Myocarditis

Inflammation of the heart muscle (myocardium) that injures cardiac myocytes; most often triggered by a viral infection.

• Major cause of sudden cardiac death in young people and can lead to chronic heart failure (dilated cardiomyopathy). It's also a classic "heart attack mimic" (chest pain, troponin elevation with clear coronaries) that's frequently tested on exams.

• Often in an otherwise healthy young adult a week or two after a viral illness, now with chest pain, dyspnea, and palpitations. Can resemble an MI (e.g., ST changes and ↑troponin) but usually in someone without risk factors; coronary angiography reveals no blockages.
• In infants or children, think unexplained heart failure: e.g., an infant with feeding difficulty, sweating, and tachypnea or an older child with fatigue and arrhythmias after a viral infection. MIS-C (post–COVID-19 inflammatory syndrome) can also cause severe myocarditis with shock in pediatric patients.
• Common causes: viral infections (especially coxsackie B, adenovirus, parvovirus B19, HHV-6, influenza, and SARS-CoV-2). Also autoimmune conditions (lupus, giant cell myocarditis, sarcoidosis), drug/toxin reactions (e.g., certain chemotherapy drugs, immune checkpoint inhibitors, clozapine), and less often bacterial (Lyme disease, diphtheria) or parasitic (Chagas disease) infections.

1. Think myocarditis in a patient (especially young, post-viral) with chest pain or new heart failure and an elevated troponin but no obvious coronary risk factors. Exclude acute MI: older patients or unclear cases may need an angiogram (myocarditis typically has clean coronaries).
2. ECG is often abnormal but non-specific: sinus tachycardia, diffuse ST elevations (if pericardium involved) or T-wave inversions, or heart block/arrhythmias – but no specific pattern is definitive.
3. Echocardiogram usually shows global hypokinesis or focal wall-motion abnormalities with reduced ejection fraction; it can also reveal a pericardial effusion if there's accompanying pericarditis.
4. Cardiac MRI can confirm the diagnosis noninvasively: shows myocardial edema and characteristic late gadolinium enhancement in a patchy mid-wall or subepicardial pattern (versus subendocardial in ischemic infarcts).
5. Endomyocardial biopsy (Dallas criteria: inflammatory infiltrates with myocyte necrosis) is the gold standard, but it's invasive. Reserve biopsy for severe, refractory, or atypical cases – especially if giant cell myocarditis is suspected, as this guides need for immunosuppression.

1. Supportive care is key: treat heart failure with ACE inhibitors, beta-blockers (once stable), and diuretics as needed; manage arrhythmias (antiarrhythmics, temporary pacing for heart block, defibrillation for ventricular arrhythmias). Ensure rest (avoid exercise) and monitor closely.
2. Address any underlying cause: stop offending drugs (e.g., clozapine or chemotherapy if implicated), treat infections (appropriate antimicrobials for Lyme, Chagas, etc.), and if giant cell myocarditis or another autoimmune cause is confirmed, initiate high-dose corticosteroids (often with other immunosuppressants). IVIG is sometimes used in acute myocarditis (especially pediatric or fulminant cases), though its benefit is not firmly proven in viral myocarditis.
3. For fulminant myocarditis with cardiogenic shock, consider advanced therapies: IV inotropes, mechanical support (IABP, ECMO or ventricular assist device), and evaluate for urgent heart transplant if recovery is not achievable. Many patients recover with time and supportive care, but some may progress to end-stage heart failure requiring transplantation.

• Coxsackie B (think B for Bad heart) is the classic virus causing myocarditis in exam questions.
• In a young patient with unexplained heart failure or arrhythmia (especially after a flu-like illness), always suspect myocarditis.
• No sports for 3–6 months after myocarditis—exercise can trigger fatal arrhythmias (a common sports medicine question).

• Syncope or sustained ventricular arrhythmias (VT/VF) in myocarditis signal high risk of sudden cardiac arrest – requires ICU monitoring and readiness for interventions (temporary pacing, defibrillator).
• Rapidly worsening hemodynamics (fulminant myocarditis with hypotension) is an emergency – initiate inotropic support and mechanical circulatory support early, and consider transfer for advanced therapies (e.g., transplant evaluation).

1. Recent viral illness + new chest pain or heart failure → suspect myocarditis.
2. Initial workup: order ECG, troponin, inflammatory markers, and echocardiogram; if it mimics MI, perform coronary angiography to exclude blockage.
3. If myocarditis is likely (e.g., positive troponin, echo dysfunction with clean coronaries) → admit if arrhythmias or low output; for severe cases, manage in ICU with inotropes and support.
4. Obtain cardiac MRI for diagnostic confirmation (typical inflammation pattern on gadolinium MRI supports myocarditis).
5. If patient deteriorates or diagnosis is uncertain → perform endomyocardial biopsy to check for specific types (e.g., giant cell) that guide therapy.
6. Rest the heart (no strenuous activity for months) and follow up frequently to monitor recovery of cardiac function.

• Young adult with a recent URI who develops chest pain, ↑troponin, and ST changes but has normal coronary arteries on angiography → Myocarditis (likely viral).
• Infant with a recent viral infection, now in heart failure (difficulty feeding, tachycardia, enlarged heart on X-ray) → Myocarditis presenting as acute myocarditis in infancy.
• Child 3 weeks after COVID-19 with fever, rash, hypotension, and reduced EF on echo → MIS-C (post–COVID multisystem inflammatory syndrome causing myocarditis).