HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION
We present the case of a 42-year-old female patient, active smoker as the only cardiovascular risk factor (15 cigarettes/day since adolescence), with no personal or family cardiological history prior to this event. On the night of admission, at around 21:00 hours and at rest at home, she began with oppressive central thoracic pain, discomfort in the left upper limb and marked vegetative cortex (emesis, diaphoresis and persistent nausea). Half an hour after the onset of the symptoms, she decided to call 061 who, on arrival at her home, performed an electrocardiogram showing ST elevation in the anterior face. In view of these findings, the haemodynamics department was contacted and the patient was transferred to our hospital for emergency coronary angiography. Coronary angiography was performed, showing dissection of the LAD from its proximal segment along its entire length with initial TIMI 2 flow (dominant RCA and RCA without lesions). After successive contrast injections, the flow in the LAD and diagonal improved, and conservative management was chosen. The patient was transferred to a monitored unit in Cardiology to continue her evolution. On arrival the patient was haemodynamically stable: BP 110/60, HR 80 bpm, SatO2 98% with nasal goggles at 2 l/min. Afebrile. Physical examination was unremarkable with no systemic/pulmonary congestive semiology or low output. Clinically, she persisted with slight retrosternal discomfort that gradually disappeared in the hours following catheterisation.

COMPLEMENTARY TESTS
Blood tests: glucose 106 mg/dl. Creatinine 0.51 mg/dl. Urea 24 mg/dl. Sodium 142 mEq/l. Potassium 4.4 mEq/litre. Lipid profile: total cholesterol 146 mg/dl. LDL-Col 37 mg/dl. LDL-Col 88 mg/dl. Triglycerides 106 mg/dl. Normal liver and thyroid profile. Glycated Hb 5.2%. Peak TNTUs 9613 ng/dl. Peak CPK 3219 mg/dl. Rheumatoid factor, CRP, ESR, ESR, proteinogram, complement, ACE, microalbumimuria and normal hormonal study. Initial leukocytosis (predominance of polymorphonuclear cells) which subsequently normalised. Hb 14 g/dl. Platelets 349,000. ANA and ANCA negative. Electrocardiograms: 061: sinus rhythm at 80 bpm. Normal axis normal PR normal. Narrow QRS with minimal R to V4 with ST elevation from V2-V6 (up to 4 mm in V4). Minimal lateral upstroke and ST rectified in AvR. At discharge: sinus rhythm at 70 bpm. Normal axis. Normal PR. Narrow QSR with QS from V1-V4. Flattened T waves in frontal plane leads. Catheterisation: left coronary trunk without lesions. Anterior descending artery with dissection from the proximal segment affecting its entire course. Double descending-diagonal system. Initial TIMI 2 flow. Circumflex artery without lesions. Dominant right coronary artery without lesions. Successive injections of contrast were repeated with improved flow in the LAD and diagonal, so conservative management was adopted. Echocardiography at discharge: LA of normal size (27 mm, 29 ml/m2). Normal mitral valve. LV: DTD 48 mm, VTD 107 ml, VTDi 71 ml/m2. EF by Simpson biplane 36%. Akinesia of the apical half of all walls. No mural thrombus seen. Septum 9 mm and inferolateral wall 7 mm. Mitral E 46 cm/sec and A 56 cm/sec. Normal aortic valve. Sinuses of Valsalva 32 mm. Non dilated right chambers with good RV systolic function. Mild TR with normal estimated PAPS. Non dilated IVC with inspiratory collapse > 50%. No pericardial effusion (Video 3-6). Angio-CT of renal arteries (conclusions): kidneys without abnormalities. No evidence of renal stenosis or fibromuscular dysplasia. Double left renal artery and fine calibre supernumerary artery in the right kidney. Ergometry at the beginning and end of CRP: clinical and electrical negatives for the level of effort reached. Adequate blood pressure response in both. No arrhythmic events. Start-final functional capacity (10-13 METS), start-final exercise time (9 min-12 min) and start-final heart rate recovery rate (17 bpm-30 bpm).

EVOLUTION
Once the diagnosis was known, the patient was re-historised, orienting the anamnesis towards the search for risk factors related to this entity. The patient was an active smoker, smoking having been related to this pathology (by facilitating endothelial damage). She had previously taken oral contraceptives and had been using an intrauterine device (IUD) as a contraceptive measure for two years. The pregnancy test performed during admission was negative. She did not remember having exercised more than usual during the previous days. She did report emotional stress the previous week in relation to her daughters' school problems. She had no symptoms compatible with connective, autoimmune, rheumatological or systemic inflammatory diseases. A blood test was performed with a lipid, thyroid and liver profile with no notable alterations. An autoimmunity study was requested (rheumatoid factor, CRP, ESR, immunogluilins, complement, ACE, hormonal study and antiphospholipid antibodies), which were normal. Angio-CT of the renal arteries was negative for renal stenosis and showed no data suggesting fibromuscular dysplasia. The patient presented a favourable clinical evolution during her admission. Echocardiography showed akinesia of the entire apical territory (without mural thrombus) and the ejection fraction (EF) was moderately depressed (Simpson biplane 36%). After clinical improvement and optimisation of medical treatment she was discharged home with double antiplatelet therapy.

The patient was referred to the cardiac rehabilitation programme (CRP) of our hospital, and was included in the high-risk group (20 sessions). She completed the programme without incident and with good adherence. Prognostic ergometry showed improvement in functional capacity (10-13 METS), exercise time (9 min-12 min) and heart rate recovery rate (17 bpm-30 bpm). Echocardiography at the end of the programme showed improvement in EF, with mild dysfunction (LVEF 49%). Finally, he has been periodically reviewed by Internal Medicine, which establishes that at the present time there are no clinical-biological data of autoimmune disease or phenotype-data of collagenopathy.

DIAGNOSIS
Anterior STEACS secondary to spontaneous coronary artery dissection of LAD. Akinesia of apical segments with moderate LV dysfunction at discharge (LVEF 36%). Negative autoimmunity/collagenopathy study. Completion of cardiac rehabilitation programme with improvement in functional capacity and partial recovery of LVEF (after CRP 49%).
