HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

Personal history
37-year-old woman with the following personal history: No adverse drug reactions. She denies drug use. No known cardiovascular risk factors. Bronchial asthma without chronic treatment. Gynaecological history: two full-term pregnancies, vaginal delivery. No usual treatment.

Current history
A 37-year-old woman with the aforementioned history presented at rest with oppressive non-radiating central thoracic pain with vegetative crust. She attended her health centre for this reason, where an electrocardiogram (ECG) was performed with pathological alterations, so it was decided to administer a loading dose of 250 mg of acetylsalicylic acid (ASA) and 300 mg of clopidogrel, sublingual nitroglycerine and contact was made with the critical care and emergency department (DCCU) for transfer to her reference hospital.

Physical examination
Acceptable general condition. Conscious, oriented and cooperative. Eupneic at rest. Normal weight. Blood pressure (BP) 95/50 mmHg, heart rate (HR) 80 bpm. Jugular venous pressure normal. Cardiac auscultation: rhythmic tones at a good frequency, no murmurs or extratonos. Pulmonary auscultation: preserved vesicular murmur without added pathological sounds. Abdomen soft and depressible, not painful on palpation. No masses or megaliths are palpable. Hydro-aerial sounds present. No oedema in the lower limbs or sloping areas. Radial, femoral and pedal pulses were preserved bilaterally.

COMPLEMENTARY TESTS
Initial ECG: sinus tachycardia at 115 bpm competing with accelerated idioventricular rhythm (RIVA). In the sinus beats, normal PR, narrow QRS, ST segment elevation of 2 mm in V1 and aVR, and 1 mm in V2-3, with ST descent of 1-2 mm in inferior face and from V4 to V6. Blood tests on admission: haemoglobin 13.5 g/dl, haematocrit 40%, leukocytes 14,000/μl with neutrophilia 12,000/μl, platelets 222,000/μl. Coagulation: INR 1.1, TTPa 28 sec. Biochemistry: urea 22 mg/dl, creatinine 0.66 mg/dl, sodium 135 mEq/l, potassium 3.87 mEq/l. CPK total/MB 252/43 -> 2.256/264 U/l. Initial high sensitivity Troponin T 176 -> peak 2,910 ng/l (normal < 13.9 ng/l). Lipid profile: total cholesterol 113 mg/dl, triglycerides 81 mg/dl, HDL cholesterol 54 mg/dl, LDL calculated 43 mg/dl, VLDL cholesterol 16 mg/dl. Echocardioscopy on arrival at the emergency department: non-dilated left ventricle with normal wall thickness, severe hypokinesia of the apical cap and hypokinesia of apical segments and middle segment of inferolateral, lateral and anterior faces, with hypercontractility of the remaining segments. Moderate-severe left ventricular dysfunction, estimated LVEF 30-35%. Right chambers of preserved size with preserved function. Non-dilated atria. Mild-moderate mitral insufficiency by colour Doppler. No pericardial effusion. Inferior vena cava 16 mm with adequate inspiratory collapse. Urgent diagnostic coronary angiography (video 1): significant stenosis of the left coronary trunk due to probable intramural haematoma causing extrinsic compression of the lumen, without significant angiographic lesions in the rest of the coronary tree. Urgent CT angiography: thoracoabdominal aorta of normal calibre, with no signs of acute pathology. No images compatible with acute aortic syndrome. Bilateral pulmonary alveolar lesions distributed throughout the upper lobes and apical segment of the lower lobes, suggesting an aspiration aetiology. Nutcracker's phenomenon with varicose dilatation of the left gonadal vein due to stenosis of the left renal vein in the aortomesenteric clamp. Bilateral adnexal cysts, functional type and free fluid in Douglas recess. No other findings of interest. Coronary revascularisation coronary angiography: the left coronary trunk was probed with an EBU 3.5 guide catheter, a guide was passed to the distal vessel of the anterior descending artery and contrast injection was performed, proving spiroid dissection of the left coronary trunk with preserved distal flow, Onyx Resolute 4 x 26 mm drug-eluting stent was implanted at 16 atm in the trunk towards the anterior descending artery with a good final angiographic result, without residual dissection. Post-catheterisation ECG: sinus tachycardia. Normal PR. Narrow QRS, axis at 30o with QS of V1-V3, QR in aVL. Persistent ST-segment elevation in aVL, V1-3, ST-segment depression of 1 mm in inferior leads and negative T in aVL. Regulated transthoracic echocardiography prior to discharge: left ventricle of normal dimensions with normal wall thickness. Mild global hypokinesia more accentuated in mid-apical segments of inferolateral and lateral region. Mild systolic dysfunction (estimated LVEF 48%). Left atrium of normal dimensions. Aortic root not dilated. Right chambers not dilated. Right ventricle with normal contractility. No organic valvular pathology. No pericardial effusion. Inferior vena cava of normal calibre. Left ventricular filling with restrictive transmitral flow pattern. Flow at the level of the pulmonary veins, with diastolic predominance. No indirect signs of significant pulmonary hypertension. Normal antegrade flow. Mild degenerative mitral regurgitation. ECG at discharge: sinus rhythm at 75 bpm. Normal PR. Narrow QRS with QS in V1-V3. Millimetre ST subleveling in V3. Negative T in DI, aVL and V1-V5. Blood tests at discharge: Haemogram: haemoglobin 12.8 g/dl, leucocytes 8,940/μl with neutrophils 6,610/μl, platelets 158,000/μl. Coagulation normal. INR 1. Biochemistry: glucose 82 mg/dl, creatinine 0.60 mg/dl, potassium 3.28 mEq/l, CRP 47.62 mg/l, total CPK 188 U/l, troponin T at discharge 658 ng/l, ProBNP 5,147 pg/ml.


CLINICAL EVOLUTION
On arrival at the ED, the patient was hypotensive (blood pressure 95/50 mmHg, heart rate 80 bpm), saturating at 97% with nasal spectacles at 2 litres/minute and with persistent chest pain. Urgent echocardiography showed moderate to severe left ventricular systolic dysfunction and segmental alterations, and the patient was transferred to the haemodynamics department for urgent coronary angiography. The coronary angiography showed significant stenosis of the left main coronary artery due to a probable haematoma causing extrinsic compression, with no significant angiographic lesions in the rest of the coronary tree. Before proceeding to revascularisation, acute aortic syndrome was ruled out by urgent aortic CT angiography. After this, percutaneous revascularisation was chosen, so coronary angiography was repeated in the following hours and a stent was implanted in the left coronary artery towards the anterior descending coronary artery with good angiographic results. During the procedure, he presented hypotension and sinus tachycardia requiring continuous perfusion of noradrenaline (0.31 microg/kg/minute). She returned to the coronary unit asymptomatic, maintaining the noradrenaline perfusion which could be progressively withdrawn in the first 48 hours after revascularisation. After a favourable evolution, he was transferred to the hospital ward. Initially, double antiplatelet therapy was maintained with ASA 100 mg and clopidogrel 75 mg; however, given the high thrombotic risk due to stenting in the left coronary trunk, it was decided to switch to ticagrelor 48 hours after catheterisation. In the post-revascularisation echocardiographic control, severe left ventricular systolic dysfunction persisted, so treatment for heart failure was started with good tolerance, presenting mild ventricular dysfunction at hospital discharge. After hospital discharge, she was included in the cardiac rehabilitation programme, which she completed without incident. She is currently being monitored in cardiology consultations and has remained asymptomatic from the cardiovascular point of view. Follow-up echocardiography showed that left ventricular systolic function had recovered and was preserved one year after the event. Treatment at discharge: ASA 100 mg (every 24 hours), ticagrelor 90 mg (every 12 hours for one year), bisoprolol 1.25 mg (every 24 hours), ivabradine 5 mg (every 12 hours), ramipril 1.25 mg (every 24 hours), omeprazole 20 mg (every 24 hours).

DIAGNOSIS
Anteroseptal ST-segment elevation acute coronary syndrome (STEMI). Spontaneous coronary artery dissection of the left main coronary artery treated with drug-eluting stent in the left anterior descending coronary artery. Acute septo-apical myocardial infarction. Severe left ventricular systolic dysfunction in acute phase with subsequent recovery.
