HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
We present a 68-year-old man, with no known drug allergies, a former smoker for three months and with alcohol consumption only at weekends.
His personal history includes arterial hypertension on treatment with torasemide 5 mg/24 hours, dyslipidaemia on treatment with simvastatin 20 mg/24 hours and chronic obstructive pulmonary disease GOLD 1A (last spirometry performed in 2017: TI 75%, FVC 104%, FEV1 83%) under follow-up by his primary care physician. She has no history of known heart disease.

In 2018 he underwent a right inguinal hernioplasty and in July 2019 he underwent a retropubic prostatic adenomectomy for benign prostatic hyperplasia with repeated acute urinary retention, having subsequently presented with episodes of haematuria.

Present illness
The patient was initially referred to the emergency department from his primary care physician for progressive exertional dyspnoea of one month's duration that began after prostate surgery. The dyspnoea was accompanied by two-pillow orthopnoea, occasional episodes of paroxysmal nocturnal dyspnoea and bilateral oedema with fovea in the lower extremities.
His regular physician had increased the dose of torasemide to double (10 mg/24 hours), after which he presented with a weight loss of 3 kg. On arrival at the emergency department, the patient was haemodynamically stable, tachycardic at 110 bpm and had a baseline saturation of 95%. Given the presence of congestive signs (hypoventilation in the right base with bilateral crackles, discrete hepatomegaly and oedema with bilateral fovea up to the thighs) and an elevation of NT-proBNP up to 4623 pg/ml (normal range 0-300 pg/ml), he was admitted to the cardiology department to study the first episode of heart failure.

Physical examination
On admission to the cardiology department, the patient was haemodynamically stable, with a blood pressure of 114/75 mmHg, tachycardic at 110 bpm and oxygen saturation around 96% baseline. There was no jugular plethora. On cardiac auscultation he was rhythmic, with no murmurs. Pulmonary auscultation (posterior plane) showed decreased vesicular murmur in the right base with bilateral crackles. He had a hepatomegaly of 3-4 cm, and on the extremities there was bilateral oedema with pitting up to the thighs.

COMPLEMENTARY TESTS
Electrocardiogram: sinus rhythm at 100 bpm, normal PR, QRS axis at 0o, narrow QRS, with known flattened T waves and frequent supraventricular extrasystoles.

Laboratory tests on admission:
Venous blood gas: pH 7.51, pCO2 32 mmHg, bicarbonate 26 mEq/ml.
Biochemistry: glucose 112 mg/dl; urea 56 mg/dl; creatinine 1.00 mg/dl; GPT 25 U/l; bilirubin 1.4 mg/dl; calcium 8.9 mg/dl; sodium 145 mEq/l; potassium 3.6 mEq/l; chloride 108 mEq/l; CRP 2.28 mg/l; creatine kinase 71 U/l; lactate dehydrogenase 188 U/l; NT-proBNP 4623 pg/ml.
Haemoglobin 10.8 g/dl; haematocrit 34.4%; mean corpuscular volume (MCV) 96.1 fl; mean corpuscular haemoglobin concentration 31.4 g/dl; mean erythrocyte corpuscular haemoglobin (MCH) 30.2 pg; erythrocyte distribution amplitude (EDA) 14.5%; platelets 209 *10^3/ƒÊL; leucocytes 6.61 *10^3/ƒÊL.
Coagulation: INR 1.3.

Other laboratory tests of interest:
Lipid profile: total cholesterol 142 mg/dl, triglycerides 85 mg/dl, HDL cholesterol 36 mg/dl, LDL cholesterol (calculated) 89 mg/dl, non-HDL cholesterol 106 mg/dl, urate 6.2 mg/dl.
Iron profile: iron 38 ug/ml, transferrin 345 mg/dl, transferrin saturation index (TSI) 8%, ferritin 50 ng/ml. Vitamin B12 406 pg/ml, folate 4.6 ng/ml.
Glycosylated haemoglobin 5.8%. Thyrotropin (TSH) 2.61 mU/l.
Serology: HCV negative, HIV negative, CMV negative, parvovirus B19 Ig-G positive (Ig-M negative), enterovirus negative, adenovirus pending.
Chest X-ray on admission: cardiothoracic index at the limit, with pinching of both costophrenic sinuses without other condensations.
Chest X-ray prior to discharge: minimal impingement of the right costophrenic sinus with significant improvement compared to the previous one.
Transthoracic echocardiogram (TTE) (videos 1, 2, 3): severely dilated left ventricle, with severely reduced systolic function (LVEF estimated by Simpson biplane 15-21%) due to severe global hypokinesia. Doppler transmitral flow pattern suggested restrictive physiology. Mildly dilated right ventricle with mildly depressed function. Moderately dilated left atrium and mildly to moderately dilated right atrium. Mitral valve leaflets thickened, with moderate mitral insufficiency. The tricuspid valve had moderate-severe insufficiency, with a maximum RV-AD gradient of 60.7 mmHg, and an estimated PSAP of 75 mmHg. Inferior vena cava was dilated and inspiratory collapse was less than 50%. The aortic valve was trivalve, with sclerodegenerative leaflets with only mild-moderate aortic insufficiency, without aortic root dilatation.
Cardiac magnetic resonance imaging (MRI) performed during outpatient follow-up: severely dilated left ventricle with severely depressed global function with diffuse hypokinesia (LVEF 29%). Mildly dilated right ventricle with mild systolic dysfunction (LVEF 44%). Late enhancement sequence shows linear intramyocardial enhancement in the basal septum and septal insertion points, non-ischaemic. In addition, a mild bilateral pleural effusion was observed as an extracardiac finding.
Catheterisation via the right radial artery:
Left coronary angiography: common trunk without lesions. The anterior descending artery shows diffuse calcified atheromatosis with mild stenosis without any significant stenosis.
The circumflex artery of medium extension and ectatic calibre at the proximal level also shows diffuse calcified atheromatosis with moderate stenosis at the marginal proximal level.
Right coronary angiography: the right coronary artery is the dominant vessel, very atheromatous and with an ectatic and irregular calibre all the way to the lumen. There is a severe ulcerated lesion at the proximal level (70%). At the end of the middle segment there is a calcified focal stenosis with severe stenosis (85%). The posterior descending branch is of medium extension and with severe focal stenosis proximally.
Pressure guidewire in the circumflex: the moderate circumflex lesion is explored with pressure guidewire without adenosine (RFR, parameter at rest) and is found not to cause ischaemia (RFR 0.96-0.98) and is therefore not treated.
Coronary intervention: the stenosis described in the middle segment of the DC is predilated with a 4.0 mm balloon with subsequent implantation of a pharmacoactive usntent with post-dilatation with a 4.5 mm balloon at 20 atm with good results. Subsequently, after predilatation with a 4.0 mm balloon, another drug-eluting stent was implanted over the ulcerated lesion described in the proximal segment. A severe residual stenosis is evident at its proximal edge, which makes it necessary to implant another stent at this level, covering the vessel ostium. These last two stents were post-dilated with a 4.5 NC balloon at high pressure with a good final result (slight under-expansion at the ostial level of around 20%).

CLINICAL EVOLUTION
The patient was a 68-year-old man admitted for a first episode of heart failure following planned prostate surgery. During admission, diuretic treatment was started, initially intravenously, and was later changed to oral therapy due to the excellent response to it, with rapid resolution of the congestive signs. In addition, after the acute phase, neurohormonal treatment was started progressively with good tolerance (nebivolol 5 mg half tablet every 12 hours as he was a bronchopathic patient, spironolactone 25 mg and finally sacubitril/valsartan 24/26 mg every 12 hours), with no alterations in renal function or symptomatic hypotension.
An echocardiogram showed dilated cardiomyopathy with severe left ventricular dysfunction due to severe global hypokinesia, and the aetiological study of this entity was initiated. A directed anamnesis was performed, in which a significant history of enolism and exposure to toxins, previous chest pain or angina pectoris, and data suspicious of myocarditis were ruled out.
Due to the characteristics of our centre and the availability of performing a catheterisation more quickly than a cardiac magnetic resonance imaging, cardiac catheterisation was performed first, which revealed severe stenosis of the right coronary artery in which three drug-eluting stents were implanted. A cardiac magnetic resonance imaging was still to be performed at the time of discharge.
On the other hand, blood tests showed normochromic normocytic anaemia with a normal range of red blood cell distribution, but with low iron, ferritin and transferrin saturation index. The digestive tract was ruled out as the origin of the anaemia, as there were no clinical signs to suggest this and the faecal occult blood test performed during admission was negative. In addition, vitamin B12 and folic acid deficiency were ruled out as possible alternative causes (although the characteristics of the anaemia did not suggest this aetiology). The anaemia was interpreted in the context of the previous episodes of haematuria and the recent surgery, and it was decided to start treatment with intravenous iron in the form of iron carboxymaltose at an initial dose of 1000 mg, without complications during the infusion.
At discharge, the patient was euvolaemic, with no congestive signs, and the heart failure unit of our hospital was contacted, who decided to include the patient in the remote telemonitoring programme for close patient follow-up.
During subsequent follow-up in the heart failure unit, the patient reported being stable since discharge, with NYHA II-III/IV dyspnoea, stable weight, minimal oedema in the ankles and good tolerance to neurohormonal treatment. Approximately two months after discharge, the patient again began to show signs of congestion (he reported an increase in his baseline dyspnoea and oedema with fovea in the lower limbs) which led to an increase in oral diuretic treatment, with a good clinical response. In addition, a control blood test showed anaemia (haemoglobin 12.6 g/dl) with a ferritin level of 49 ng/ml and a transferrin saturation index of 11.1%, without the patient reporting bleeding at any level, so it was decided to start a new course of intravenous iron carboxymaltose with the aim of improving the patient's exercise capacity and quality of life. After the administration of an initial dose of 1000 mg in the day hospital of our centre, with no incidents during the same, a new evaluation of the patient is pending to assess the need to complete the regimen with intravenous iron.

DIAGNOSIS
Heart failure, first episode.
Dilated cardiomyopathy, non-ischaemic, with severely depressed LVEF (LVEF estimated by Simpson biplane 15-20%).
Moderate functional mitral regurgitation.
Moderate-severe tricuspid regurgitation with severe pulmonary hypertension.
Severe single-vessel coronary artery disease (right coronary) treated with implantation of three drug-eluting stents, and moderate single-vessel coronary artery disease (obtuse marginal). Normocytic normochromic anaemia with iron deficiency.
