HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
36-year-old woman, with the following medical history: No known adverse drug reactions. Never smoked. No consumption of alcohol or other intoxicants. No previous cardiological history. No history of heart disease in the family. Pregestational arterial hypertension with debut at 33 years of age, currently on treatment with labetalol 100 mg every 12 hours. Dyslipidaemia (LDL 200 mg/dl). Primiparous woman in recent puerperium after scheduled caesarean section performed 10 days ago, without immediate complications, with a healthy male newborn weighing 2,930g. The patient consulted the emergency department for several episodes in the last 3 days of oppressive precordial pain without associated irradiation or vegetative cortex, lasting between 5 and 30 minutes, of variable intensity and unrelated to exertion, with a tendency to hypertension during the episodes. Consultation for a new episode of greater intensity and duration. On arrival at the ED, blood pressure (BP) 165/104 mmHg; heart rate (HR) 79 bpm, oxygen saturation 98% FiO2 0.21; temperature 36.5 oC. On physical examination, the patient was conscious, oriented, eupneic at rest, without jugular ingurgitation. Cardiac auscultation with regular tones and no murmurs. Pulmonary auscultation with preserved vesicular murmur without aggregates. Radial and pedial pulses present and symmetrical. Absence of peripheral oedema.

COMPLEMENTARY TESTS
Electrocardiogram 1 (ECG) on arrival, with pain: sinus rhythm at 75 bpm, PR 180 ms, narrow QRS with axis at +30o, ST-segment depression < 0.5 mm in V4 to V6, flattened T in III. Painless ECG 2: sinus rhythm at 60 bpm, PR 180 ms, narrow QRS with axis at +60o, J-point rise of 0.5 mm in V2, biphasic T from V2 to V5, negative in I and aVL. Chest X-ray: normal cardiomediastinal silhouette, without images of consolidation or pleural effusion. Laboratory tests: Myocardial damage marker curve: ultrasensitive troponin T (TnTus) 58.7 to 420 pg/ml at 3h (normal values < 14 pg/ml). N-terminal pro-brain natriuretic peptide (NT-proBNP) 157 pg/ml. D-dimer 1560 ng/ml. Other biochemistry, haemogram and coagulation anodine. Bedside echocardioscopy: non-dilated left ventricle with preserved LVEF and anterior hypokinesia at mid-apical level. Non-dilated right ventricle with good systolic function. Absence of significant valvular heart disease. Absence of pericardial effusion. Abdominal ultrasound: placental debris ruled out. Coronary angiography 1: abrupt decrease in the calibre of the middle and distal anterior descending artery after the exit of the second diagonal developed, image compatible with spontaneous coronary dissection. Distal flow TIMI 3. Rest of arteries without lesions.

CLINICAL EVOLUTION
The patient was admitted to the coronary unit with stable, pain-free condition, with low-dose nitroglycerine perfusion and controlled blood pressure, and early coronary angiography was performed with the findings described. Given the absence of angina and TIMI 3 distal flow, conservative management in the coronary unit was initially decided. In the following days, the patient presented several short episodes of precordial pain lasting a few minutes, with no electrical changes or increase in markers of myocardial damage. On the third day of admission, she presented a new episode of pain of greater intensity, with an electrocardiogram (ECG 3) showing ST-segment elevation >1mm in V1 to V4 and 0.5mm in III and aVF. It was decided to perform a new coronary angiography (video 2. Coronary angiography 2) which showed distal progression of the dissection, with worsening of the lumen of the artery at the medial level and complete collapse of the same in the apical segment, with weak homolateral collaterals (Rentrop 1). Given the haemodynamic stability, the disappearance of pain with electrocardiographic improvement after medical treatment and the location of the occlusion in the distal-apical segment, conservative management was again decided, with good initial evolution and progressive decrease in markers of myocardial damage. Six days later, the patient presented a new episode of intense precordial pain accompanied by haemodynamic deterioration with hypotension (TAS 70 mmHg) requiring vasoactive drugs, respiratory deterioration, radiological worsening compatible with acute pulmonary oedema (chest X-ray) and new elevation of myocardial damage markers from 500 to 3750 pg/ml. The ECG (ECG 4) shows ST-segment elevation > 2 mm in V4-V5 and 0.5 mm in II, III and aVF. It was decided to perform a new coronary angiography (Coronary angiography 3) which showed progression of the dissection at the proximal level, with complete occlusion of the vessel at the middle level and distal vessel weakly visualised by homocoronary collaterals (Rentrop 1). In view of the shock situation and TIMI 0 flow, it was decided to intervene guided by intravascular ultrasound (IVUS), and after placing the angioplasty catheter and passing the guidewire to ADA and diagonal, an image of dissection in the distal left coronary artery (possibly facilitated by the tip of the catheter on a susceptible intima) with TIMI 0 flow in all branches was observed. A 3.5 x 28 mm drug-eluting stent was implanted in the coronary trunk to the proximal anterior descending coronary artery and a second 3.5-3.0x60 mm stent was implanted distally, restoring TIMI 3 flow in the distal anterior descending artery although with persistent non-occlusive dissection, and first diagonal with TIMI 1 flow. Finally, conservative management of the circumflex artery ostium was chosen after restoring distal TIMI 3 flow, once the entry port had been sealed. The patient evolved favourably over the following days, with resolution of the shock situation and discharge to the cardiology ward. Regular echocardiography was performed (video 4) and the study was completed with cardiac magnetic resonance imaging (video 5), showing dilatation of the left ventricle with severe depression of its systolic function (LVEF 34%) secondary to alterations in segmental contractility in apical segments and on the lateral side, transmural necrosis of 4 segments of the LAD territory (apical segments) and non-transmural necrosis on the lateral side. During follow-up at discharge from the heart failure unit, prognostically evident drugs were prescribed and, given the absence of improvement in systolic function, an ICD was placed for primary prevention.

DIAGNOSIS
Spontaneous coronary artery dissection associated with pregnancy.
Non-ST-segment elevation acute coronary syndrome (NSTEACS).
ST-segment elevation acute coronary syndrome (NSTEMI).
