Myocarditis 

🔹 Definition

Myocarditis is defined as inflammation of the myocardium associated with myocyte necrosis that is not secondary to ischemia.
It is a clinicopathological diagnosis, encompassing a spectrum from subclinical disease to fulminant cardiogenic shock or sudden cardiac death.

🔹 Etiology and Classification

1. Infectious Causes

2. Immune-Mediated / Autoimmune

• Systemic autoimmune diseases: SLE, sarcoidosis, rheumatoid arthritis.
• Idiopathic giant-cell myocarditis — often rapidly fatal without immunosuppression.
• Eosinophilic myocarditis — drug hypersensitivity or hypereosinophilic syndrome.

3. Toxic / Drug-Related

• Clozapine, Methyldopa, Amphotericin B, Cocaine, Alcohol, Immune checkpoint inhibitors (e.g., nivolumab).

4. Hypersensitivity / Radiation / Post-infectious

• Associated with immune dysregulation and molecular mimicry.

🔹 Pathophysiology — Stepwise Mechanistic Understanding

Phase 1: Direct Injury

• Viral replication in cardiomyocytes → release of damage-associated molecular patterns (DAMPs).
• Activation of TLR-mediated innate immune response → cytokine surge (IL-1β, TNF-α, IL-6).

Phase 2: Immune-Mediated Myocyte Damage

• Molecular mimicry: Viral proteins mimic cardiac antigens → auto-reactive T cells attack myocardium.
• Predominant lymphocytic infiltration (CD8+ T cells).

Phase 3: Chronic Remodeling

• Failure to clear infection → chronic inflammation → fibrosis, chamber dilatation → DCM phenotype.

Histological Patterns

🔹 Clinical Presentation

1. Prodromal Phase

• Viral-like illness: fever, malaise, myalgia, sore throat.

2. Cardiac Phase

Symptoms range from mild chest pain to cardiogenic shock:

• Chest pain (mimics ACS)
• Palpitations (arrhythmias)
• Dyspnea, orthopnea, fatigue (heart failure)
• Syncope / sudden cardiac death (ventricular arrhythmia or heart block)

3. Clinical Variants

🔹 Examination Findings

• Tachycardia out of proportion to fever.
• S3 gallop, murmurs of MR/TR (due to annular dilation).
• Soft heart sounds, hypotension (in shock).
• May have signs of pericardial friction rub (myopericarditis).

🔹 Diagnostic Approach

Step 1: Clinical Suspicion

• Young patient with new-onset HF after viral illness.
• Troponin rise + normal coronaries on angiography.
• ECG changes without coronary distribution.

Step 2: Laboratory Investigations

Step 3: ECG(non specific)

• Sinus tachycardia most common.
• Diffuse ST elevation (pericarditis-like) or localized (mimicking MI).
• T-wave inversion, QT prolongation.
• Conduction blocks or ventricular arrhythmias.

Step 4: Imaging

Echocardiography

• Global LV dysfunction > regional.
• Pericardial effusion possible.
• Fulminant: non-dilated ventricles, thickened walls (edema).

Cardiac MRI – Diagnostic Gold Standard (non-invasive)

• Lake Louise 2018 Criteria:
• T2-based marker: Myocardial edema.
• T1-based marker: LGE in mid-wall/subepicardial pattern.
• T1/T2 mapping abnormalities.

MRI helps differentiate ischemic vs. non-ischemic necrosis.

Step 5: Endomyocardial Biopsy (EMB)

Gold standard for definitive diagnosis but reserved for select cases.

AHA/ESC Indications:

• New-onset HF (<2 weeks) with hemodynamic compromise.
• HF (2 wks–3 mo) with arrhythmias or AV block, or poor response to therapy.
• Suspected giant-cell or eosinophilic myocarditis.

Dallas Criteria (Histologic Diagnosis):

• Active myocarditis: inflammatory infiltrate + myocyte necrosis.
• Borderline myocarditis: inflammation without necrosis.

🔹 Differential Diagnoses

• Acute coronary syndrome (ACS)
• Takotsubo (stress) cardiomyopathy
• Pericarditis / Myopericarditis
• Sepsis-induced cardiomyopathy

🔹 Management

I. General / Supportive Measures

• Admit to ICU if hemodynamically unstable.
• Oxygen / mechanical ventilation as needed.
• Avoid volume overload.
• Avoid NSAIDs and strenuous exercise.

II. Hemodynamic Support

• Inotropes: Dobutamine, Milrinone for low-output states.
• Vasopressors: Norepinephrine if hypotensive.
• Mechanical support:
• VA-ECMO for refractory cardiogenic shock.
• Impella / IABP as bridge to recovery or transplant.

III. Etiology-Specific Therapy

IV. Heart Failure Management

• Once stable:
• ACEI/ARB/ARNI, β-blocker, MRA per HF guidelines.
• Avoid these during shock phase.

V. Arrhythmia Management

• Treat ventricular arrhythmias per ACLS.
• Temporary pacing for high-grade AV block.
• ICD may be indicated for persistent ventricular arrhythmias after 3 months.

🔹 Prognosis

🔹 Follow-Up

• Repeat echocardiography at 3–6 months.
• Avoid competitive sports for 6 months.
• Long-term HF therapy if residual dysfunction.

🔹 References

1. Harrison’s Principles of Internal Medicine, 21st Edition – Ch. on Myocarditis.
2. Caforio ALP et al. Eur Heart J. 2020;41:2129–2152.
3. Bozkurt B et al. Circulation. 2021;144:e123–e135 (AHA Scientific Statement).
4. Ammirati E et al. J Am Coll Cardiol. 2022;79:1959–1976.
5. Kindermann I et al. NEJM. 2008;359:1526–1538.
6. McDonagh TA et al. Eur Heart J. 2021;42:3599–3726 (ESC HF Guidelines).