HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
59-year-old woman. No cardiovascular risk factors or previous pathological history. No chronic treatment.   Present illness On 8 March the patient was giving a speech at a rally for Women's Day. Suddenly and before she could finish reading her manifesto, she suffered a sudden syncopal episode, without prodromes and with spontaneous recovery after a few seconds. On regaining consciousness she presented with epigastric pain radiating to the left hemithorax with associated vegetative cortex. The patient had no palpitations or dyspnoea prior to syncope. Unable to finish her speech, she was referred to the emergency department for assessment.

Physical examination
Blood pressure 104/60 mmHg, heart rate 75 bpm, oxygen saturation by pulse oximetry 97% on room air. Afebrile. Good general condition. Conscious and oriented. Eupneic at rest, tolerates decubitus. No jugular ingurgitation. Cardiac auscultation: regular, rhythmic heart sounds, no murmurs or pathological sounds. Pulmonary auscultation: normal ventilation in all lung fields. Abdomen: soft, depressible, non-painful, without megaliths. Lower extremities: no oedema, distal pulses present.



COMPLEMENTARY TESTS
Electrocardiogram on admission: sinus bradycardia at 58 bpm. Normal PR. Narrow QRS, normal axis at -10o. ST segment elevation of 1mm in V5-V6. QTc 388 ms.
Electrocardiogram at discharge: sinus bradycardia at 44 bpm. Normal PR, narrow QRS, axis at 0o. Negative T wave in V4-V6, I and aVL, II; flat T wave in III and aVF. QTc 391 ms.
Chest X-ray: normal cardiothoracic index. No alveolar consolidation or pleural effusion.
Laboratory tests: biochemistry: normal thyroid function. Creatinine 0.57 mg/dl. Total cholesterol 225 mg/dl (HDL 31 mg/dl; LDL 176 mg/dl). Serum total bilirubin 0,59 mg/dl. Total proteins 6.1 g/dl, albumin 3 g/dl. Chlorine 108 mEq/l, potassium 4.7 mEq/l, sodium 141 mEq/l. CK 138 U/l, FA 87 U/l, GGT 19 U/l, GOT 32 U/l, GPT 13 U/l, LDH 158 U/l. Glycosylated haemoglobin 5.5%. Troponin I 4,468 ng/l (normal < 11.6 ng/l), proBNP 1,909 pg/ml. Haemogram: leucocytes 5000/mm3 (N 2,600/mm3; L 1,900/mm3), haemoglobin 14.2 g/dl, platelets 171,000/mm3.

Cardiac catheterisation: Coronary angiography: right dominance. Left common trunk without angiographic stenosis. Anterior descending (AD) with angiographically mildly moderate stenosis in the proximal third, the rest of the main vessel has no angiographic stenosis. Rest of vessels without angiographic stenosis.
Optical coherence tomography (OCT) was performed on the LAD, which in the proximal segment showed a minimal luminal area of 4.22 mm2 with integrity of the endothelium despite plaque burden. Functional assessment shows RFR 0.93, after hyperemia with i.v. adenosine FFR 0.90 and microcirculation study shows CFR 2 and IMR 44: evidence of microvascular dysfunction. Ventriculography shows a left ventricle (LV) of normal size with akinesia of all apical segments and hypercontractility of the basal segments. No intraventricular or aortic transvalvular gradient was detected.

Cardiac magnetic resonance: findings compatible with takotsubo syndrome. Diffuse hypersignal indicating the presence of oedema in the middle segments, apical segments and apex segment in T2-weighted T2-weighted TSE-FAT SAT sequences in short axis and two chambers. Absence of late gadolinium enhancement. Currently no apical dyskinesia is identified (with synchronous and homogeneous contractility), left ventricular ejection fraction 71%. No associated apical thrombus is observed. Right ventricle (RV) with normal function.

Echocardiogram at discharge: left ventricle of normal size and thickness. Left ventricular ejection fraction normal, without contractile asymmetries. Left ventricular end-diastolic pressure data not elevated. Right ventricle normal in structure and function. Mitral valve normal in structure and function with minimal insufficiency. Normal tricuspid valve, with minimal tricuspid insufficiency allowing estimation of a pulmonary artery systolic pressure (PSAP) of 25 mmHg. Trivalve aortic valve. The aortic root is of normal size. There is no pericardial effusion.

CLINICAL EVOLUTION
The patient was referred to the emergency department of our hospital, where an electrocardiogram was performed, showing ST segment elevation of 1 mm in the lower lateral face. It was decided to perform emergent coronary angiography. Cardiac catheterisation revealed a coronary tree with no lesions, except for angiographically mild-moderate stenosis in the proximal LAD. To assess the stenosis of the LAD, it was decided to perform an optical coherence tomography (OCT) study. The OCT showed a luminal area greater than 4 mm2 with integrity of the endothelium. The haemodynamic study was completed with an assessment of the microcirculation showing microvascular dysfunction with a low coronary flow reserve (CFR) and a high microvascular resistance index (MRI). Ventriculography was performed, showing akinesia of the apical segments with hypercontractility of the basal segments; all highly suggestive of tako-tsubo syndrome. The patient was admitted haemodynamically stable and pain-free to the cardiac intermediate care unit. She progressed favourably, with no new chest pain, no signs of heart failure and no arrhythmic events. Electrocardiographically, there was a progressive negativisation of the T wave in the anterolateral and inferior face. The study was completed with a cardiac MRI scan showing oedema in the middle and apical segments with absence of late gadolinium enhancement, findings compatible with tako-tsubo syndrome. Prior to discharge, an echocardiogram was performed showing recovery of myocardial contractility. In view of the good evolution, hospital discharge was decided with treatment with bisoprolol 2.5 mg every 24 hours, enalapril 2.5 mg every 24 hours and atorvastatin 40 mg every 24 hours.

DIAGNOSIS
Tako-tsubo syndrome. Microvascular dysfunction. Global and segmental left ventricular systolic function recovered at discharge.
Mild-moderate atherosclerotic lesion in the anterior descending artery without functional repercussions.
