HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
79-year-old woman, with no known drug allergies, hypertensive on treatment with olmesartan 40 mg and amlodipine 5 mg per day and independent for ABVD. She presented with oppressive chest pain at rest, not radiating or associated with vegetative cortex, of three days' evolution, accompanied by an increase in her usual dyspnoea until it became minimal effort. On examination she was normotensive and afebrile with preserved vesicular murmur and no pathological sounds, rhythmic and without murmurs. There is no oedema.
The neurological and abdominal examination was unremarkable. The ECG showed sinus rhythm, with ST-segment depression in V2-V6, DI and aVL (maximum 2 mm in V2), which partially corrected after becoming asymptomatic (figure 1). First enzyme measurement: ultrasensitive troponin T 1890 ng/L [0-14], CK 319 U/L [26-167]. Treatment was started with double antiplatelet therapy (ASA and clopidogrel), low molecular weight heparin, atorvastatin, candesartan and bisoprolol. The patient was admitted to the cardiology department with a diagnosis of STEMI.

COMPLEMENTARY TESTS
Laboratory tests: glucose 98 mg/dl; urea 60 mg/dl, creatinine 1.71 mg/dl; GFR 31 ml/min; sodium 140 mmol/l; potassium 4.7 mmol/l, CK 319 U/L [26-167]; ultrasensitive troponin T 1890 ng/L [0-14]; leukocytes 9.95x103; neutrophils 5.92x103 (59.4%); lymphocytes 1.38x103 (19.9%); monocytes 1.01x103 (10.2%); eosinophils 1.63x103 (16.4%) [normal 0-6], basophils 0.01x103 (0.1%) Hb 12.5 g/dl; Hto 38.9%; MCV81.7 fl; platelets 61 x 103; leukocytes and eosinophils were as high as 20.950 and 46% respectively.
Chest X-ray: CTI< 0.5, no infiltrates. C costophrenic sinuses were free.
Echocardiography: LV not dilated, with slightly depressed systolic function and no contractility alterations. Right chambers not dilated with normal systolic function. LA dilated. Impaired relaxation. Mild MI and TR.
Coronary angiography: right dominance. Coronary arteries without significant lesions.
Cardiac MR and viability: non-dilated LV with slightly depressed LVEF (50%). Apparent thickening of the wall without being able to specify whether it corresponds to cardiac muscle, which is more significant in the lateral wall, with a maximum end-diastolic thickness of 18 mm. In the early study after intravenous gadolinium administration, an area of hyperenhancement was observed in the lower basal segment and hypocaptive foci of subendocardial location on the lateral wall, which could correspond to small thrombi. Dilated LA. Mild MI and TR.
Cerebral MRI: multiple ischaemic lesions affecting both cerebral and cerebellar hemispheres. No images suggestive of intraparenchymal bleeding. The ventricular system is symmetrical and of normal calibre.
Parasites in stool: negative.
Determination of IgE: negative: ECA: 40; ANA negative Hep-2: 1/320; ANCA IFI positive. P-ANCA and c-ANCA negative. Tumour markers: CA 125: 40 [0-35]; Beta-2-microglobulin 3494 [1200-2500]; CYFRA 21-1: 4.4 (0-3.3) IF plasma/orine: absence of monoclonal peaks. ACS. Antiphospholipids: negative. Bone marrow aspirate: flow cytometry: MO with 19% lymphocytes, of which 73% are T lymphocytes and 16% are B lymphocytes. A TCR Beta sequencing study was performed and no clonal population was identified.
Cytogenetics: absence of FIP1L/PDGFRRa and PDGFRb mutations.
Helminth serology: Strongyloides, Toxocara, Trichinella, Echinococcus, Fasciola negative.
Electroencephalogram: marked destructuring and global slowing of brain activity. These findings indicate the existence of moderate to severe diffuse encephalic involvement.
Thoracoabdominal CT: no pulmonary thromboembolism was identified in the main lobar or segmental arteries. Bronchiectasis of the anterior segment of the LSI. Discrete thickening of the subpleural interstitium. Two right apical perilymphatic nodules of 4mm are identified, probably corresponding to intrapulmonary lymph nodes. Global cardiomegaly associated with myocardial thickening in the left ventricle up to 21 mm in its lateral aspect. Minimal bilateral laminar pleural effusion. 10 mm prevascular adenopathy with no evidence of other significant mediastinal adenopathy. No significant retroperitoneal adenopathy. Normal liver. Bilateral cortical renal cysts. Uncomplicated digmoid diverticulosis.

EVOLUTION
On admission, coronary angiography showed coronary arteries without lesions. Transthoracic echocardiography showed a non-dilated LV with slightly depressed LVEF (51%). Dilated LA. Impaired relaxation. Mild MI and TR. Due to persistent eosinophilia (16-45%) it was decided to request cardiac MRI which was compatible with eosinophilic cardiomyopathy. Ten days after admission the patient had a stroke with left hemiplegia and decreased level of consciousness. Brain MRI showed multiple infarcts in both cerebral and cerebellar hemispheres. Doppler ultrasound of the supra-aortic trunks was normal.
A study of hypereosinophilic syndrome was initiated: ANA 1/320; ANCA (+) IFI; no paraproteins were detected in blood or urine. Bone marrow aspirate ruled out eosinophilic leukaemia. Parasitological stool culture was also negative and IgE values were within normal range.
Corticotherapy was started with prednisone 60 mg/day (1 mg/kg/day). Given the persistence of hypereosinophilia with systemic repercussions (cardiac and CNS), treatment was started with bolus methylprednisolone, without response or neurological improvement. Treatment was started with imatinib while awaiting the results of FIP1L/PDGFRa, obtaining a transitory decrease in the levels of eosinophils in the blood. Imatinib was discontinued after a further increase in eosinophils and hydroxyurea was started. He also presented with a polymicrobial infection of a decubitus ulcer, isolating SAMS. A month and a half after admission, he presented with abundant rectorrhagia, for which 2 red blood cell concentrates were transfused and due to the clinical situation it was decided not to perform a colonoscopy. After 48 hours he presented a new episode of rectorrhagia together with a worsening of his general and neurological condition. In consensus with the family, it was decided to start perfusion sedoanalgesia, and the patient died a few days later.

DIAGNOSIS
Primary hypersosinophilic syndrome with severe cardiac and neurological involvement
Eosinophilic cardiomyopathy
Multiple cerebral ischaemic infarcts
Renal failure
Thrombocytopenia
Polymicrobial infection
Lower gastrointestinal bleeding
AHT
