HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

PERSONAL HISTORY
Allergic reaction to sulphonamides.
Denies toxic habits.
Cardiovascular risk factors (CVRF): arterial hypertension (AHT).
Stage IIIB endometrial carcinosarcoma, treated by surgery and adjuvant chemotherapy (cisplatin and ifosfamide) in 2011. Recurrence at the level of the vaginal vault in 2012, for which she received radiotherapy and brachytherapy. Currently free of disease.
Infiltrating colon adenocarcinoma over tubular adenoma resected in 2011.
Currently free of disease.
Chronic normocytic anaemia.
Surgical history: hysterectomy and double adnexectomy in 2011; resection of colonic polyp in 2011; bilateral inguinal hernia, nasal septoplasty.
Usual treatment: enalapril/hydrochlorothiazide 20/12.5 mg/day, lorazepam 1 mg/day.

CURRENT ILLNESS
A 79-year-old female patient attended the emergency department of our centre presenting with progressive dyspnoea of one month's duration until becoming minimal effort in the last 48-72 hours, together with accompanying asthenia and weakness. He denied clinical signs of chest pain. No cough, no expectoration, no fever, no dysthermic sensation.

PHYSICAL EXAMINATION
General condition was normal, normohydrated, normal colour. Eupneic at rest with no use of accessory muscles. Conscious, oriented and cooperative, with no apparent neurological focality.
Blood pressure (BP) 95/55 mmHg, heart rate (HR) 130 bpm, oxygen saturation (SatO2) 98% (ambient air).
Cardiac auscultation: regular sounds, tachycardic, no audible murmurs.
Pulmonary auscultation: generalised hypoventilation, no rales.
No oedema in the lower limbs.

COMPLEMENTARY TESTS
During his stay in the intensive care unit (ICU) the following complementary tests were performed:
Electrocardiogram (ECG) on admission: sinus rhythm at 96 bpm, normal PR, narrow QRS with axis at 0o, ST underlevel of up to 2 mm in V3-V6 with 1 mm sublevel in aVR. Isolated ventricular extrasystole.
Chest X-ray: hyperventilated lungs with normal parenchymal density, no nodular condensation. No alveolar space condensation.
Normal mediastinal silhouette and pulmonary hilarity, with no space-occupying lesions.
Laboratory tests on admission: creatinine 1.65 mg/dl, C-reactive protein (CRP) 111.6 mg/l, leukocytes 11.71x10^9/l, neutrophils 4.58 x10^9/l, lymphocytes 0.96 x10^9/l, monocytes 0.28 x10^9/l, eosinophils 5.88 x10^9/l, basophils 0.01 x10^9/l, haemoglobin 10 g/dl, ultrasensitive troponin T 1.911 pg/ml.
Coronary angiography: normal epicardial coronary arteries. Ventriculography normal.

During his hospitalisation in cardiology the following complementary tests were performed:
Transthoracic echocardiography: normal sized left ventricle with moderate concentric hypertrophy without apparent alterations in segmental contractility and with preserved systolic function. Diastolic filling pattern of impaired relaxation.
Mild aortic insufficiency on degenerative valve with normal transvalvular gradients. Non-dilated right ventricle with normal systolic function.
Mild tricuspid insufficiency (TI) allowing estimation of a systolic pulmonary artery pressure (PAPs) of 32 mmHg. No significant pericardial effusion is observed.
Cardiac magnetic resonance (CMR): left ventricle with concentric hypertrophy (14 mm), preserved mass (IMVI: 71 g/m2), concentric remodelling pattern, reduced volumes (IVTDVI 38 ml/m2; IVTSVI 14 ml/m2) and segmental and global systolic function within normal (LVEF 64%). Widespread patchy subendocardial and intramyocardial oedema, more marked on the lateral aspect, basal anterior and apex. Right ventricular volume (IVTDVD 26 ml/m2; IVTSVD 11 ml/m2) and systolic function preserved (RVEF 58%). Atria and great vessels of preserved dimensions. First-pass perfusion at rest (IV dimeglumine gadobenate 0.0075 mmol/kg) with patchy subendocardial defects. Absence of myocardial necrosis. Presence of small foci of subendocardial uptake at the level of the basal anterior and medial lateral aspect, also affecting papillary muscles. Slight pericardial effusion. In summary, acute myocarditis pattern with pseudohypertrophy due to multifocal myocardial oedema, preserved systolic function and small foci of late uptake in the left ventricle.
Peripheral blood smear: discrete erythrocyte anisopoikilocytosis with the presence of some isolated spherocytes and elliptocytes. Normocytic anaemia with a tendency to hypochromia is confirmed. No other morphological findings of interest. Manual leukocyte formula: 26% segmented, 6% lymphocytes, 68% mature-looking eosinophils.
Specific proteins: complement C3 110 mg/dl, complement C4 47 mg/dl, total IgE (immunoglobulin E) 306.3 IU/ml.
Parasite studies: negative.
Serology: only positive for Toxoplasma gondii IgG.
Bone marrow aspirate: abundant lump that is conspicuously absent of cellularity. Only some plasma cells and peripheral blood cells are seen. Conclusion: bone marrow with abundant lump empty of cellularity.
Bone marrow biopsy: bone marrow aplasia, without correlation with peripheral blood.


CLINICAL EVOLUTION
When an ECG was performed in the emergency department, ST segment alterations were observed (ST-segment depression of up to 2 mm in V3-V6 with a 1 mm depression in aVR), and a blood test for ultrasensitive troponin T was requested, the result of which was 1,911 pg/ml. In view of these findings, the patient was admitted to the ICU with initial suspicion of high-risk non-ST-segment elevation acute coronary syndrome (NSTEACS).
During her stay in the ICU, coronary angiography was performed which ruled out coronary artery disease and ventriculography showed no alterations, and she was discharged to the cardiology ward with a diagnosis of MINOCA (acute myocardial infarction without obstructive atherosclerotic coronary disease) to complete studies and appropriate treatment.
After admission to cardiology, the patient remained asthenic with stable haemoglobin levels of around 10 g/dL and eosinophilia that progressively increased to a maximum of 8.35x10^9/l absolute eosinophils. Treatment with beta-blockers was started and he remained at absolute rest with progressive control of heart rate and without tachy or bradyarrhythmias, nor presenting symptoms suggestive of these. At no time did she present symptoms compatible with heart failure.
In view of the CMR findings and the hypereosinophilia in peripheral blood, the patient was diagnosed with eosinophilic myocarditis and treatment was started with prednisone 50 mg per day with overall symptomatic improvement, with a gradual decrease in peripheral eosinophilia, as well as a decrease in ultrasensitive troponin T. Therefore, the dose of prednisone was gradually reduced. Therefore, the dose of beta-blocker was progressively reduced and she started to ambulate with good tolerance.
During her admission, she was studied by the internal medicine and haematology departments and various complementary tests were performed, such as bone marrow biopsy, among others, labelling the symptoms as hypereosinophilia of uncertain origin, without finding an underlying aetiology (negative autoimmunity, negative OM biopsy, negative parasites), and so she was left to continue follow-up after discharge from outpatient clinics.
After 10 days of hospitalisation, with the patient stable and asymptomatic from the cardiovascular point of view, tolerating ambulation without symptoms of heart failure or arrhythmic complications, with markers of myocardial damage in decline and electrocardiographic normalisation, it was decided to discharge her from hospital with close outpatient monitoring and treatment with prednisone in a descending pattern until a maintenance dose of 10 mg was achieved for at least 6 months depending on her evolution.

DIAGNOSIS
Acute eosinophilic myocarditis.
Hypereosinophilia of uncertain origin.
Arterial hypertension.
Chronic anaemia.
Disease-free uterine carcinosarcoma.
Disease-free adenocarcinoma of the colon.
