Clinical meaning
Myocarditis is inflammation of the myocardium (heart muscle) that can result from infectious, autoimmune, or toxic causes, with viral infection being the most common etiology. Coxsackievirus B (an enterovirus) is historically the most frequently identified causative agent, though adenovirus, parvovirus B19, human herpesvirus 6 (HHV-6), influenza, SARS-CoV-2, and Epstein-Barr virus are also important causes. The pathophysiology of viral myocarditis proceeds through three overlapping phases. In Phase 1 (viral invasion, days 1-3), the virus enters the body through the respiratory or gastrointestinal tract and reaches the heart via the bloodstream. Coxsackievirus B binds to the coxsackievirus-adenovirus receptor (CAR) on cardiomyocytes, gaining entry to the cardiac muscle cells. Once inside, the virus hijacks cellular machinery to replicate, causing direct cardiomyocyte necrosis and releasing intracellular contents (troponin, CK-MB) into the bloodstream. In Phase 2 (immune response, days 4-14), the innate and adaptive immune systems mount an inflammatory response. Natural killer cells, macrophages, and T lymphocytes infiltrate the myocardium to destroy virus-infected cardiomyocytes. While this immune response is necessary to clear the virus, it causes significant collateral damage to uninfected cardiomyocytes, creating patchy areas of myocardial inflammation and necrosis. Pro-inflammatory cytokines (TNF-alpha, interleukins) further injure the myocardium and depress contractile function. In Phase 3 (resolution or progression, weeks to months), the inflammation either resolves with myocardial healing and fibrosis, or progresses to chronic inflammation leading to dilated cardiomyopathy. Approximately 10-20% of patients with acute myocarditis develop dilated cardiomyopathy, which is a leading cause of heart transplantation in young adults. The inflamed, edematous myocardium has impaired systolic function (reduced ejection fraction) because damaged and necrotic cardiomyocytes cannot contract effectively. Diastolic function is also impaired as the stiff, inflamed muscle resists normal filling. These functional impairments produce symptoms of heart failure: dyspnea, orthopnea, fatigue, peripheral edema, and reduced exercise tolerance. The inflammation can also disrupt the cardiac conduction system, producing arrhythmias ranging from premature ventricular contractions to ventricular tachycardia and complete heart block. Myocarditis is a significant cause of sudden cardiac death in young adults and athletes, which is why patients must be placed on activity restriction during the acute phase. Cardiac MRI with gadolinium enhancement is the most sensitive noninvasive diagnostic tool, showing myocardial edema and late gadolinium enhancement in areas of inflammation and fibrosis. Endomyocardial biopsy remains the gold standard for definitive diagnosis but is invasive and rarely performed except in fulminant cases. For the practical nurse, care focuses on hemodynamic monitoring, activity restriction, medication administration, recognition of heart failure and arrhythmia signs, and patient education about the importance of prolonged activity modification during recovery.