Article Text

Eosinophilic myocarditis mimicking acute coronary syndrome in a young man with T-lymphoblastic lymphoma and hypereosinophilia
  1. Mohd Asyiq Al-Fard Raffali,
  2. Beh Boon Cong,
  3. Syawal Faizal Muhammad and
  4. Hamat Hamdi Che Hassan
  1. Department and Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Cheras, Malaysia
  1. Correspondence to Dr Mohd Asyiq Al-Fard Raffali; ashkashick{at}


A man in his 20s with underlying chemorefractory primary T-lymphoblastic lymphoma and hypereosinophilia developed acute chest pain in the ward after readmission for disease progression. ECG showed widespread ST depression and serum troponin was markedly elevated. Transthoracic echocardiography showed diffused thrombus deposition with preserved ejection fraction consistent with eosinophilic myocarditis. The patient ultimately succumbed to the disease, after complications with severe hospital-acquired pneumonia.

  • Cancer - see Oncology
  • Pericardial disease
  • Haematology (incl blood transfusion)

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Eosinophilic myocarditis is a rare complication of hypereosinophilia and may manifest as acute coronary syndrome. This case report demonstrates the importance of ruling out this condition before subjecting patients with invasive procedures that might bring more harm than benefit for the patient.

Case presentation

A man in his 20s with underlying chemorefractory primary T-cell lymphoblastic lymphoma was admitted to the ward for disease progression. He had a fall 2 days earlier and had a body weakness and lethargy. After a few days in the ward and initiation of tyrosine kinase inhibitor, dasatinib, he developed sudden acute chest pain, which was compressing in nature, which does not relieve on rest. On examination, he was alert but distressed. His blood pressure was 92/55 mm Hg, with a pulse rate of 96 per minute, and peripheral oxygen saturation of 100% on room air.

He was diagnosed with primary T-cell lymphoma 2 years ago after having generalised neck and groin swelling accompanied with constitutional symptoms. Lymph node biopsy was done confirming the disease. His disease was chemorefractory after failed second line of chemotherapy, hyper-CVAD (cyclophosphamide, vincristine, doxorubicin) and ICE (ifosfamide, carboplatin, etoposide) regimen. The latest PET-CT (positron emission tomography and computed tomography) scan 3 months earlier showed disease progression. He had no history of bronchial asthma, no known drug and food allergies, and no signs and symptoms of parasitic infection.


ECG on episode of chest pain showed diffused ST depression over inferolateral leads with dynamic changes, as compared with baseline ECG which was normal (figure 1). High sensitivity cardiac troponin-I was elevated, 2718 pg/mL. His full blood count showed normocytic normochromic anaemia with haemoglobin of 71 g/L, platelet count of 14×109/L and markedly elevated absolute eosinophil count of 51.9×109/L (normal range 0.02–0.5×109/L) which was 73% of the leucocyte count. His baseline eosinophil count before he was diagnosed with lymphoma was 0.8×109/L. COVID PCR was negative. Chest radiography showed clear lung fields with no evidence of pneumothorax nor widened mediastinum (figure 2).

Figure 1

(A) Baseline ECG of the patient nearly 10 months before. (B) ECG of the patient at the time of acute chest pain showing diffused ST segment depression over inferolateral leads. aVR: augmented vector right. aVL: augmented vector left. aVF: augment vector foot.

Figure 2

Chest radiography on admission showing a right-sided chemo port, no cardiomegaly, widened mediastinum nor pneumothorax.

Differential diagnosis

The differential diagnoses of the acute chest pain include acute coronary syndrome, myopericarditis, aortic dissection, pleuritis and pneumothorax.


The patient was initially treated as type II acute coronary syndrome by the attending physician. Antithrombotic therapy was not started in view of the severe thrombocytopenia. He was transfused with one unit of packed red cells and multiple units of apheresis platelets. After formal consultation with cardiology was done, echocardiography was ordered and showed diffused thrombus deposition over the endocardium with preserved left ejection fraction of 65% with no regional wall motion abnormality. There was also moderate pericardial effusion present (figure 3). The patient was treated as eosinophilic myocarditis based on suggestive features from echocardiography, supported by the very high absolute eosinophil count. The patient was further planned for cardiac MRI. However, he developed claustrophobia as he was put on the gantry during CMR (cardiac magnetic resonance), thus the procedure was abandoned. Plan for endomyocardial biopsy was put on hold due to severe thrombocytopenia.

Figure 3

Transthoracic echocardiography showing diffused superficial layer of thrombus deposition over the endocardium, papillary muscle atrophy and moderate pericardial effusion: (A) apical four chamber, (B) apical two chamber, (C) apical three chamber, (D) parasternal short axis at the level of mitral valve, (E) parasternal short axis at the level of papillary muscles and (F) parasternal short axis at the level of apex.

Outcome and follow-up

Unfortunately, the patient’s condition deteriorated as severe hospital-acquired pneumonia set in. As he was already in a chemorefractory disease, the decision was made with the family for only conservative therapy and to optimise palliative care. He ultimately succumbed after 3 weeks in the ward, and the family refused for postmortem.


EM (eosinophilic myocarditis) is a rare infiltrative disease of the myocardium, which has a potential catastrophic outcome for the affected patient. The association of eosinophilia and myocardial damage has been established in numerous studies, and many aetiologies have been identified such as hypereosinophilic syndrome, parasitic infection and bronchial asthma.1

The clinical presentation of EM varies from being asymptomatic to acute fulminant heart failure. Naturally, it has three stages, necrotic, thrombotic and fibrotic stages depending on the current pathophysiological process. As our patient has preserved ejection fraction, and echocardiography showed diffused superficial layer of thrombus, he was probably at the thrombotic stages.

In our patient’s case, the most likely cause for the severe hypereosinophilia was the progression of the T-lymphoblastic lymphoma. Various cytokines and growth factors are secreted by malignant lymphoma cells which stimulate the bone marrow to induce granulocyte precursors towards differentiation into eosinophils.2 As the patient has no history of bronchial asthma or parasitic infection, other causes for the hyperosinophilia were unlikely.

We described a case of EM mimicking acute coronary syndrome, as the patient had classical compressive chest pain accompanied with widespread ECG changes and elevated troponin levels. As the patient was young, and echocardiography showed no regional wall motion abnormality even at a tachycardic state, possibility of ischemia was unlikely. Thambidorai et al and Galiuto et al described in their case reports of EM mimicking myocardial infarction after excluding coronary angiography. The diagnosis was made on suspicion of EM due to elevated absolute eosinophil count, and after EMB (endomyocardial biopsy) was done.3 4 The true cause of the chest pain in this case was most likely due to myopericarditis, as evident by the elevated troponin levels and presence of pericardial effusion.

Although, we were unable to perform CMR and EMB for this patient due to unavoidable consequences, the diagnosis of EM was very likely in this patient, as echocardiography shows pathognomonic changes of diffused thrombus deposition with pericardial effusion supported by the very high eosinophil count.5 Baseline echocardiography which was done a few months earlier was normal (figure 4), followed by a full body F-18 FDG (fluorodeoxyglucose-18) PET-CT scan 2 weeks earlier which showed normal myocardium uptake and absent pericardial effusion (figure 5).

Figure 4

Baseline transthoracic echocardiography showing normal endocardial borders. Larger papillary muscles and absence of pericardial effusion: (A) modified apical four chamber view, (B) parasternal short axis view at the level of papillary muscles and (C) subcostal view.

Figure 5

F-18 FDG PET-CT scan of the chest 3 weeks earlier showing normal myocardial uptake, and no obvious pericardial effusion: (A) transverse view, (B) frontal view and (C) sagittal view.

Treatment for the disease is to treat the underlying cause, with systemic corticosteroids to reduce the inflammation associated by the EM. This patient was already on a tyrosine kinase inhibitor for his disease and oral high-dose dexamethasone as prophylaxis for tumour lysis syndrome.

In terms of prognosis of the disease, as it is rare, there are no large real-world data available. However, data from single-centre studies show mortality of 10% during hospitalisation and 30% survival rate after 3 years.5

Patient’s perspective

After a long battle with lymphoma, my son is finally at peace. I hope with this case report, other doctors can benefit by learning how does the disease present and manifest.

Learning points

  • To understand the possibility of differential acute chest pain in a patient with hypereosinophilia is EM.

  • To learn about the echocardiographic features of EM.

  • To learn about the progression of EM and the difficulty in managing it.

Supplementary video

Supplementary video

Ethics statements

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Supplementary materials

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  • Twitter @asyiqraffali

  • Contributors MAA-FR wrote the case under continuous supervision of HHCH and SFM. MAA-FR and BBC discussed the case presentation, investigation and management. HHCH and SFM supervised and provided guidance on management of the patient.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.