HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
70-year-old woman. No drug allergies. No toxic habits. High blood pressure. No history of diabetes mellitus or dyslipidaemia. Neoplasia of the left kidney with nephrectomy in 2010. Secondary chronic renal failure with usual creatinine 1.4 mg/dL (GFR 37 ml/min). Iron deficiency anaemia. History of trigeminal neuralgia. Osteoporosis. Diagnosed with irritable colon. In 2013, tubular adenoma with low-grade dysplasia in colon. Anxiety syndrome under treatment. IQ: left total hip prosthesis in March 2014. Left nephrectomy (hypernephroma) in 2010. Cardiological: first episode of paroxysmal atrial fibrillation in 2013, prescribed pill in the pocket. New episode in March 2014 in postoperative femur fracture, which reversed spontaneously. Echocardiogram with no alterations. He started treatment with acenocoumarol and flecainide.
Usual treatment: amlodipine 5 mg/d, flecainide 50 mg/d, acenocoumarol as prescribed, valsartan 160 mg/d, ferrous sulphate 80 mg/d, lorazepam 1.5 mg/d, calcium/VitD 1000/880 IUI, tramadol/paracetamol 37.5/325 mg.

Present illness
At rest, the patient began to experience central thoracic pressure radiating to both arms and interscapular region, intensity 10/10 and accompanied by profuse sweating, nausea and pallor. On arrival of the ambulance, an ECG was performed showing RS at 60 bpm, axis 60, PR 0.16s, narrow QRS with slight ST rectification in V3-V4. Nitrates and up to 6 mg of morphine chloride were administered, with improvement in pain. He was transferred to the emergency room where he arrived without pain with BP 120/70 mmHg and HR 55 bpm. ECG showed persistent ST rectification in V3-V4. Analyses showed positive troponin. Double antiplatelet therapy was started and the patient was admitted for study.  Physical examination Patient in good general condition, conscious and oriented, eupneic at rest, afebrile. Cardiac auscultation: rhythmic tones with aortic systolic murmur I/VI. Pulmonary auscultation: VCM, without added sounds. IIUS: no oedema or signs of DVT. Pedial pulses present and symmetrical.

COMPLEMENTARY TESTS
Emergency laboratory tests: creatinine 1.53 mg/dl, urea 80 mg/dl, Na 140 meq/l K 4.8 meq/l Hb; 11.2 g/dl, Ht 35.5 %, leukocytosis 12,500 76 % neutrophils, platelets 228000. INR 1.44. Serial troponin I: 1.478 -7.55- 5.13 ng/ml. Chest X-ray: cardiomegaly, no signs of vascular redistribution. Control ECG: RS 57 bpm, QR wave in I and aVL, narrow QRS, symmetrical negative T wave from V2 to V6, DI, DII and aVL. Coronary angiography: coronary arteries without significant angiographic lesions. Transthoracic echocardiogram: non-dilated, hypertrophic left ventricle, moderately depressed systolic function (EF 4C 40 %), with anterolateral mid-apical akinesia and mid-lower akinesia and hyperrefringence with hypertrabeculation in these territories. Diastolic pattern of impaired relaxation. Right ventricle of normal size, preserved function. Dilated left atrium. Tricuspid valve with mild insufficiency that allows estimating PSAP of at least 44 mmHg. Inferior vena cava not dilated. No pericardial effusion. No evidence of intracardiac masses. Admission blood tests (14/03): glucose 78 mg/dl, urate 4.93 mg/dl, urea 59 mg/dl, creatinine 1.29 mg/dl, cholesterol 176 mg/dl, HDL cholesterol 69 mg/dl, LDL cholesterol 86.42 mg/dl, triglycerides 102 mg/dl, AST 30 U/L, ALT 14 U/L, GGT 30 U/L, sodium 144.0 mEq/L, potassium 4.9 mEq/L. CBC: haemoglobin 12.5 g/dl, haematocrit 40.0 %, leucocytes 8730/L, N 63.3 %, platelets 222000/L. Cardiac MRI: dilated LV, dyskinesia of anterior, anterior/lateral, infero/lateral and inferior and lateral apical midwall segments. Hyperdynamia of the rest of the apical cap and basal segments. EF 40%. Dilated LA. Edema in the middle segments of the anterior wall, anterior/lateral, infero/lateral and inferior and lateral apical. No abnormalities in gadolinium uptake. ID: study compatible with tako-tsubo syndrome with midventricular involvement.

EVOLUTION
On admission, an echocardiogram was performed showing hypertrophic LV with moderately depressed systolic function with mid-apical anterolateral akinesia and mid-lower akinesia and hyperrefringence. Coronary angiography ruled out angiographically visible coronary lesions. With the diagnosis of stress cardiomyopathy, cardiac MRI was requested and a diagnosis of midventricular tako-tsubo syndrome was confirmed. She was discharged home and a month later, after a repeat transthoracic echocardiogram was performed, showing an improvement in the segmental alterations.

DIAGNOSIS
Tako-tsubo syndrome with midventricular involvement.
