HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
We present a 65-year-old man with no known drug allergies. Background As personal history, he is being treated with ezetimibe/atorvastatin 10/80 mg for familial hypercholesterolaemia (last available LDL 50 mg/dl). No other known cardiovascular risk factors, no toxic habits. Body mass index (BMI) 26.7 (overweight). With regard to family history, history of early ischaemic heart disease in a brother at 50 years of age (he died for this reason).

Current disease
A 65-year-old patient with the aforementioned history came to the emergency department referred by 061 after presenting at home with oppressive central thoracic pain with associated vegetative crusade lasting 15 minutes. He had not presented with previous episodes of chest pain. The electrocardiogram performed by the emergency department showed anterolateral ST elevation, so ticagrelor (180 mg) and aspirin (300 mg) were administered and the infarction code was activated.

Physical examination
During transfer by 061 and on arrival at the haemodynamics room, the patient was haemodynamically stable, well perfused, with the need for low-flow oxygen. Vital signs: blood pressure 121/85 mmHg, heart rate 75 bpm. Oxygen saturation 93% with nasal goggles at 2 bpm. Eupneic at rest. On cardiac auscultation rhythmic tones without audible murmurs. Pulmonary auscultation with bibasal crackles. No megaliths, mild jugular ingurgitation. No oedema in the lower extremities.

COMPLEMENTARY TESTS
Electrocardiogram (ECG): sinus rhythm at 75 bpm, q v1-v2, ST V1-V4, I and AVL with specular decrease in inferior face. Blood tests on admission: acid-base balance PH 7.44, PCO2 34 mmHg, bicarbonate 23.1 mmol/l, lactate 3.8 mmol/l, sodium 142 mmol/l and potassium 3.6 mmol/l. Biochemistry urea 37mg/dl, creatinine 1.24 mg/dl. Troponin I ultrasensitive peak 196000 μg/l. NT-proBNP 8682 pg/ml. Coronary angiography: Acute complete occlusion of distal common trunk (CT). Left anterior descending artery (LAD): occluded vessel with homolateral perfusion TIMI 0. After opening, ectasia is seen in its proximal portion, with diffuse mild to moderate involvement of the entire vessel and thin distal bed. Second septal branch ectatic, with a long course and severe ostial lesion. Left circumflex artery (CX) proximal occluded vessel with homolateral perfusion TIMI 0. Right coronary artery (CD): dominant vessel, large calibre, ectatic and with moderate diffuse disease. Percutaneous coronary intervention was performed by implanting drug-eluting stents at distal CT level directed towards the LAD and subsequently at distal CT level towards Cx-first obtuse marginal. Echocardiogram (prior to discharge): dilated left ventricle (LV) (LVED 61 mm) with severe systolic dysfunction. Estimated LVEF 34% with contractile asymmetries. Right chambers of normal size and contractility. Mild aortic insufficiency (AIo). Moderate mitral insufficiency (MI) (II/IV). Estimated pulmonary pressure normal. Blood tests prior to discharge: NT-proBNP 6009 pg/ml (previous 8682), urea 36 mg/dl, creatinine 0.89 mg/dl, LDL 51 mg/dl, chlorine 105 mEq/l, sodium 139 mEq/l, potassium 4.4 mEq/l, haemoglobin 10.7 g/dl, haematocrit 31.5%, HbA1c 6.6%. Echocardiogram (after completion of phase II of cardiac rehabilitation; videos 5 and 6): Dilated LV (LVED 61 mm) with slightly depressed function. Estimated LVEF 46% with contractile asymmetries. Right chambers of normal size and contractility. Mild AoI. Moderate MI (II/IV). Blood tests after end of phase II: NT-proBNP 2178 pg/ml, creatinine 1.25 md/dl, LDL 50 mg/dl, HbA1c 6.3%.

CLINICAL EVOLUTION
During the percutaneous intervention in the haemodynamics room, our patient presented a progressive clinical worsening. Tendency to arterial hypotension with poor peripheral perfusion, requiring the initiation of vasoactive drugs (dobutamine and noradrenaline) at medium doses, as well as respiratory failure requiring non-invasive mechanical ventilation. Prior to leaving the haemodynamic ward, a balloon counterpulsation device (IABP) was implanted. During his stay in the intensive care unit he evolved favourably, allowing the weaning of vasoactive drugs and the removal of the IABP on the fourth day. During admission to the hospital ward (18 days of hospitalisation), congestive data persisted with very slow resolution despite forcing a negative water balance with intravenous diuretic, as well as borderline blood pressure and transient worsening of renal function that made it difficult to initiate neurohormonal treatment, and he was discharged in NYHA functional class (FC) II. The echocardiogram performed showed severely depressed ventricular function. Regarding treatment at discharge, priority was given to oral diuretic treatment with furosemide and eplerenone, together with low doses of beta-blockers, given the circumstances described above. After hospital discharge, our patient was referred to the cardiac rehabilitation unit (CRP) and, in parallel, began follow-up in the advanced heart failure unit. During phase II of the CRP, our patient underwent the educational programme, dietary recommendations, review of cardiovascular risk factors (CVRF) and home medical treatment. Subsequently, he successfully completed 8 weeks of face-to-face training guided by ergospirometry, supervised by the cardiologist and rehabilitation physician. Regarding treatment, drugs with prognostic benefit were prioritised (quadruple therapy), suspending furosemide treatment and reducing the dose of eplerenone, which allowed the progressive initiation, with close monitoring of renal function, of sodium-glucose cotransporter type 2 inhibitor (iSGLT2) and angiotensin receptor neprilysin inhibitor (ARNI) at low doses. Finally, intravenous ferric carboxymaltose was administered on an outpatient basis in day hospital (iron profile: iron 50 μg/dl, ferritin 150 ng/dl, haemoglobin 13.3 g/dl, haematocrit 44%). After close comprehensive management, our patient showed a clear improvement 4 months after the event, improving both in functional class (stable CF I) and in analytical data (final NTproBNP 2178 pg/ml; initial 8682 pg/ml) and echocardiographic data, with an estimated ventricular function of 46%.

DIAGNOSIS
Acute ST-segment elevation myocardial infarction (STEMI) anterior Killip-Kimball IV
Coronary artery disease of the common coronary trunk: distal CT occlusion
Ischaemic dilated cardiomyopathy (DCM) with severely depressed ventricular function
Impaired basal glycaemia Iron deficiency anaemia. Familial hypercholesterolaemia.
