HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
Male, 68 years old.
No known drug allergies. He denies current consumption of toxic substances.
Episode of right renal colic in 2010, with discrete ectasia at pyelocaliceal level. Normal renal function.

Cardiological history:
Cardiovascular risk factors (CVRF): arterial hypertension (AHT) and dyslipidaemia on pharmacological treatment. Ex-smoker for 20 years (IPA of 30 packs/year).
No diabetes mellitus.
Known left bundle branch block (LBBB).
Chronic coronary syndrome that debuted in 1986 with AMI, with surgical revascularisation with double aortocoronary bridge (marginal saphenous-obtuse and anterior saphenous-descendant). Subsequently, several episodes of unstable angina in 2002 and 2003, with percutaneous revascularisation: percutaneous coronary intervention (PCI) with implantation of a drug-eluting stent in the LAD distal to the saphenous graft, two stents in the first proximal-medial diagonal branch, and a stent in the middle DC. In 2010 a new coronary angiography was performed, on a scheduled basis, where a severe stenosis of 70% was observed in distal CT, with stent placement, with a good result.
Last control echocardiogram (2018): dilated cardiomyopathy with severe ventricular dysfunction (LVEF 25%) with moderate-severe mitral insufficiency due to tenting and mild pulmonary hypertension.
Cardiac magnetic resonance imaging (MRI) of the same year: severely dilated left ventricle (LV) with severe dysfunction. LVEF 25.5%. Dyskinesia of the true apex, akinesia of the basal half of the inferior, inferolateral and anterolateral sides, as well as of the basalmost posterior septum.
Thinning of the inferior and inferolateral aspect (3 mm). Abnormal septal motion. Non-dilated right ventricle (RV) with preserved global and segmental function. RVEF 52.5%. Mitral insufficiency jet is seen. Late enhancement sequences showed ischaemic enhancement in regions of the basal and medial posterior septum, basal and medial inferolateral, and basal anterolateral.
In outpatient follow-up in heart failure consultation, with six-monthly/annual check-ups. Clinically asymptomatic, NYHA I/IV, with no new episodes of angina. Follows cardiac rehabilitation programme.
Usual treatment: omeprazole 20 mg, acetylsalicylic acid 100 mg/day, bisoprolol 5 mg/12 hours, furosemide 20 mg/day, sacubitril/valsartan 97/103 mg/day, rosuvastatin 20 mg/day.

Present illness
The patient consulted the emergency department of our centre due to a progressive increase in dyspnoea during the last week, to the point of minimal effort, associated with orthopnoea and oliguria during the last 3 days. No angina or palpitations. Poor compliance with hygienic-dietary measures during the last few days, with increased water intake. No infections or changes in medication.

Physical examination
Blood pressure (BP) 120/70 mmHg, heart rate (HR) 100 bpm, SO2 90% baseline improving with O2 2 bpm to 95%. Afebrile.
Minimal jugular plethora. Cardiac auscultation: rhythmic with systolic murmur in mitral focus III/IV, AP with bibasal crackles up to midfields. Abdomen was nondescript. Bilateral oedema with fovea in EEII to pretibial level.
In view of symptoms compatible with decompensated heart failure, it was decided to admit the patient to the cardiology department for treatment and clinical evolution.

COMPLEMENTARY TESTS
In the emergency department:
ECG: sinus rhythm at 70 bpm, PR 220 ms, with known LBBB, with QRS complex duration of 170 ms.
Chest X-ray: borderline cardiothoracic index, with pinching of both costophrenic sinuses, without infiltrates in the lung parenchyma.
Blood tests: glycaemia 80mg/dl, urea, creatinine and hepatic battery normal. Na 135 mEq/l, K 4.2 mEq/l. Hb 15 g/dl, leukocytes 4,800, platelets 205,000. Coagulation normal, with INR 1.1. NTproBNP in the ED 1,050 pg/ml.
On the cardiology ward:
Extended CBC with ferric profile, TSH and HbA1c: ferritin 250 ug/l with TSI 12%. TSH normal.
HbA1c 5.4%.
Transthoracic echocardiogram (video 1): ischaemic dilated cardiomyopathy with severely dilated LV. Mild LVH. Severe dysfunction (LVEF 22%) with global hypokinesia. Severe mitral insufficiency (MI) due to tenting. Asynchronous septal motion in relation to LBBB. Moderate tricuspid insufficiency (TI). Normofunctioning RV with moderate pulmonary hypertension (PH). Similar to previous echocardiographic findings.


CLINICAL EVOLUTION
The patient remained in hospital with good clinical evolution and excellent response to intravenous diuretic treatment, with notable clinical improvement and complete resolution of the congestive semiology, which made it possible to de-escalate the diuretic treatment to the usual oral dose at home. The pre-discharge NT-proBNP test was repeated, with notable improvement (600 pg/ml).
The patient was already on outpatient neurohormonal treatment, which was not modified (previously, the introduction of ivabradine had been attempted in consultations, but was poorly tolerated and therefore discontinued).
The patient was re-interviewed and reported episodes of increased dyspnoea during the last 4 months. It was decided to raise the case with the electrophysiology section of our department for the implantation of an ICD-CRT for primary prevention, which was accepted. The implantation took place without incident, achieving partial correction of the interventricular asynchrony.
At the analytical level, it is worth noting ferropenia data, without associated anaemia. As this was a patient with heart failure with reduced ejection fraction and symptoms (NYHA III-IV on admission), and given the data on improved exercise capacity, quality of life and functional capacity demonstrated by intravenous ferrotherapy in these patients, it was decided to administer iron carboxymaltose in a single dose of 500 mg.
The patient was again educated in hygienic-dietary measures, was discharged and continued regular check-ups at the heart failure clinic.
Eight months after discharge, he was clinically stable, asymptomatic, with baseline NYHA I/IV, with no new episodes of HF decompensation. A repeat echocardiogram showed an improvement in LVEF to 33%, with mild-moderate mitral regurgitation. The control analysis again showed an iron deficiency profile (ferritin 80 ug/l with TST 10%), with associated microcytic anaemia (Hb 11 g/l, with MCV 80 fl), which was not present on admission. In this case, our patient was clinically asymptomatic for his heart failure (NYHA I), but with associated anaemia, so it was decided to re-administer IV ferrotherapy (1000 mg of ferric carboxymaltose in a single dose, with a further administration of another 500 mg the following week in the day hospital).
A faecal occult blood test was requested, which was positive, so the patient was referred to the gastrointestinal department for further evaluation with the relevant studies.

DIAGNOSIS
Chronic decompensated heart failure, with severely reduced LVEF.
Ischaemic dilated cardiomyopathy.
Chronic coronary syndrome with trivial coronary artery disease with multiple surgical and percutaneous revascularisations.
Microcytic anaemia with iron deficiency profile pending digestive study.
Procedures performed: first implantation of automatic implantable cardioverter defibrillator with cardiac resynchronisation therapy (ICD-CRT) in primary prevention and intravenous ferrotherapy.
