HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
A 68-year-old woman, with no medical or surgical history of interest, was referred to the emergency department of our hospital for oppressive central thoracic pain.
The patient denies known drug allergies. Cardiovascular risk factors include obesity and type 2 diabetes mellitus on metformin. She has no family history of early ischaemic heart disease or sudden cardiovascular death.
Previously asymptomatic from the cardiovascular point of view, on the day of admission, during an intense discussion in the neighbourhood, she reported the onset of oppressive central thoracic pain, radiating to the back and left upper limb, lasting approximately 45 minutes, for which she alerted the emergency services, who transferred her to the emergency department of our hospital.
At our assessment, she persisted with central thoracic pain of similar intensity, with no significant improvement after nitrates. The patient denied other accompanying symptoms (no associated vegetative cortex, dizziness or dyspnoea).
On physical examination, the patient was in relatively good general condition, eupneic at rest (baseline sats O2 100%), well perfused, with blood pressure around 180/83 mmHg, heart rate 45 bpm. Cardiac auscultation is rhythmic, with no audible murmurs. No evidence of congestion (normal jugular venous pressure, preserved vesicular murmur without added noise, lower extremities without oedema), and with preserved pulses at all levels.

COMPLEMENTARY TESTS
ECG on admission: complete atrioventricular block (AVB) with wide QRS leak with morphology of left bundle branch block (LBBB) at 50 bpm.
Repolarisation consistent with LBBB.
Chest X-ray: normal cardiothoracic index, with no evidence of pulmonary congestion or other pathological findings.
Laboratory tests on admission: haemogram: leucocytes 6,600/μl, haemoglobin 12.2 g/dl, platelets 227,000/μl. Coagulation: INR 1, PT 100%. Biochemistry: glucose 164 mg/dl, urea 31 mg/dl, creatinine 0.89 mg/dl, glomerular filtration rate 67 ml/min/1.73 m2, sodium 143 mEq/dl, potassium 3.5 mEq/dl, proBNP 3,664 pg/ml (at discharge 314 pg/ml). Peak myocardial damage markers: CK 193 (10-195 IU/l), troponin US 194.8 (0-13 ng/l).
Transthoracic echocardiogram (TTE) (videos 1-5): left ventricle not hypertrophic and size at the high limit of normal (LVEDD 52 mm, IVS 11 mm, PP 9 mm). Mid-apical septal akinesia, mid-apical lateral, mid-apical anterior and the rest of the apical segments, with hypercontractility of the bases and moderately depressed global systolic function (EF 35%). Right ventricle of normal size and function (TAPSE 21 mm, S wave 0.14 m/s). Mitral valve with sclerosed leaflets and mild insufficiency. Conclusion: segmental alterations compatible with transient apical dyskinesia syndrome, with moderately depressed systolic dysfunction.
Emergent haemodynamic study: 1-vessel coronary artery disease due to severe stenosis of small diagonal 1a, with the rest of the vessels without significant lesions (moderate stenosis in the middle third of the anterior descending artery). Ventriculography was performed, showing a dilated ventricular chamber, with akinesia of the apical segments and hypercontractility of the basal segments, suggestive of tako-tsubo syndrome.
Cardiac magnetic resonance imaging (MRI): normal sized left ventricle (53 mm) with akinesia of the apical anterior wall, apical inferior wall and apical septum. Hypokinesia of the basal and medial inferior wall. Oedema of the mid septum, mid anterior, apical segments except lateral wall and LV apex. No areas of hypoperfusion or late enhancement are identified. LVEF 52%. LV-DVT: 91mL. LV-STV: 44mL.
LV-LV: 47mL. Right ventricle of normal size with no abnormalities in contractility and preserved morphology. Atria of normal size. Conclusion: study compatible with clinical suspicion of tako-tsubo syndrome.

CLINICAL EVOLUTION
In view of the clinical manifestations and the alterations in the electrocardiogram, the patient was admitted to the coronary unit of our department to complete studies and initiate therapeutic measures.
An echocardiogram was performed which showed segmental alterations compatible with transient apical dyskinesia syndrome, with moderately depressed systolic dysfunction (LVEF 35%), and it was decided to perform an emergent haemodynamic study which described 1-vessel coronary artery disease due to severe stenosis of small diagonal 1a, with the rest of the vessels without significant lesions (moderate stenosis in the middle third of the anterior descending coronary artery).
Ventriculography was performed, in which a dilated ventricular chamber was observed, with akinesia of the apical segments and hypercontractility of the basal segments, suggestive of tako-tsubo syndrome.
In the following days, the studies were completed with a cardiac MRI consistent with the diagnosis of transient apical dyskinesia, in which an improvement in LV ejection fraction was observed.
However, the patient persisted with complete AVB 1 week after her debut, so it was decided to implant a DDDR permanent pacemaker.

DIAGNOSIS
Transient apical dyskinesia syndrome. LVEF 52% at discharge.
Complete BAV with wide QRS escape rhythm.
DDDR pacemaker implantation.
1-vessel coronary artery disease: significant stenosis of D1 (small calibre vessel).
