HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
A 70 year-old man attended the emergency department of our centre due to dyspnoea.

History
Cardiovascular risk factors: no arterial hypertension, no diabetes mellitus, no dyslipidaemia. Active smoker of 1 pack a day since the age of 20 (50 packs/year). Obesity grade II (body mass index [BMI] 37 kg/m2).
No previous cardiological history.
Moderate chronic obstructive pulmonary disease, chronic bronchitis type (FEV1 51% of predicted), non-exacerbating. Follow-up in outpatient pulmonology department.
Stage IIIb colon adenocarcinoma (p3T3N1M0) diagnosed in 2015, treated with laparoscopic right colectomy + adjuvant chemotherapy with 5-fluoruracil + oxaliplatin which ended in 2017, free of disease with normal serial colonoscopies to date.
Benign prostatic hypertrophy.
Usual treatment: tamsulosin + solifenacin 0.4/6 mg, 1 tablet per day. Salmeterol + fluticasone 25/250 mcg, 1 inhaled capsule per day.

Present illness
Progressive increase in baseline dyspnoea of 2 weeks' evolution (usual CF NYHA II, in the context of bronchopathy) until presenting dyspnoea at rest, associated with orthopnoea that forced him to sleep in a sitting position, oedematisation of the lower limbs and subjective decrease in the volume of diuresis.


Physical examination
Blood pressure (BP) 137/70 mmHg, heart rate (HR) 90 bpm, Sat 2O89% on room air. Jugular venous pressure at 12 cm H2O. Cardiac auscultation: rhythmic, with a systolic murmur in mitral focus III/VI, radiating to the axilla. Pulmonary auscultation: bilateral crackles in midfields and bases. Abdomen: soft and depressible, not painful on palpation, no masses or megaliths. Hepatojugular reflux positive Extremities: oedema up to the knees +++/++++, peripheral pulses preserved and symmetrical, no signs of phlebitis.
Echocardioscopy performed at the bedside in the emergency department revealed dilatation and biventricular dysfunction, as well as significant mitral regurgitation, so it was decided to admit the patient for stabilisation and study.

COMPLEMENTARY TESTS
Electrocardiogram: sinus rhythm at 90 bpm. Narrow QRS, axis at 30o. ST-segment depression of 1 mm from V3 to V5 with negative T wave. Asymmetric negative T wave in lateral face as a sign of systolic overload.
Chest X-ray on admission: posteroanterior projection. Increased cardiothoracic index. Free costophrenic sinuses. Prominent pulmonary hilae. Signs of vascular redistribution to upper fields.
Laboratory tests on admission:
Haemoglobin 14.7 g/dl, MCV 89 fl, MCH 28.3 pg, leukocytes 5.5 x 10`9/l, platelets 183 x 10^9/l.
Haemostasis: I. Quick 93.7%, INR 1.1, TTPa ratio 0.95.
Biochemistry: glucose 110 mg/dl, HbA1c 5.6%, sodium 141 mEq/l, potassium 3.9 mEq/l, creatinine 1 mg/dl, urea 41 mg/dl, NT-proBNP 6,789 pg/ml, LDL-C 92 mg/dl.
Myocardial damage biomarker curve (hsTnI, normal < 19.8 ng/l): 32.6 - 37.8 - 35.4 ng/l.
Echocardiogram: moderately dilated left ventricle, with normal thickness. Global hypokinesia, with LVEF 30%. Transmitral filling type relaxation disturbance with estimated normal left ventricular end-diastolic pressures (E/E' = 7). Severely dilated left atrium. Moderate functional mitral regurgitation with ORE by PISA of 0.2 cm. Sclerosed, normofunctioning aortic valve. Aortic root not dilated. Right ventricle of normal diameters and mild ventricular dysfunction (TAPSE 15 mm). Mild tricuspid insufficiency that allows estimating PSAP of 60 mmHg. Inferior vena cava 19 mm with respiratory variation < 50%.
Coronary angiography 1: calcified left main coronary artery with 20-30% stenosis distally. LAD with severe proximal and middle disease with stenosis around 80%. Borderline lesion in the ostial circumflex artery (50%) and significant lesion in the first marginal branch. Right coronary artery with 70% lesion in the proximal segment and 50% at the level of the crux cordis.
Cardiac magnetic resonance imaging (MRI): left ventricle with increased volumes (VTD 107 ml/m, VTS 75 ml/m) with mild eccentric hypertrophy (IMVI 97 g/m2), generalised global hypokinesia and severe depression of global systolic function (LVEF 30%). No myocardial oedema is seen on STIR sequences. Non-dilated right ventricle (RVOT 58 ml/m, STV 33 ml/m) with slightly depressed global systolic function due to generalised hypokinesia (RVEF 43%). Aortic root diameters at the upper limit of normal (sinus portion 38 mm) with moderate dilatation of the tubular portion of 47 mm. Fallen 32 mm. Descending aorta 29 mm. Left atrium slightly dilated (maximum diameter 50 mm, area 15 cm2/m2). Increased pulmonary vascular resistance, estimated at 6 UW (mean pulmonary velocity 8.4 cm/sec). No perfusion defects detected at rest. Necrosis and viability detection study: presence of late gadolinium enhancement suggestive of linear intramyocardial fibrosis at septal-anterior basal and medial level and focal at septal-inferior and inferior basal and medial level, at the LV and RV junction.
Coronary angiography 2 (videos 5-7): Impella device is positioned by right femoral access. Angiography is performed via left radial access. Severe LAD lesions are pre-dilated and everolimus-eluting drug-eluting stents 3 x 48 mm and 3.5 x 18 mm are implanted. The distal circumflex guidewire was crossed and IVUS aostium was performed, detecting a luminal area > 6 mm2 and therefore not significant. The lesion was treated in the first obtuse marginal area with a constant everolimus-releasing drug 2.5 x 33 mm with good results. The guidewire was crossed to the distal DC, predilatation of the lesion in the proximal segment and implantation of a 3.5 x 15 mm everolimus-eluting drug-eluting stent. Good result. Finally, the Impella device is removed according to protocol. Femoral haemostasis with Proglide intravascular suture device.

CLINICAL EVOLUTION
On admission to the cardiology ward, intensive depletive treatment was started, with 40 mg of i.v. furosemide every 6 hours, with excellent response to the same, with dyspnoea disappearing at rest and progressive toleration of ambulation without incident.
A regulated echocardiogram confirmed the presence of severe left ventricular dysfunction, so treatment was started with enalapril 2.5 mg daily, bisoprolol 2.5 mg daily and spironolactone 25 mg daily with good tolerance.
As part of the aetiological study of the ventricular dysfunction, elective coronary angiography was performed, which revealed 3-vessel disease, with a SINTAX score of 26.
The case was presented at a medical-surgical session. Given the patient's comorbidities (moderate-severe chronic obstructive pulmonary disease [COPD], obesity, severe ventricular dysfunction, STS score 3.7%, EuroScore II of 6.7%), despite the SINTAX score favourable to surgical revascularisation, it was decided to perform percutaneous revascularisation assisted with Impella device as the procedure was considered high risk, to be performed on an outpatient basis.
The patient was discharged with the following medical treatment: acetylsalicylic acid 100 mg per day, enalapril 2.5 mg per day, bisoprolol 2.5 mg per day, spironolactone 25 mg per day, furosemide 40 mg 1 tablet at breakfast and lunch for 2 weeks followed by 1 tablet at breakfast, tamsulosin + solifenacin 0.4/6 mg 1 tablet per day, salmeterol + fluticasone 25/250 mcg 1 inhaled capsule per day, atorvastatin 40 mg per day, pantoprazole 20 mg per day. The importance of weight loss, physical exercise and smoking cessation was stressed.
She consulted the emergency department one week after discharge due to palpitations lasting 2 hours, with new onset paroxysmal atrial fibrillation detected on electrocardiogram. A rhythm control strategy was followed, achieving pharmacological cardioversion after an intravenous bolus of 300 mg of amiodarone. At discharge, treatment with apixaban 5 mg every 12 hours was added due to CHADs-VASc of 3 and oral amiodarone 200 mg 5 days a week.
Subsequently, percutaneous revascularisation was programmed with mechanical assistance with Impella CP device, which was performed without incident. He received clopidogrel 300 mg the night before admission. After 24 hours of hospitalisation, he was discharged with the addition of clopidogrel 75 mg per day to the aforementioned treatment. After 1 month of triple therapy (ASA + clopidogrel + apixaban), treatment with acetylsalicylic acid was discontinued.
Six months after revascularisation, the patient attended a clinical control visit, and was found to be practically asymptomatic for dyspnoea or other symptoms of heart failure, in NYHA functional class I. He is currently awaiting echocardiography. He is currently awaiting a follow-up echocardiogram. No further visits to the emergency department were required due to decompensation.

DIAGNOSIS
Acute heart failure due to ischaemic dilated cardiomyopathy with severe left ventricular dysfunction (LVEF by cardiac MRI 30%).
Three-vessel coronary artery disease with a SINTAX score of 26 points.
Paroxysmal atrial fibrillation (CHADs-VASc = 3, HAS-BLED = 2).
High risk device assisted PCI with Impella CP device with complete revascularisation (proximal LAD, mid LAD, distal DC and 1OM with excellent angiographic outcome).
Moderate COPD phenotype chronic bronchitis. Smoking on admission. Obesity.
