Eosinophilic myocarditis (EM) is a highly specific and often underdiagnosed inflammatory condition involving eosinophil-driven infiltration of myocardial tissue.

Though rare, its progression can be rapid and life-threatening if not promptly identified and treated.

Unlike typical myocarditis, which often results from viral pathogens, EM is usually a hypersensitivity or autoimmune-mediated phenomenon that requires targeted immunosuppressive therapy rather than supportive care alone. A recent study emphasize the disease's polymorphic presentations, ranging from mild fatigue to fulminant cardiogenic shock, challenging even seasoned clinicians.

Pathophysiology: More Than Just Inflammation

At the core of eosinophilic myocarditis is eosinophil degranulation, which releases cytotoxic mediators such as major basic protein (MBP) and eosinophil cationic protein (ECP). These substances exert direct myocardial toxicity, provoking necrosis, fibrosis, and microvascular injury.

Dr. Michael D. Bristow, a cardiology researcher, remarks "Eosinophils are potent effectors—not benign bystanders. In eosinophilic myocarditis, they don't just migrate they destroy." Histological studies typically reveal dense eosinophilic infiltration with varying degrees of myocardial cell death and interstitial edema. Without intervention, this inflammation may evolve into restrictive cardiomyopathy or provoke arrhythmogenic complications.

Etiological Spectrum: Beyond Drug Reactions

Though hypersensitivity to medications such as antibiotics, antiepileptics, or chemotherapeutics—remains a leading cause, the differential diagnosis must remain broad. Other recognized etiologies include:

- Parasitic infections, particularly in endemic areas (e.g., Toxocara, Trichinella)

- Hypereosinophilic syndrome (HES)

- Eosinophilic granulomatosis with polyangiitis (EGPA)

- Neoplastic infiltration, especially in hematologic malignancies

Clinical Presentation: A Diagnostic Challenge

Symptoms are heterogeneous and often mimic other cardiomyopathies. Some patients present with nonspecific complaints—fever, chest discomfort, shortness of breath while others deteriorate rapidly, developing hypotension, conduction abnormalities, or pulmonary congestion.

Key warning signs include:

- Persistent peripheral eosinophilia (>500 cells/µL)

- Unexplained myocardial injury on imaging or labs

- Electrocardiographic changes, including T-wave inversions and ventricular irritability

In fulminant cases, multisystem involvement may accompany cardiac dysfunction, reflecting systemic eosinophilic infiltration.

Diagnostic Tools: Biopsy Is Still the Gold Standard

While echocardiography and cardiac MRI can detect structural abnormalities and edema, endomyocardial biopsy remains the definitive diagnostic modality.

A recent study emphasize early biopsy when EM is suspected, particularly when eosinophilia is present alongside cardiac dysfunction. Cardiac MRI may demonstrate late gadolinium enhancement with non-ischemic patterns, but cannot reliably distinguish eosinophilic inflammation from lymphocytic forms.

Management: Time-Sensitive Immunosuppression

Treatment hinges on the prompt initiation of corticosteroids, often in high doses (e.g., methylprednisolone 1 g/day IV for 3 days). Delay in therapy can lead to irreversible fibrotic remodeling or hemodynamic collapse. In patients refractory to corticosteroids or with recurrent episodes, immunomodulatory agents such as azathioprine, cyclophosphamide, or mepolizumab (an IL-5 inhibitor) have demonstrated efficacy.

Prognosis and Long-Term Outcomes

Prognosis varies by etiology and response to treatment. Drug-induced cases that receive early corticosteroids typically show complete recovery within weeks.

In contrast, cases secondary to systemic eosinophilic disorders often have a relapsing course and require chronic immunosuppression. Long-term surveillance with echocardiography and inflammatory markers is essential, as late fibrotic changes or recurrent inflammation can manifest even after initial resolution.

Eosinophilic myocarditis exemplifies the intersection of immunology and cardiology. Although infrequent, its potential for rapid deterioration demands heightened clinical suspicion and immediate action. In any patient with unexplained cardiac dysfunction and peripheral eosinophilia, EM must be considered and biopsied if necessary.

Medical professionals across specialties should recognize the broad spectrum and systemic associations of eosinophilic myocarditis, ensuring timely diagnosis and targeted immunotherapy to reduce mortality and improve recovery.