HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
Female patient aged 43 years, without CVRF or toxic habits. No medical or cardiological history, without taking regular medication.  Present illness She presented with syncope during her work activity, preceded by a feeling of dizziness and instability with rapid recovery afterwards. He began with central thoracic oppression and interscapular irradiation, haemodynamic instability, with an electrocardiogram suggestive of LMCA involvement. A chest CT scan was requested which ruled out acute aortic syndrome, the Infarction Code was activated, a loading dose was administered (ASA 300 mg and ticagrelor 180 mg) and the patient was referred to the reference hospital for urgent coronary angiography.

Physical examination (on arrival at the haemodynamics ward)
Poor general condition. Conscious and oriented, generalised pallor. Tachypnoea, sweating, hypoperfused BP 60/40 mmHg, HR 120 bpm. SatO2 (with Oxiplus at 8 litres): 92 %. Afebrile. Cardiac auscultation: rhythmic without audible murmurs, tachycardic. Pulmonary auscultation: bilateral crackles up to midfields. Abdomen: soft, depressible, non-painful, no masses or megaliths, no signs of peritoneal irritation, no oedema or indirect signs of DVT.

COMPLEMENTARY TESTS
ECG (initial): sinus rhythm, PR 0,18. Axis 60 o. ST elevation suggestive of subepicardial lesion up to 3 mm in I, avL, V5 (V6 without elevation due to probable artefact, V6 poorly positioned). Concomitant ST-segment elevation in inferior face up to 4 mm. Blood tests: cardiac markers (peak numbers) Trop I 56.39, myoglobin 300, proBNP 9500. Biochemistry: glucose 140 mg/dl, urea 24, creatinine 0.62 mg/dl, Chlorine 99 mEq/l, Na 134 mEq/l, K 4.6 mEq/l. Thyroid function: TSH 6,30. T4L 0.89. Iron metabolism: ferritin 265.9, transferrin 250, SatTf 15.4 %. Vitamin B12 and folic acid normal. Autoimmunity and coagulation studies negative. Haemogram: 25,500 leucocytes, Hb 12.2 g/dl, Hto 37.8%, 197,000 platelets. Coronary angiography: aortography: no images suggestive of acute aortic syndrome. Coronary angiography: right dominance. Left main coronary artery (LMCA): subocclusion compatible with spontaneous mid-distal dissection involving the ostium of the anterior descending (LAD) and proximal segment of the CX. Anterior descending: except ostial dissection, vessel of good calibre and development without lesions, initial flow TIMI 1-2. Cx: ostial and proximal dissection involving first marginal (Mo) of small entity. Second Mo of good development without lesions. Right coronary: no significant angiographic lesions. Percutaneous coronary interventionism: PCI on LMCA: during the procedure he presented sustained ventricular tachycardia at 160 bpm, with haemodynamic instability, which required synchronised CVE at 100 J with success. Synergy 4 x 24 mm direct drug-eluting stent was implanted in the LMCA with good results, TIMI 3 flow in the LAD, with angiographic improvement of the ostial-proximal CX. It was decided to finalise the procedure by implanting an intra-aortic balloon counterpulsation device (IABP) and noradrenaline perfusion.

Transthoracic echocardiogram (at discharge): LV slightly dilated (LVEDD 54 mm). Severe systolic dysfunction (LVEF estimated by Simpson "s 30%). Medial and apical septal akinesia and all apical segments, medial lateral (these segments being thinned). Inferoapical dyskinetic aneurysm. Medial lateral and anterior medial hypokinesia. Rest of segments contractility preserved. Pseudonormal diastolic pattern, without current data of elevated preload. Left atrium of normal dimensions. Normal right chambers, RV normocontractile. Normal aortic root and visualised portion of proximal ascending aorta. MV: thin leaflets, mild central reflux. VAo: trivalva, thin leaflets, competent. Minimal TR. IVC not dilated with inspiratory collapse. Estimated normal PAPs. Slight pericardial effusion adjacent to the right cavities, with no current signs of haemodynamic echocardiographic compromise. Intravenous contrast was administered which ruled out the presence of apical thrombus, but slow flow in the area of inferoapical aneurysm.  EVOLUTION Admitted to the coronary ICU in cardiogenic shock and acute pulmonary oedema requiring high-dose inotropic support, non-invasive mechanical ventilation (NIV) and IABP, presenting at the acute moment with SVT and haemodynamic instability requiring effective ECV. Slow and progressive clinical improvement allowed withdrawal of IABP and lowering of inotrope, with a control echocardiogram in ICU showing moderate LV dysfunction (low intravenous inotrope), with no secondary mechanical complications. During his stay on the ward, he was clinically stable, with no arrhythmic events. A repeat echocardiogram at discharge showed severe LV dysfunction, with akinesia of apical segments, inferoapical dyskinetic aneurysm, with no evidence of systemic congestion or significant valvular heart disease. She presented fair blood pressure figures that prevented treatment with ACE inhibitors and beta-blockers, so ivabradine was started for optimal heart rate control; double antiplatelet therapy was maintained for at least one year, eplerenone and diuretics at low doses, and she was discharged. A new control echocardiogram was performed in 40 days with no improvement in echocardiographic data, so it was decided to implant a subcutaneous ICD for primary prevention. She continued to be reviewed by the Heart Failure and Cardiac Rehabilitation Unit, with current functional class II/IV NYHA.

DIAGNOSIS
Acute coronary syndrome with ST segment elevation (STEACS) anterolateral Killip IV. Spontaneous coronary artery dissection of LMCA to LAD and CX. Percutaneous coronary intervention on LMCA-AD (1 drug-eluting stent). Severe LV dysfunction with contractile segmental asymmetries. Subcutaneous ICD implantation for primary prevention.
