Eosinophilic myocarditis due to parasitic infection: A case-based minireview

Abstract

Eosinophilic myocarditis (EM) is a rare inflammatory condition of the heart, often associated with eosinophilic infiltration. While its causes range from allergies to autoimmune and infectious diseases, parasitic infections are an uncommon but critical etiology. This mini-review focuses on a case of EM in a 47-year-old male from Vietnam, linked to Schistosoma spp., Strongyloides stercoralis, and Toxocara spp. infections. The patient presented with severe chest pain and recovered fully after treatment with corticosteroids and albendazole. Drawing insights from this case and existing literature, we discuss the pathophysiology, diagnostic approaches, and therapeutic strategies for parasite-induced EM. Early diagnosis and tailored treatment are essential to improve clinical outcomes, especially in endemic parasitic areas.

Key Words: Eosinophilic myocarditis; Parasitic infection; Corticosteroids; Albendazole; Diagnosis; Vietnam

Core Tip: Eosinophilic myocarditis induced by parasitic infections is often underrecognized despite its severity. A 47-year-old Vietnamese patient with Schistosoma spp., Strongyloides stercoralis, and Toxocara spp. infections highlights that early diagnosis via serological and clinical evaluation, paired with corticosteroids and albendazole, can reverse cardiac dysfunction and prevent fatal outcomes, advocating for heightened awareness in endemic settings.

INTRODUCTION

Eosinophilic myocarditis (EM) is a rare, potentially life-threatening inflammatory condition characterized by eosinophilic infiltration of the myocardium[1-3], with etiologies ranging from hypersensitivity[4,5] and autoimmune disorders to infections[6-9], including parasitic causes prevalent in endemic areas. This condition can lead to severe complications, including myocardial necrosis, heart failure, and sudden cardiac death, necessitating early diagnosis and intervention[10-13]. Clinically, EM poses diagnostic challenges due to its nonspecific presentation, ranging from chest pain to fulminant cardiac dysfunction, often requiring a combination of laboratory, imaging, and histopathological assessments[14]. This mini-review examines the clinical presentation, pathophysiology, diagnostic strategies, and management of EM, with a focus on its parasitic origins, using a real-world case to illustrate these complexities.

CASE PRESENTATION

A 47-year-old male with a medical history of gout and habitual consumption of fermented meats, raw fish dishes, and fresh vegetables presented to our clinic with severe retrosternal chest pain radiating to the back, associated with dyspnea on exertion. On admission, physical examination revealed tachycardia (heart rate: 108 beats/min), blood pressure of 90/60 mmHg, body temperature of 38 °C, and a respiratory rate of 22 breaths per minute. Cardiac auscultation disclosed muffled heart sounds, suggestive of pericardial involvement.

Initial laboratory investigations demonstrated normal creatine kinase levels but markedly elevated cardiac biomarkers, including high-sensitive cardiac troponin T (hs-cTnT) at 1.95 ng/mL (reference: < 0.014 ng/mL) and N-terminal pro B-type natriuretic peptide (NT-proBNP) at 12740 pg/mL (reference: < 125 pg/mL), which is consistent with myocardial injury and heart failure. Additional findings included hyperuricemia (uric acid: 469.5 μmol/L), hypokalemia (potassium: 2.95 mmol/L), and a normal cortisol level (283 nmol/L). Hematological analysis revealed a white blood cell count of 12.4 × 10³/µL with significant eosinophilia (19.7%; reference range: 0%-7%). Inflammatory markers were elevated, with C-reactive protein (CRP) at 6.53 mg/L and interleukin (IL)-6 at 17.37 pg/mL.

Electrocardiography (ECG) on admission showed an irregular rhythm (110 beats/min), right axis deviation, QS waves in leads V1-V3, and inverted T waves in leads V4-V6, raising initial suspicion of subacute myocardial infarction with lateral ST elevation.

Transthoracic echocardiography was performed to evaluate cardiac structure and function, revealing hypokinesia of the anterior septum and apex, left ventricular systolic dysfunction with a left ventricular ejection fraction (EF) of 39%, and pericardial effusion, supporting a diagnosis of myocarditis with pericardial involvement. To exclude an ischemic etiology, coronary angiography was conducted, demonstrating no evidence of coronary artery stenosis (Figure 1A and B), effectively ruling out acute coronary syndrome.

Figure 1 Coronary angiography and cardiac magnetic resonance imaging findings in a patient with suspected myocarditis. A and B: Coronary angiography reveals normal coronary anatomy with no evidence of luminal stenosis, effectively excluding obstructive coronary artery disease; C and D: Cardiac magnetic resonance imaging demonstrates focal myocardial injury indicated by arrows, characterized by increased signal intensity on T2-weighted imaging (edema) and late gadolinium enhancement in a subepicardial distribution of the lateral wall, consistent with acute myocarditis.

Cardiac magnetic resonance (CMR) was subsequently undertaken to further characterize the myocardial pathology. CMR findings included reduced left ventricular end-diastolic volume (44.6 mL), and late gadolinium enhancement affecting > 75% of the myocardial wall thickness in the lateral wall, extending toward the apex (Figure 1C and D). Additionally, bone marrow examination, performed to investigate potential hematologic disorders, revealed eosinophilic hyperplasia (Figure 2).

Figure 2 Eosinophilic activation and myocardial infiltration in the context of parasitic infection. A: Bone marrow smear from the patient reveals a markedly increased number of eosinophils, as demonstrated on the peripheral blood film, suggesting eosinophilic hyperplasia; B: Schematic illustration of the proposed pathophysiological mechanism: Parasitic infection triggers immune activation, leading to eosinophil proliferation and activation. Activated eosinophils subsequently infiltrate the myocardium, contributing to tissue inflammation and injury.

Given the clinical presentation, eosinophilia, and imaging results, a diagnosis of EM was established. The patient’s dietary history prompted serological testing for parasitic infections, which returned positive for Schistosoma spp., Strongyloides stercoralis, and Toxocara spp. (Table 1). Detailed serological testing methodologies, including assay specifications, cutoff values, and local validation protocols, are provided in the Supplementary material. These findings strongly suggested a parasitic etiology as the underlying cause of EM in this case, guiding subsequent treatment decisions.

Table 1 Results of serological testing for parasitic infections.

Test name	Result	Reference range
Cysticercus cellulosae	Negative (6.265 NTU)	< 9.0 NTU; Grayzone: 9-11
Echinococcus granulosus	Negative (6.598 NTU)	< 9.0 NTU; Grayzone: 9-11
Fasciola gigantica	Grayzone (0.227 OD)	< 0.2 OD; Grayzone: 0.2-0.3
Schistosoma	Positive (1.127 OD)	< 0.2 OD; Grayzone: 0.2-0.3
Strongyloides stercoralis	Positive (0.865 OD)	< 0.2 OD; Grayzone: 0.2-0.3
Toxocara	Positive (32.445 NTU)	< 9.0 NTU; Grayzone: 9-11
Trichinella spiralis	Grayzone (0.351 OD)	< 0.3 OD; Grayzone: 0.3-0.4

Treatment was initiated with a 5-day course of oral prednisolone (40 mg/day) and albendazole (400 mg/day), alongside standard heart failure therapy. Rapid clinical improvement ensued, with hs-cTnT decreasing to 0.051 ng/mL and NT-proBNP to 1311 pg/mL within days. The white blood cell count normalized to 5.2 × 10³/µL, and eosinophilia resolved.

At one-month follow-up, repeat echocardiography demonstrated full recovery of left ventricular ejection fraction (EF: 64%). Eosinophil levels remained within normal limits, and the patient was asymptomatic, indicating a favorable response to therapy. A detailed timeline of the patient’s clinical presentation, diagnostic workup, treatment, and follow-up is provided in Figure 3.

Figure 3  Timeline of clinical presentation, diagnostic workup, treatment, and follow-up in the reported case.

DISCUSSION

Epidemiology of EM

EM is a rare subtype of myocarditis that can affect individuals across all age groups. It is defined by the presence of diffuse or localized myocardial inflammation accompanied by eosinophilic infiltration, typically associated with elevated peripheral eosinophil counts[1-3,15]. However, accurately determining the incidence of EM remains challenging due to its often nonspecific and subtle clinical presentation, which frequently results in diagnoses being made post-mortem through biopsy[16]. Among patients undergoing endomyocardial biopsy (EMB) for suspected myocarditis, EM is identified in 2%-46% of cases, highlighting its rarity and the limited understanding of its pathogenesis[17-21]. The true incidence of myocarditis remains uncertain, partly due to the infrequent use of EMB and the low sensitivity of the Dallas criteria[22]. Systematic studies have revealed that EM is more commonly observed in Caucasian populations, with a mean age of diagnosis around 41 years among those confirmed histologically[23]. Furthermore, two systematic reviews have consistently demonstrated that systemic disorders, such as hypereosinophilic syndrome (HES) or eosinophilic granulomatosis with polyangiitis (EGPA), are associated with EM in 64% to 71% of cases. The remaining cases are classified as idiopathic, where no specific underlying cause is identified[23,24]. Globally, EM is associated with a significant mortality risk of 22% in-hospital and up to 30% within five years if untreated-underscoring the urgency of early diagnosis, particularly in endemic regions[23,25].

Importance of early diagnosis

Early diagnosis of EM is essential for improving patient prognosis, although many complex and rare underlying clinical conditions may delay the diagnostic process. The first step involves hematologic and biochemical testing. Increase in cardiac biomarkers (particularly troponin and NT-proBNP), inflammatory markers (CRP, erythrocyte sedimentation rate, and procalcitonin), and leukocytes (especially eosinophils) are commonly observed[14,23]. It is important to maintain a high level of clinical suspicion, as eosinophilic cardiac involvement can occur even in the absence of peripheral eosinophilia or atopic manifestations at presentation. EM is not always associated with peripheral hypereosinophilia at time of evaluation. Getz et al[26] and Watanabe et al[27] described a patient with EM who never developed peripheral hypereosinophilia. Galiuto et al[28] similarly described a patient in whom EM was confirmed by cardiac biopsy, despite the fact that the initial peripheral blood eosinophil count was only 530/mm³ and never exceeded 870/mm³. However, patients without eosinophilia at admission could develop peripheral eosinophilia during hospitalization infiltration[15]. In our patient, laboratory findings of eosinophilia (19.7%), hs-cTnT (1.95 ng/mL), and NT-proBNP (12740 pg/mL) aligned with these expectations, indicating myocardial injury and heart failure.

Diagnostic criteria of EM

The definitive diagnosis of EM requires meeting at least two out of four standard criteria for myocarditis, as outlined by the European Society of Cardiology guidelines. First, the patient must fulfill the four standard criteria for diagnosing myocarditis: ECG, Holter, or stress test abnormalities; elevated myocardial injury markers (troponin I or T); evidence of functional or structural abnormalities on cardiac imaging; and myocardial tissue changes observed on cardiac magnetic resonance imaging (MRI), alongside histological evidence of inflammatory eosinophilic infiltration[14]. The degree of myocardial eosinophilic infiltration depends on the underlying cause, as well as the extent and duration of eosinophil exposure, with parasitic infections often inducing pronounced infiltration due to chronic antigenic stimulation[29,30].

Etiologies of EM

EM has been associated with various conditions. In cases where no specific cause is identified, the condition is considered idiopathic. One recognized form of EM is Loeffler endocarditis. EM is also associated with eosinophilic vasculitides, most notably EGPA (Churg-Strauss syndrome). Other causes include infections, allergic diseases, transplant rejection in heart transplants, and certain malignancies, particularly myeloproliferative disorders and hypersensitivity myocarditis, which are among the most commonly reported etiologies[13,31]. A recent review of the literature indicated that idiopathic cases represented the largest share, approaching one-third of all reported cases. EGPA followed as the next most frequent etiology, accounting for close to one-fifth of all cases. Drug-induced EM and HES each contributed to roughly one in every eight cases. Less commonly, this condition has been linked to parasitic infections, malignancy-related eosinophilia, and post-vaccination reactions[32].

In our patient, marked eosinophilia suggested a possible association with parasitic infections, such as Schistosoma spp, Strongyloides stercoralis, and Toxocara spp. This link was further supported by positive serological results for specific antibodies. Nonetheless, we conducted a comprehensive evaluation, including medication history review and specialized testing, to rule out other common causes of eosinophilia and myocarditis. This evaluation helped exclude other etiologies, such as viral infections, malignancies, or vasculitis, ensuring a focused diagnostic approach[33]. The serological detection of Schistosoma spp, Strongyloides stercoralis, and Toxocara spp antibodies in our patient provides compelling but indirect evidence of parasitic etiology. While serologic testing remains the clinical mainstay in resource-limited settings, several diagnostic limitations warrant consideration. First, antibody tests cannot distinguish active infection from prior exposure, potentially overestimating disease causality. Second, cross-reactivity among helminth antigens may yield false positives.

In light of the eosinophilia and positive serological results, additional diagnostic methods could help support the presumed parasitic origin of myocarditis. These include both routine and advanced techniques-such as stool examination, cytokine profiling, and PCR-that may offer further diagnostic confirmation when invasive procedures like EMB are not feasible.

Stool ova and parasite examination remains a fundamental parasitological technique for detecting intestinal helminths and protozoa. It is widely used in endemic settings and for patients with eosinophilia. Although cost-effective, its sensitivity can be limited by intermittent parasite shedding and reliance on experienced microscopists, especially when only a single sample is tested. Therefore, collecting and examining multiple samples over consecutive days is recommended to improve diagnostic sensitivity[34,35].

Cytokine profiling, particularly involving type 2 immune mediators such as IL-5, IL-13, IL-4, and eotaxin, has been proposed as a potential tool to better understand the pathophysiology of eosinophilia related to parasitic infections. IL-5 plays a central role in eosinophil activation and survival, while eotaxin facilitates eosinophil recruitment to inflamed tissues[36,37]. IL-4 and IL-13 contribute to Th2 immune polarization and promote IgE production. However, the evidence for their diagnostic utility remains limited, with most data derived from animal models and experimental studies. Notably, the roles of IL-4 and IL-13 in parasitic infections are complex and sometimes contradictory, as some studies suggest that they may impair host defense mechanisms[38]. To date, there are no established clinical guidelines recommending cytokine assays for diagnosing EM, and these biomarkers have not been integrated into routine clinical practice. Therefore, while cytokine profiling may offer insights into disease mechanisms and Th2-driven immune activation, its application remains investigational and requires further clinical validation before widespread use can be recommended.

PCR-based detection of parasitic DNA in blood, stool, or cardiac tissue can provide direct evidence of infection and may support the diagnosis of EM in suspected parasitic cases. Recent studies have demonstrated the value of PCR in detecting parasites with higher sensitivity than traditional microscopy or serology[35,39,40]. Moreover, multiplex and real-time PCR assays have improved diagnostic efficiency and the ability to detect co-infections[41]. Despite these benefits, PCR remains underutilized in routine clinical practice because of its high cost, lack of standardization for myocardial specimens, and limited availability of molecular diagnostic platforms in low-resource settings. Thus, while promising, its application in parasitic EM remains largely investigational.

Pathophysiology

Cardiac damage mechanisms related to eosinophilic infiltration progress through three stages (Figure 2). The initial phase, known as acute necrosis, is often clinically silent. In this stage, myocarditis is characterized by both inflammation and the presence of eosinophils within the myocardial tissue, occasionally accompanied by granulomatous formation[42]. Throughout this stage, a variety of cytotoxic molecules-such as eosinophil cationic protein, major basic protein, eosinophil-derived neurotoxin, eosinophil peroxidase, and reactive oxygen species-are released. These agents contribute to mitochondrial dysfunction within cardiomyocytes[43-45]. These substances cause myocardial necrosis and programmed cell death (apoptosis). The second stage is thrombotic endocarditis, where eosinophil granule proteins act as potent procoagulants. They stimulate platelet aggregation and impair the anticoagulant properties of the endothelium, leading to thrombus formation adherent to blood vessel walls or cardiac chambers, which may result in embolic events[42]. Take et al[46] reported the finding of intraventricular thrombi in 15% of 110 cases of hypereosinophilia. The final stage is fibrosis, characterized by scarring in the damaged myocardium due to thrombus formation, ultimately leading to restrictive cardiomyopathy and atrioventricular valve dysfunction[47,48].

Clinical manifestations and complications

The manifestations of myocarditis are closely related to underlying pathogenic factors and inflammation, which can cause myocardial tissue damage of varying severity[49]. The clinical spectrum seen in EM is markedly heterogeneous, and disease severity often fails to correlate directly with the level of peripheral eosinophilia. Individuals may experience symptoms such as fever, skin eruption, palpitations, chest pain, and dyspnea, with more severe cases presenting with impaired cardiac function or hemodynamic collapse. Arrhythmias, abnormal impulse conduction, and alterations in ST and T waves have also been observed, although myocarditis does not present with a characteristic ECG phenotype[11]. Furthermore, complications such as arterial embolism, pericarditis, and sudden death can occur. EM is also associated with myocardial infarction through mechanisms such as coronary artery inflammation-induced stenosis, left coronary artery dissection, and coronary spasm. Eosinophil-derived proteins and vasoactive cytokines can cause vascular smooth muscle spasms, increasing the risk of myocardial infarction and serious cardiovascular events[28,50,51].

Diagnostic modalities

In some cases, differentiating myocarditis from a myocardial infarction can be challenging because of overlapping clinical features. The broad spectrum and nonspecific characteristics of clinical manifestations in EM, along with the absence of well-established diagnostic criteria, require a high level of clinical suspicion and the integration of multiple factors and tests for diagnosis[14]. First and foremost, a thorough patient history should always be reviewed, especially for allergies, systemic diseases, prior infections, travel history, and medication use before symptom onset[52]. Laboratory findings are also essential; although nonspecific and not always present, eosinophilia in blood tests may suggest EM[53,54]. Studies have demonstrated that eosinophil degranulation products and serum eosinophil cationic protein may serve as useful indicators for diagnosing and tracking disease progression during management[55]. Additionally, markers of inflammation and elevated cardiac troponin I and T levels are often present but are nonspecific. Even normal troponin levels do not entirely rule out myocarditis[56,57]. Echocardiographic findings in EM are diverse, depending on the disease's progression, and may manifest as dilated, hypertrophic, restrictive, or ischemic cardiomyopathy[16,58]. Our patient had normal chamber sizes but showed regional wall motion abnormalities in the anterior, anteroseptal, and apical left ventricular segments. Coronary angiography is mandatory to detect coronary artery disease, such as stenosis, arteritis, or thrombotic lesions[14]. CMR provides critical information regarding myocardial tissue characteristics, perfusion, ventricular function, and fibrosis[59]. It is the only non-invasive method that can be used before EMB to aid in diagnosing myocarditis and monitor disease progression during treatment[33]. Mavrogeni et al[60] also reported CMR as an emerging modality for evaluating Kawasaki disease, a type of systemic vasculitis, with the ability to visualize myocardial inflammation, blood flow, cardiac function, and fibrosis, providing essential and detailed clinical insight for diagnosing EM. Nonetheless, while CMR has been shown to outperform EMB in both sensitivity and specificity, it still cannot fully characterize the extent of inflammation or determine the precise etiology of the condition[33,61].

Role of EMB

EMB, using the Dallas criteria, is considered the gold standard for diagnosing and classifying myocarditis based on cellular infiltration[62]. In EM, EMB reveals diffuse myocardial necrosis associated with eosinophilic infiltration and interstitial fibrosis along with focal myocyte damage and perivascular infiltration[63]. The use of EMB in the routine evaluation of myocarditis has remained controversial. Despite being widely regarded as the definitive diagnostic modality, its clinical application is often limited due to factors such as low diagnostic yield, limited accessibility, elevated costs, and the procedural risks associated with its invasive nature. Nevertheless, EMB is still considered the diagnostic “gold standard” for confirming myocarditis[64]. EMB has limited sensitivity and specificity, around 50%, as the infiltrates are often localized[59]. EMB is advised in three clinical contexts. The first involves patients with acute-onset heart failure of less than two weeks' duration, accompanied by either normal ventricular dimensions or dilated ventricles and signs of hemodynamic compromise. The second applies to individuals experiencing heart failure for two to twelve weeks with left ventricular dilation, particularly when associated with new-onset ventricular arrhythmias, advanced atrioventricular block (second or third degree), or a lack of clinical improvement despite appropriate treatment within one to two weeks. The third scenario concerns cases of heart failure-regardless of its duration-in which dilated cardiomyopathy is suspected to be linked to hypersensitivity reactions and/or peripheral eosinophilia[65]. Acute myocardial infarction, left ventricular thrombus, or aneurysm formation are contraindications for myocardial biopsy. The risk of myocardial biopsy increases in cases of marked cardiomegaly, severe heart failure, or recent infection, especially when other pathologies cannot be excluded[59]. Therefore, myocardial biopsy is limited. However, EMB is the only method capable of identifying the histologic characteristics and subgroups of cardiac inflammation. Specifically, acute myocarditis with interstitial eosinophilic infiltration can be detected through hematoxylin and eosin staining[65].

Application to our case

In our patient, who was admitted with acute chest pain, no risk factors for coronary artery disease were identified. Ischemic changes on the ECG and significantly elevated cardiac enzyme levels, along with regional wall motion abnormalities in the anterior, anteroseptal, and apical left ventricular segments on echocardiography, clearly indicated myocardial injury. CMR showed abnormal perfusion in the territories of the left anterior descending artery and left circumflex artery, pericardial effusion, and mild pericardial thickening. Normal coronary arteries excluded acute coronary artery disease, yet raised the issue of distinguishing myocarditis from myocardial infarction with non-obstructive coronary arteries (MINOCA). Diagnosing MINOCA is inadequate if myocarditis has not been excluded[66]. While myocarditis was yet to be ruled out, significant peripheral eosinophilia and positive serology for Schistosoma spp., Strongyloides stercoralis, and Toxocara spp. pointed towards a likely diagnosis of parasitic EM in the patient, enabling prompt treatment with albendazole and prednisolone, which improved clinical symptoms, laboratory parameters, and normalized ECG and echocardiographic findings. In this case, myocardial biopsy was not conducted because the patient declined the procedure, despite the significant value of EMB in confirming the diagnosis.

Treatment

Currently, there are no clear guidelines or consensus for treating EM. Management depends on the underlying cause, clinical presentation, and disease stage, including discontinuing harmful factors, standard heart failure therapy, and early administration of high-dose steroids[51]. In many instances, the administration of glucocorticoids has led to significant improvement in clinical symptoms, likely attributable to their potent anti-inflammatory properties. Initiating steroid therapy at an early stage may help prevent progression to the subsequent phase characterized by thrombotic necrosis, mural thrombus formation, and fibrosis[59].

In most cases, glucocorticoids alleviate symptoms via potent anti-inflammatory effects, and early administration may help prevent disease progression[59]. Corticosteroids were administered in approximately four out of five EM cases associated with systemic conditions such as EGPA and HES, and in just over two-thirds of those related to hypersensitivity reactions. In many instances, cardiac function showed substantial improvement following treatment[23]. Although no clinical trials have evaluated steroid efficacy in parasitic EM, the use of antiparasitic drugs like albendazole is strongly recommended[59]. Globally, some EM case reports related to parasitic infections, such as Ascaris lumbricoides, Trichinella spiralis, and Toxocara canis, treated with dual therapy of high-dose albendazole and prednisolone, have demonstrated efficacy with favorable outcomes[51,67,68]. Additionally, symptomatic treatment to sustain life and prevent sudden death is essential, as most patients exhibit signs of cardiac dysfunction. Alongside conventional heart failure therapies, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers and aldosterone receptor antagonists may aid in cardiac remodeling[59]. Furthermore, since most patients suffer from arrhythmias, close attention should be given to prevent malignant arrhythmias, which can lead to sudden cardiac death[69]. In cases where standard medical treatment is ineffective, mechanical support therapies, such as ventricular assist devices (VADs), intra-aortic balloon pump counterpulsation, and extracorporeal membrane oxygenation, may be considered to help patients overcome the most critical phase of heart failure[70]. After one month of this therapy, our patient showed significant improvement, with a left ventricular EF recovering from 39% to 64% and eosinophil counts returning to normal.

The therapeutic efficacy of corticosteroids combined with albendazole, while demonstrated in our patient should be interpreted as hypothesis-generating rather than definitive. Three key contextual factors may limit generalizability: (1) Treatment response appears optimal in early-stage disease before fibrotic myocardial remodeling occurs; (2) Therapeutic benefit requires confirmed parasitic etiology through serological or histopathological evidence; and (3) This approach may be particularly relevant in resource-limited settings where EMB remains inaccessible. Importantly, the absence of controlled clinical trials and potential confounding from concomitant cardiovascular therapies necessitates cautious interpretation. Future investigations should focus on prospective validation in endemic populations, with particular attention given to treatment duration optimization and identification of predictive biomarkers.

The role of immunosuppressive therapy in the treatment of EM remains controversial, but it may help prevent recurrence. Treatment with cytotoxic agents such as cyclophosphamide and imatinib can be employed as a specific therapeutic approach in EM associated with EGPA or myeloproliferative syndromes[51]. Recently, mepolizumab-a monoclonal antibody against IL-5-has emerged as a novel option in the management of EM associated with idiopathic HES, reducing eosinophil counts and mitigating the long-term side effects of corticosteroid therapy[71]. Inotropic agents and left VADs are valuable for patients with hemodynamic instability, heart failure, or arrhythmias[71]. The role of anticoagulation in acute EM for preventing intracardiac thrombi and arterial embolism is still under discussion; however, no studies have yet demonstrated the efficacy of this therapy[59].

CONCLUSION

EM caused by parasitic infections represents a rare but treatable cause of acute cardiac injury. Our case features eosinophilia and confirmed seropositivity for Schistosoma spp., Strongyloides stercoralis, and Toxocara spp. - emphasizes that parasitic EM should be considered in patients presenting with chest pain, elevated cardiac markers, and peripheral eosinophilia, particularly in endemic regions. While cardiac MRI provides valuable diagnostic information and EMB remains definitive, targeted serologic testing is crucial when parasitic etiology is suspected.

Early combined treatment with corticosteroids and antiparasitic agents (e.g., albendazole) may lead to favorable outcomes, as observed in our patient. However, these therapeutic observations should be interpreted cautiously, as current evidence derives primarily from case reports rather than controlled studies. This approach appears most reasonable for patients with clear serological evidence of parasitic infection, especially when biopsy confirmation is not feasible. More robust clinical studies are needed to establish standardized treatment protocols and better define which patient populations would benefit most from this strategy.

ACKNOWLEDGEMENTS

We gratefully acknowledge the patients and their families for their participation and trust, which made this study possible. We also extend our appreciation to the Heart and Metabolic Innovations Research Team (HMIRT) for their collaborative spirit and valuable contributions to this research.