-like illness to fulminant heart failure and sudden cardiac death. Common symptoms include dyspnea, chest pain, palpitations, and fatigue. Chest pain is often pleuritic or sharp and may mimic acute coronary syndrome due to local inflammation or coronary spasm. Dyspnea on exertion is frequent, and orthopnea or paroxysmal nocturnal dyspnea suggests the development of congestive heart failure. Syncope is concerning and may indicate malignant ventricular dysrhythmias or high-grade conduction block. In children, myocarditis is the most common cause of heart failure in previously healthy patients and often presents with nonspecific findings such as poor feeding, respiratory distress, sweating with feeds, or new murmurs.


Physical examination findings depend on severity and may include fever, tachycardia disproportionate to fever, hypotension, cyanosis, jugular venous distention, bibasilar crackles, peripheral edema, hepatomegaly, ascites, and gallop rhythms. A diminished S1, murmurs of mitral or tricuspid regurgitation, or a pericardial friction rub may be present, particularly when myocarditis is associated with pericarditis. Hypotension and cardiogenic shock are uncommon early but indicate a poor prognosis when present.


Evaluation in the emergency setting includes electrocardiography, chest radiography, and targeted laboratory testing. ECG findings are often nonspecific and commonly show sinus tachycardia, ST- and T-wave changes, atrial or ventricular dysrhythmias, and conduction delays; up to 20% of patients may develop heart block or bundle branch block. Cardiac biomarkers may be elevated, reflecting myocardial necrosis, though normal values do not exclude myocarditis. Echocardiography is essential to assess ventricular function, wall-motion abnormalities, pericardial effusion, and intracardiac thrombus. Cardiac MRI with gadolinium enhancement is increasingly valuable, as it can identify myocardial inflammation and necrosis with high diagnostic accuracy. Endomyocardial biopsy is reserved for select cases, such as transplant recipients or patients with unexplained, rapidly progressive disease.


Management is largely supportive and focused on treating complications. All patients require close monitoring with attention to airway, breathing, and circulation. Dysrhythmias should be treated promptly, and patients with Mobitz II or complete heart block require pacing. Heart failure is managed with oxygen, diuretics, ACE inhibitors, and cautious use of digoxin. NSAIDs are contraindicated in the acute phase due to potential worsening of myocardial injury. Anticoagulation is indicated in patients with severe left ventricular dysfunction or documented intracardiac thrombus. In pediatric viral myocarditis, intravenous immunoglobulin has been shown to improve ventricular function and outcomes. Sympathomimetic agents and β-blockers should generally be avoided in the acute setting.


Disposition depends on severity. All symptomatic patients, particularly those with dysrhythmias, new-onset heart failure, conduction abnormalities, thromboembolic events, or cardiogenic shock, require hospital admission, often to a monitored or intensive care setting. Asymptomatic patients without evidence of cardiac dysfunction or arrhythmia may be considered for discharge with close follow-up. Early recognition and careful monitoring are critical, as myocarditis carries significant morbidity and mortality, and progression to chronic cardiomyopathy or need for cardiac transplantation can occur despite initial stabilization.


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