HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION
A 56-year-old male ex-smoker, with insulin-dependent type 2 diabetes mellitus, hypertensive, dyslipidaemic, hyperuricaemic and obese, with peripheral arterial disease (bilateral femoropopliteal stenosis not requiring revascularisation after evaluation by vascular surgery) whose cardiological history was ischaemic heart disease in the dilated phase.
In 2003 she had an anteroseptal fibrinolysis AMI and coronary angiography was not performed.
A new posteroinferior AMI in 2005 with coronary angiography showed chronic occlusion of the middle anterior descending artery, 90% lesion in the posterolateral artery, 40% lesion in the proximal right coronary artery and 80% lesion in the obtuse marginal artery.
Echocardiogram showed LVEF of 26%. Surgical revascularisation was performed with bypass of the internal mammary artery to the anterior descending artery, saphenous artery to the obtuse marginal artery and saphenous artery to the posterior descending artery. In 2013, a single-chamber defibrillator implant was indicated for primary prevention. Currently being monitored by Cardiology in NYHA functional class II.
Usual treatment: carvedilol 12.5 mg every 12 hours, ivabradine 5 mg every 12 hours, enalapril 2.5 mg every 12 hours, furosemide 80 mg per day, omeprazole 20 mg, atorvastatin 80 mg, ASA 100 mg, eplerenone 25 mg, allopurinol 300 mg, insulin lantus 40 units per day and insulin novorrapid.
The patient came to the emergency department for progressive dyspnoea in recent weeks until he became resting, with three-pillow orthopnoea and paroxysmal nocturnal dyspnoea. He also reported oedema in both legs and decreased diuresis.
He did not report palpitations or chest pain.
Physical examination showed blood pressure 145/70 mmHg, HR 80 beats/minute, BMI 41.2 kg/m2, baseline oxygen saturation 90 %, tachypnoea, and he was afebrile. He showed jugular ingurgitation up to the mandibular angle, moist crepitant rales up to midfields, rhythmic hypophonic tones with systolic murmur in mitral focus II/VI, a globular abdomen with no palpable megaliths, no signs of ascites and tibio-malleolar oedema with fovea up to the proximal third.
Chest X-ray, electrocardiogram, blood tests showed: absence of anaemia, slightly impaired renal function, normal ions and mild elevation of cardiac biomarkers in plateau, and tristatic echocardiogram showed severe dilatation of the left ventricle, severely depressed LVEF and severe functional mitral regurgitation.

COMPLEMENTARY TESTS
Chest X-ray: cardiomegaly at the expense of the left cavities, fluid in the medial cisure, vascular redistribution and perihilar alveolar-interstitial infiltrate.

Electrocardiogram: sinus rhythm at 75 beats/minute, intraventricular conduction disorder with QRS of 170 ms, Q wave in aVL and secondary repolarisation disorders.
CBC: leukocytes 8,600/mm3, haemoglobin 11.5 g/dl, MCV 86 mm3, MCH 28/cell, platelets 220.000/mm3, normal coagulation, creatinine 1.34 mg/dl, urea 50 mg/dl, glomerular filtration rate 50 ml/min/1.73 m2, Na 137 mEq/L, K 4.5 mEq/L, CPK 130 IU/L, troponin I 0.8 ng/ml, NT pro BNP 9350 pg/mL, glycosylated haemoglobin 10 %.
Echocardiogram: regular acoustic window. Severely dilated left ventricle. Very severely depressed LVEF (15 % by Simpson biplane) with impaired global contractility. Pseudonormal diastolic pattern with average E/e" of 15.6. Mitral valve with mild leaflet thickening and mild annular calcification. Severe central mitral regurgitation of functional origin predominantly with central tenthering. Contracted vein of 8 mm and ORE by PISA of 0.31 cm2. Normofunctioning aortic valve. Severely dilated left atrium. Moderately dilated right chambers with moderately depressed right ventricular systolic function with fractional shortening of 25%. Moderate tricuspid regurgitation with PSAP of 60 mmHg. Pericardium without effusion. Inferior vena cava 22 mm with reduced inspiratory collapse.
Coronary angiography: left common trunk without significant lesions.
Anterior descending artery with moderate proximal diffuse atheromatosis and chronic occlusion of the middle portion, after origin of 1st diagonal being visible the distal vessel with severe diffuse atheromatosis by bypass of internal mammary to anterior descending artery.
Circumflex with severe proximal lesion anterior to 1st obtuse marginal. Distal vessel of obtuse marginalis without significant lesions visible through patent saphenous bypass.
Right coronary artery with chronic occlusion in middle portion. Chronically occluded right saphenous to coronary artery immediately after its origin.
Adenosine SPECT: severe dilatation of the left ventricle with severe and extensive anterior hypoperfusion as well as moderate hypoperfusion in mid-basal segments of the inferolateral wall, all without significant changes in the study at rest.

EVOLUTION
The patient was admitted to Cardiology and perfusion of furosemide and nitroglycerine was started, achieving negative water balance and clinical improvement, despite which dyspnoea persisted on minimal effort. Hygrotona was added and the dose of antialdosterone was increased to achieve resolution of the congestion. In addition, the remaining treatment for heart failure was titrated. Given the clinical deterioration of the patient, coronary angiography was performed, which showed patent bypasses from mammary to anterior descending and from saphenous to obtuse marginal 1a and very proximal occlusion of the saphenous bypass to the right coronary artery. This artery showed chronic occlusion in its middle segment, and was not considered to be susceptible to percutaneous treatment as a viability test was performed with SPECT, which showed no viability in this territory. He was discharged with 120 mg of furosemide per day, spironolactone 100 mg per day, hygrotona 50 mg every 48 hours, carvedilol 25 mg every 12 hours, ivabradine 7.5 mg every 12 hours, enalapril 2.5 mg every 12 hours, ASA, omeprazole, atorvastatin, allopurinol and insulin therapy.
Based on the electrocardiographic findings, the clinical situation and the patient's LVEF, an upgrade to resynchronisation therapy was indicated. In this procedure, venography was performed, showing occlusion at various levels of the coronary sinus without identifying any practicable subsidiary vein. Only a middle cardiac vein independent of the coronary sinus was observed, which could not be cannulated despite the use of several subselectors and angioplasty guides, so cardiac resynchronisation therapy by percutaneous approach could not be performed.
A few months later, he was readmitted due to decompensation of his heart failure related to a respiratory infection and was discharged with an increased dose of diuretic. Given the patient's age and NYHA functional class II-III, the patient was referred to a reference centre for evaluation for inclusion on the heart transplant waiting list. Right heart catheterisation was performed and showed a PCP of 30 mmHg, mean PAP of 34 mmHg, PVR 2.6 uW and cardiac output of 2.6 L/min, and ergospirometry showed a peak oxygen consumption of 14 ml/kg/min. Due to comorbidities, poorly controlled diabetes, obesity and peripheral arterial disease, he was not considered a candidate for heart transplantation.
On outpatient follow-up, the patient maintained NYHA functional class II-III with NT-proBNP of 4350 pg/mL. It was decided to switch from enalapril to sacubritil/valsartan 49/51 mm every 12 hours after the 36-hour washout period. After one week of treatment and without worsening renal and ion function, the dose was titrated to 97/103 mg every 12 hours. The patient reported significant clinical improvement after this medication change and diuretic dose reduction was possible. As resynchronisation therapy was not possible due to the unfavourable anatomy of the cardiac veins, the possibility of electrode implantation in the epicardium of the left ventricle by cardiac surgery was offered. With the clinical improvement after the introduction of sacubritil/valsartan, the patient decided to postpone this intervention. On the other hand, the patient had severe functional mitral regurgitation and occlusion of the right saphenous-coronary bypass. At the medical-surgical session, he was not considered a candidate for mitral repair and a new coronary artery bypass given the lack of viability of the lower territory, obesity and surgical risk. However, the possibility of Mitraclip implantation for treatment of mitral insufficiency was offered. Given the patient's symptomatic improvement with the change from ACE inhibitors to sacubitril/valsartan, this therapeutic option has not been implemented for the time being.

DIAGNOSIS
Heart failure with reduced EF.
Ischaemic heart disease in dilated phase with severely depressed systolic function.
Severe functional mitral regurgitation.
Severe three-vessel coronary artery disease with occlusion of saphenous to right coronary artery bypass and permeable mammary to anterior descending and saphenous to first obtuse marginal bypass.

Secondary diagnoses:
Insulin-dependent type 2 diabetes mellitus.
Arterial hypertension.
Dyslipidaemia.
Grade 2 obesity.
Chronic lower limb ischaemia.
