Background: Eosinophilic myocarditis (EM) is a rare, potentially life-threatening condition. Diagnosis is challenging due to heterogeneous clinical presentation, imaging phenotype overlapping with other cardiomyopathies, suboptimal timing and use of endomyocardial biopsy (EMB), and misconceptions, notably that EM can be excluded in the absence of peripheral eosinophilia. Delayed recognition may lead to irreversible myocardial injury and adverse outcomes. Case summary : We describe four EM cases highlighting distinct diagnostic and therapeutic challenges. Case 1 presented with chest pain and was initially misclassified as apical hypertrophic cardiomyopathy on cardiovascular magnetic resonance (CMR) due to apical psuedohypertrophy, delaying EM diagnosis and resulting in endomyocardial fibrosis with severe mitral regurgitation requiring annuloplasty. Case 2 presented while on chronic corticosteroid therapy for eosinophilic asthma, with severe biventricular dysfunction and mild eosinophilia; EMB revealed a polymorphous inflammatory infiltrate. In Case 3, EMB performed for severe LV dysfunction during steroid therapy for a prior diagnosis of eosinophilic granulomatosis with polyangiitis revealed lymphocytic myocarditis; eosinophilic infiltration became evident on repeat EMB only after steroid tapering. Case 4 presented with chest pain, peripheral eosinophilia and ST-elevation myocardial infarction due to coronary embolism, with biventricular apical thrombosis; idiopathic hypereosinophilic syndrome was later diagnosed and EMB during high-dose IV steroids showed a lymphocytic infiltrate. In our case series, treatment included corticosteroids with azathioprine (Case 1) and long-term anti–IL-5 monoclonal antibodies (mepolizumab) in systemic eosinophilic disorders (Cases 2–4); in all cases treatment was well tolerated without EM relapses, and enabled corticosteroid withdrawal, sustained control of peripheral eosinophilia, improved NYHA class and normalization of left ventricular ejection fraction and cardiac biomarkers. Conclusions: EM can manifest as isolated cardiac disease without extracardiac involvement or eosinophilia. Prognosis depends on timely diagnosis. Diagnostic pitfalls arise from overreliance on non-invasive imaging and smoldering disease course, particularly when chronic corticosteroids mask clinical and histological features. Targeted IL-5 pathway biologics are a promising, well-tolerated treatment option even in advanced EM.