HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
Male, 61 years old. No known allergic reactions to medication. Cardiovascular risk factors: arterial hypertension. Obesity grade 2 (body mass index 37.86 kg/m2). No diabetes mellitus or dyslipidaemia. No toxic habits. Surgical history: operated for left trimalleolar fracture with osteosynthesis of peroneal malleolus with 6-hole tube third plate and osteosynthesis of tibial malleolus with a screw in 2009. Non-cardiological medical history: Moderate chronic obstructive pulmonary disease (COPD), under follow-up by the outpatient pulmonology department of his referral hospital. Sleep apnoea-hypopnoea syndrome (SAHS) being treated with continuous positive airway pressure (CPAP) and home oxygen. Prostate adenocarcinoma diagnosed in 2016, treated with radiotherapy and hormone blockade. Unfiliated renal tumour, first detected in 2017. Not operated on at his referral hospital due to high surgical risk. Abdomino-pelvic CT scan performed at his reference hospital in 2020: mixed nodule measuring 20 x 18 mm in the right kidney, close to the lower pole, eccentric, without clear perirenal fatty infiltration. Stability in radiological follow-up, so it has been considered non-malignant. Cardiological history: non-ischaemic dilated cardiomyopathy diagnosed in 2003, with severe left ventricular dysfunction. Loss of follow-up until 2012. In 2012 the patient returned to the cardiology outpatient clinic at his referral hospital. Echocardiogram at that time showed a severely dilated left ventricle (LV), with biplane EF 29%, with diffuse global hypokinesia. Coronary angiography showed irregularities in the right coronary artery, the rest of the coronary tree showed no alterations. Implantable cardioverter defibrillator implantation with cardiac resynchronisation therapy (ICD-CRT) was decided in March 2012 for primary prevention of sudden death.

An appropriate shock due to non-sustained monomorphic ventricular tachycardia (NSMVT) occurred in December 2012. In reviews of the ICD, multiple episodes of sustained monomorphic ventricular tachycardia (SMVT) treated with overstimulation were detected, so amiodarone was started. In February 2020, a new ventricular tachycardia (VT) occurred with appropriate ICD discharge, and the patient was admitted to his referral hospital. The last transthoracic echocardiogram, performed during this admission, showed a severely dilated left ventricle (DTD 104 mm, VTDi 207 ml/m2, VTSi 157 ml/m2), with severe depression of function (LVEF 23% biplane), with severe global hypokinesia. Dilated left atrium (34 cm2). Diastolic dysfunction grade I with signs of increased filling pressures (E/e" 20). Mitral valve with mild regurgitation due to dilatation of the annulus. Aortic flow with slightly increased gradients (11/5 mmHg), without aortic insufficiency. Mild tricuspid insufficiency (LAD electrode) that does not allow adequate estimation of systolic pressure in the pulmonary artery. Dilated right ventricle (44 mm baseline), with RVEF at the lower limit (TAPSE 18 mm). No pericardial effusion. Usual treatment: atorvastatin 80 mg (1 tablet daily), amiodarone 200 mg (1 tablet every 12 hours), furosemide 40 mg (2 tablets daily), carvedilol 12.5 mg (1 tablet every 12 hours), sacubitril/valsartan 24/26 mg (1 tablet every 12 hours), esomeprazole 20 mg (1 tablet every 24 hours), indacaterol/glycopyrronium bromide 85/43 mcg (1 inhalation every 24 hours), tamsulosin 0.4 mg (1 tablet per day). Present illness A 61-year-old male who, referred from his referral centre, was admitted in May 2020 to the cardiology inpatient ward of the advanced heart failure and heart transplant unit to assess treatment options. The patient was diagnosed with dilated cardiomyopathy with severe left ventricular dysfunction in 2003 and had stopped attending check-ups until 2012. At present, the patient reports NYHA functional class III/IV, with sustained symptoms for the last few months. He has orthopnoea. He can walk only 50 metres without having to stop, with difficulty climbing a floor. No episodes of palpitations, syncope or presyncope, nor new ICD discharges. No other associated symptoms. Physical examination Conscious and oriented, eupneic at rest. Blood pressure 118/71 mmHg, heart rate 53 bpm, peripheral oxygen saturation 98% (FiO2 21%). Weight 112 kg, height 172 cm, body mass index (BMI) 37.86 kg/m2 (obesity grade 2) Cardiac auscultation: regular heart tones, no murmurs or audible friction rubs. Pulmonary auscultation: preserved vesicular murmur with no added sounds, although some generalised hypoventilation was observed. Extremities: slight tibiomalleolar oedema with fovea, with no signs of deep vein thrombosis (DVT).

COMPLEMENTARY TESTS
12-lead electrocardiogram on admission: sinus bradycardia at 50 beats per minute, with ventricular rhythm due to pacemaker in VAT.
Chest X-ray on admission PA: no infiltrates or masses were identified. No costophrenic sinus impingement. ICD-CRT correctly positioned. SARS-CoV2 CRP: not detected. Transthoracic echocardiogram at bedside: poor acoustic access due to obesity. The left ventricle is severely dilated (DVItd 9.7 cm, DVIts 9.1 cm, indexed DVItd (cm/m2) 4.4 cm/m2, indexed DVIts (cm/m2) 4.1 cm/m2). Left ventricular systolic function is severely reduced (EF [Teich] 13.8%). Estimation of EF by Simpson's method is poorly assessable due to poor acoustic access. Right ventricle of normal dimensions (baseline RV dimensions 3.8 cm, indexed baseline RV dimensions (cm/m2) 1.72 cm/m2, RV diastolic area 19.6 cm2, RV end-systolic area 15.4 cm2). Right ventricular systolic function is mildly to moderately reduced (TAPSE 3.6 cm, RV FAC 21.7%). Difficult to assess correctly due to poor acoustic access. Mild left atrial dilatation (LA diameter 4.3 cm). Right atrial size is normal. Mitral valve with degenerative changes. Mild to moderate mitral regurgitation detected. Difficult to quantify. Holosystolic flow but low density (Vmax E MV 75.0 cm/s, Vmax A V: 88.4 cm/s, E/A MV 0.85, mitral E/e' (medial) 15.7 {ratio}, E' peak velocity lat. 3.5 cm/s, E' peak velocity med. 4.8 cm/s, mitral E/e' (lateral) 21.4 {ratio}). Tricuspid valve normal in structure and function. No tricuspid insufficiency. No indirect signs of significant pulmonary hypertension (PHT). Trivalve aortic valve normal in appearance. The pulmonary valve is not well visualised. The aortic root is of normal size. No signs of increased central venous pressure (CVID 1.84 cm, CVID inspiration 0.58 cm). There is no pericardial effusion. Blood tests: Biochemistry: glucose 108 mg/dl, creatinine 1.05 mg/dl, glomerular filtration rate (CKD-EPI) 76 ml/min, sodium 142 mEq/l, potassium 4.1 mEq/l, chlorine 103 mEq/l, uric acid 5,9 mg/dl, total bilirubin 0.86 mg/dl, AST/GOT 19 U/l, ALT/GPT 13 U/l, GGT 37 U/l, alkaline phosphatase 69 U/l, NT-proBNP 497 pg/ml, total protein 6.0 g/dl. Lipid profile: total cholesterol 162 mg/dl, HDL cholesterol (direct) 51 mg/dl, LDL cholesterol (calculated) 91 mg/dl, triglycerides 99 mg/dl. Iron profile: iron 89 μg/dl, total Fe binding capacity 291 μg/dl, transferrin desaturation index 31%, ferritin 186 ng/ml, transferrin 225 mg/dl. Haemogram: red cells 4.07 x 10^6/μl, haemoglobin 12.2 g/dl, haematocrit 38.0%, MCV 93 fl, MCH 30.0 pg, leucocytes 6.66 x 10^3/μl, neutrophils 3.53 x 10^3/μl, lymphocytes 2.00 x 10^3/μl, monocytes 0.84 x 10^3/μl, eosinophils 0.25 x 10^3/μL, basophils 0.04 x 10^3/μl, platelets 228 x 10^3/μl. Thyroid hormones: TSH 0.53 mU/l, free T4 1.70 ng/dl. Glycosylated haemoglobin A1c 6.4%, mean estimated glucose 137 mg/dl.

CLINICAL EVOLUTION
The patient remained stable throughout admission. The case was referred to the endocrinometabolic surgery unit, which decided that the patient was not a candidate for bariatric surgery due to a history of prostatic neoplasia under active treatment (less than 5 years). On discharge, his usual treatment was maintained. However, given that during admission he was diagnosed with diabetes mellitus (HbA1c 6.4%), it was decided to start treatment with semaglutide 0.5 mg, one injection per week for 4 weeks, subsequently increasing to 1 mg per week indefinitely, with good tolerance.

Treatment was also started with dapagliflozin 10 mg 1 tablet per day and eplerenone 25 mg 1 tablet per day. Education in heart failure is started. Periodic scheduled admissions were decided (the patient lives far from our hospital) for treatment with levosimendan under monitoring. During successive admissions, all of which were uneventful, a gradual weight loss was observed as follows: in June 2020, the patient weighed 107 kg, in July 2020 he weighed 100 kg, and in August 2020 he weighed 94 kg. The patient reports a marked improvement of his functional class, almost NYHA class I. Laboratory tests show a reduction in glycosylated haemoglobin (HbA1c) from 6.4% in May to 5.7% at 3 months. On admission in September 2020, the patient weighs 89 kg and in October 2020, the weight is maintained at 89 kg. Subsequent outpatient follow-up is carried out at our hospital. The patient indicates that he has reduced his weight to 84 kg (BMI 28.39 kg/m2, overweight grade 2). He reports some fatigue on exertion, but denies dyspnoea. He is able to climb several floors without stopping. He has stopped taking furosemide tablets. Therefore, and as a summary, since the introduction of antidiabetic treatment (semaglutide 1 mg weekly and dapagliflozin 10 mg daily), the patient has started a progressive and constant weight reduction until reaching a weight of 84 kg, managing to maintain the loss over time. From an initial weight of 112 kg and a BMI of 37.86 kg/m2 (grade 2 obesity), the patient reduced his weight by a total of 28 kg in approximately 6 months, reaching a BMI of 28.39 kg/m2 (grade 2 overweight). At the same time, the patient reports progressive improvement in symptoms and functional class. Initially, in our first assessment, he was considerably limited by his heart disease, with NYHA functional class III, and was practically asymptomatic on discharge from our centre (NYHA class I). As a result, the patient was no longer indicated for intervention by the advanced heart failure and heart transplant unit, and was therefore followed up by the cardiology department of his referral hospital.

DIAGNOSIS
Heart failure with severely reduced left ventricular ejection fraction.
Non-ischaemic dilated cardiomyopathy.

Other diagnoses:
Obesity grade 2.
Type 2 diabetes mellitus.
