HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

PERSONAL HISTORY
Male, 56 years old, from Colombia, with no known drug allergies.
No family history of heart disease or sudden death.
His toxic habits include moderate alcohol consumption until several years ago. He was a non-smoker.
Cardiovascular risk factors include arterial hypertension and dyslipidaemia, both without pharmacological treatment or control by any physician, and morbid obesity (BMI 57 kg/m2).
Other history of interest: severe sleep apnoea syndrome without treatment and hypothyroidism.
She denies regular treatment for any of her comorbidities.

CURRENT ILLNESS
She came to the emergency department for progressive dyspnoea of 15 days of evolution until she became resting, together with orthopnoea, increased abdominal perimeter and oedema in the extremities. She reported no chest pain, palpitations, dizziness or syncope in the weeks prior to consultation.

PHYSICAL EXAMINATION
Weight 171 kg; height 173 cm; body mass index (BMI) 57 kg/m2.
Afebrile; blood pressure (BP) 100/60 mmHg; heart rate (HR) 132 bpm; baseline SatO2 98%.
Conscious and oriented, normohydrated, eupneic at rest, jugular ingurgitation present at 45 ̊.
Cardiac auscultation: arrhythmic heart sounds at 132 bpm without murmurs.
Pulmonary auscultation: bibasal crackles.
Abdomen: soft, depressible, very globular, not painful to deep or superficial palpation, peristalsis present, without peritonism.
Lower extremities: bilateral oedema with pitting up to the knee.

COMPLEMENTARY TESTS
ECG on admission: atrial fibrillation (AF) with ventricular response at 132 bpm.
Q wave in DIII. Low voltages.
Chest X-ray: radiological cardiomegaly. Interstitial oedema.
Blood tests: biochemistry: glucose 93 mg/dl; HbA1c 6.2%; urea 0.44 g/l; creatinine 1.19 mg/dl; glomerular filtration rate 67 ml/min; total cholesterol 223 mg/dl; LDL cholesterol 150 mg/dl; HDL cholesterol 23 mg/dl; triglycerides 250 mg/dl; sodium 145 mEq/l; potassium 4.8 mEq/l. TSH 2.01 mcU/ml. Normal liver function tests.
Haemoglobin 14.8 g/dl; haematocrit 45.7%; leucocytes 8,100/mm3; platelets 198,000/mm3.
Transthoracic echocardiogram (with Sonovue echocontrast): severely dilated left atrium (A4C: 60 cm2). Thin leaflet mitral valve with preserved mobility and opening; mild regurgitation grade I/IV. Moderately dilated left ventricle (indexed biplane LVEDV: 93 cm3/m2) with severely depressed systolic function (LVEF 32%) due to global impairment. Thin aortic valve with good opening and mobility; no regurgitation. Slightly dilated aortic root. Slightly dilated right atrium (A4C: 26 cm2). Dilated right ventricle (basal diameter 53 mm; mean 37 mm); with slightly depressed contractility (TAPSE 15 mm). Tricuspid valve with good opening and mobility; grade II/IV insufficiency. Dilated inferior vena cava with inspiratory collapse. Estimated pulmonary arterial systolic pressure 51 mmHg.
No pericardial effusion.
Left heart catheterisation: ventriculography: dilated left ventricle with severe systolic dysfunction. No mitral regurgitation. Coronary angiography: left dominance. No angiographically significant lesions in the epicardial coronary arteries.
Respiratory function tests: spirometry: moderate decrease in obstructive ventilatory function. FEV1 2.12 l (59%); FVC 3.38 l (73%); FEV1/FVC 62.67%.
Bronchodilator test: positive; significant improvement in FEV1 (+18% = 320 ml).
Electrocardiogram at discharge: atrial fibrillation with ventricular response at 80 bpm. Q wave in III. Low voltages.

CLINICAL EVOLUTION
Initial cardiological assessment in the emergency department revealed clinical signs of congestive heart failure, atrial fibrillation with rapid ventricular response at 132 bpm and left systolic dysfunction on echocardioscopy, and the patient was admitted for appropriate treatment and to complete aetiological studies.
The patient showed significant clinical improvement during the first days of admission with depletive treatment with intravenous diuretics, reaching a dry weight of 156 kg compared to the initial 171 kg. A regulated echocardiogram was performed with echocontrast due to a poor echocardiographic window, which confirmed the echocardiographic findings, also showing elevated filling pressures with significant pulmonary hypertension and associated right-sided dysfunction. Furthermore, the aetiological study was completed with coronary angiography to rule out ischaemic aetiology of dilated cardiomyopathy, showing no angiographically significant lesions in the epicardial coronary arteries. Therefore, the condition was interpreted as heart failure with reduced ejection fraction in the context of non-ischaemic dilated cardiomyopathy, without being able to rule out a toxic origin (enolic) together with a certain component of associated tachycardiomyopathy.
During admission, treatments with prognostic value in heart failure with depressed systolic function were successfully initiated, with good tolerance to them, achieving good heart rate control with beta-blockers at medium doses and being discharged with ACE inhibitors, beta-blockers and antialdosteronics at maximum doses tolerated by blood pressure.
In addition, during his hospitalisation the patient received nutritional education for changes in eating habits, as well as instructions to begin physical exercise. In the case of a patient with pre-diabetes and morbid obesity with LDL 150 mg/dl, statins were started to achieve target LDL < 100 mg/dl.
In collaboration with the pulmonology department, CPAP treatment was started during admission for his sleep apnoea, with good tolerance.
Regarding his atrial fibrillation of uncertain onset, with a CHADS-VASc score of 2 and HASBLED of 0, he was anticoagulated on admission with weight-adjusted LMWH. An initial strategy of rate control was proposed so that, after clinical stabilisation and one month of anticoagulation, programmed electrical cardioversion was performed for rhythm control purposes.
Regarding the choice of anticoagulation therapy at discharge, the patient refused to take VKA for personal reasons, which added to his high weight and BMI posed a major dilemma. In agreement with the haematology service, it was decided to start rivaroxaban 20 mg and laboratory measurements of his peak and trough levels were performed to check that they were in therapeutic range. After this, he was discharged with this treatment on a continuous basis.
In the outpatient follow-up, the patient has improved clinically, has reduced his weight to 130 kg (BMI 43 kg/m2) and is in functional grade II. Titration of prognostic drugs in heart failure has continued, replacing ACE inhibitors with sacubitrilo-valsartan. Two unsuccessful attempts at electrical cardioversion were made, opting to continue with heart rate control, which was proving adequate. In the control echocardiography after 3 months of optimised medical treatment, an improvement in LVEF of up to 50% was observed.

DIAGNOSIS
Heart failure with depressed left ventricular ejection fraction.
Non-ischaemic dilated cardiomyopathy (possible toxic damage due to enolism and associated tachycardiomyopathy).
Atrial fibrillation (AF) of undetermined onset (CHADSVASc 2, HASBLED 0).
Coronary arteries without significant lesions.
Very severe sleep apnoea syndrome.
Morbid obesity.
Arterial hypertension with good control at discharge.
Prediabetes.
