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A 56-year-old woman with high CRP and lateral ST-depression in the ECG

Case presentation

A 56-year-old woman was referred to the hospital because of high CRP and lateral ST-depression in the ECG.
She had been previously healthy except for asthma, which was diagnosed for about two years earlier. Her regular medication comprised budesonide and formoterol fumarate inhalations.

Myocardial Disease

She had had for more than two weeks before admission intermittent pain in the left shoulder, some aura-like visual disturbances and dyspnea, but no chest pain. The patient had also underwent helicobacter eradication slightly earlier. Laboratory examinations were carried out at the local health center. Her erythrocyte sedimentation rate was 41, CRP was 96 mg/l (<3) and leukocyte count was 14.4 x 109/l (normal range 3.4-8.2).

Fig 1. ECG showed mild st-depression in lateral leads.

The patient was referred to the hospital. On admission, bed-side echocardiography demonstrated anteroseptal and apical hypokinesia. Left ventricle was 48/40mm and EF was 27-34%, diminished. Mitral inflow was compatible with diastolic dysfunction. Septum thickness was 11mm and there was some pericardial fluid (1-2mm). Acute myocardial infarction and heart failure were suspected and nitro infusion, LMWH, enalapril and bisoprolol were initiatedOn admission to the hospital the patient was febrile (37.8oC), normotensive and had sinustachycardia 122/min. Chest X-ray demonstrated enlarged heart and mild pulmonary congestion. Serum troponine T (TnT) concentration was 2.63 ng/l (<0.03), serum creatinine concentration was within normal range, leukocyte count was 14.9 x 109/l and CRP was 142mg/l.

Fig. 2. In follow-up, echocardiography revealed septal hypokinesia

ECG showed inferolateral T-inversions. CRP was 107 and transaminases mildly elevated. Leukocytosis and elevated TnT concentration persisted for over one week’s time while there was no anemia and the thrombocyte count was normal. Invasive evaluation revealed open coronaries. LV cineangiography demonstrated global hypokinesia, the myocardium appeared stiff and there was some mitral regurgitation.

Fig. 3. Cardiac MRI showed that LVEDV was 167 ml (96 ml/m2), ESV 108 ml (61 ml/m2) and SV 62 ml. Wall thicknesses were normal and global EF was 36%. There was late enhancement in basal septum and posterior wall.


1. What is your differential diagnosis?
2. Which further investigations would you suggest to be done next?

In follow-up the patient experienced ventricular extrasystolia, paroxysmal atrial fibrillation and atrial flutter. Laboratory examinations revealed remarkable peripheral blood eosinophilia 6.44x 109/l  /47% (normal range 0.03-0.44x109/l). The concentration of serum eosinophilic cationic protein (ECP) was also high, 29.5 ug/l (<16). Serum IgE concentration was 607kU/l (0-110) while the concentrations of S-IgA and S-IgM were within normal range.
The  main clinical clue was thus eosinophilia. Eosinophilic syndromes can be divided into secondary, clonal or idiopathic forms. The possible causes of eosinophilic myocarditis include asthma, collagen diseases, hematologic malignancies, carcinoma, parasitic infections and allergic reactions to drugs.
Endomyocardial biopsies showed eosinophilic infiltration among the myocytes, some necrosis and fibrosis. Viral analyses of endomyocardial biopsies remained negative for parvo-, adeno-, picorna - and cytomegalo- viruses. The findings were compatible with eosinophilic myocarditis. The hematologist was consulted. Bone marrow aspirate and biopsy showed eosinophilia but no signs of a myeloproliferative or lymphoproliferative disease or mastocytosis.
The results of the cytogenetic studies of the bone marrow aspirate were normal. Using FISH-method, no chromosome 4q12 -related to FIP1L1-PDGFRA- (FIP1-like 1- platelet –derived growth factor) fusion gene was found. There was no clonal rearrangement of T-lymphocyte receptor gamma chain gene. Peripheral blood samples did not reveal BCR-QR- fusion transcripts or JAK2-gene (Janus kinase 2) V617F mutation.

The conclusion was that there was no evidence of a clonal hematologic disease.  Serology for connective tissue diseases remained negative. The patient was not predisposed to parasitic infections and also the laboratory results remained negative for them. Corticosteroid treatment, ramipril and bisoprolol were initiated and eosinophil count in the peripheral blood and left ventricular systolic function normalized within few weeks.
Eosinophilic myocarditis is a rare disease. The patients may present with fever, tachycardia and skin rash or non-specific st-t-abnormalities, which may simulate acute coronary syndrome. Without treatment eosinophilic myocarditis may be fatal. The histopathological findings comprise focal or diffuse infiltrates of inflammatory cells and eosinophils in the myocardium. Positive EMB may confirm the diagnosis but as it is not very sensitive, a negative finding does not necessarily exclude the possibility of eosinophilic myocarditis. Peripheral blood eosinophilia may be seen but not always. The possible causes of eosinophilic myocarditis include asthma, collagen diseases, hematologic malignancies, carcinoma, parasitic infections and allergic reactions to drugs. However, often the cause eosinophilia and eosinophilic myocarditis may remain unknown.
In our case, the possibility of parasite infections, collagen diseases and hematologic malignancies were excluded by laboratory examinations, bone marrow biopsy and molecular genetic and cytogenetic studies. The possible ethiologic roles of lansoprazol or amoxicillin remained speculative. Some patients have reportedly responded  well to corticosteroid therapy . After diagnosis, our patient was also given corticosteroids.
At the moment, for more than one year later, her prednison dose has been tapered to 7.5 mgx1, bisoprolol, ramipril and budesonide and formoterolfumarate inhalations have been continued and her cardiac condition is stable.


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2. Al Ali AM, Straatman LP, Allard MF, Ignaszewski AP. Eosinophilic myocarditis: case series and review of literature. Canadian Journal of Cardiology. 2006;22(14):1233-7.
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5.Tefferi A, Patnaik MM, Pardanani A. Eosinophilia: secondary, clonal and idiopathic. British Journal of Haematology 2006;133:468-92.

Notes to editor

Author: Dr Tiina Heliö, Department of Cardiology, Helsinki University Central Hospital, Helsinki, Finland.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.

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