HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

BACKGROUND:
No known drug allergies. No toxic habits. Arterial hypertension. Diabetes mellitus type 2. Hypercholesterolemia. Osteoporosis. Symptomatic cholelithiasis and hepatic steatosis under follow-up by digestive specialist.
Surgical history: ovarian cyst and urinary incontinence.
Admission to cardiology in 2013:
Sinus rhythm at 60 bpm, complete left bundle branch block pattern (LBBB).
Transthoracic echocardiography (23/04/13): severe left ventricular (LV) systolic dysfunction, with ejection fraction (EF) 24%. Mitral valve with degenerative changes, moderate fibrosis and severe mitral insufficiency (MI). Severe pulmonary hypertension.
Moderate tricuspid insufficiency.
Cardiac catheterisation (20/08/13): reduced cardiac output and cardiac index. Right atrial, pulmonary artery and pulmonary venocapillary pressures within normal range. Coronary arteries free of obstructive lesions. LV of normal size and morphology with severely depressed global contractility, with EF 30%.
Stress test with O2 consumption: peak O2 consumption 17.3 ml/kg/min, which is 80% of the calculated theoretical. 7.9 METs achieved. Weber-Janicki Class B.
Cardiac magnetic resonance imaging (MRI): dilated cardiomyopathy of uncertain origin with severe left ventricular dysfunction, LV ejection fraction (LVEF) 30%.
Assessment in 2014: O2 consumption stress test: peak O2 consumption 16.2 ml/kg/min. Weber-Janicki Class C. Normal BP and no arrhythmias.
Admitted to cardiology in 2016:
Transthoracic echocardiography with severe systolic dysfunction with LVEF 33%. Severe MI.
Mild pulmonary hypertension. Mild-moderate tricuspid insufficiency.
Boston type resynchronising defibrillator (ICD-CRT [cardiac resynchronisation therapy]) implanted.
Follow-up in a monographic HF clinic with stable New York Heart Association (NYHA) functional class II
Association (NYHA) functional class II.
Usual treatment: acetylsalicylic acid 100 mg (0-1-0), spironolactone 25 mg (0-1-0), bisoprolol 1.25 mg (1-0-1), sacubitril/valsartan 49/51 mg (1-0-1), furosemide 40 mg (1-0-0), omeprazole 20 mg (1-0-0), pravastatin 40 mg (0-0-1), empaglifozin/metformin 5/1000 mg (1-0-0).

CURRENT ILLNESS:
Admitted for dyspnoea on moderate exertion in recent months, which has been worsening in recent days, for which reason he is no longer able to leave his home. He reports walking 1-2 metres and getting tired and having to sit down due to dyspnoea. No increase in oedema in the lower limbs or other symptoms. No infectious symptoms. No chest pain or palpitations.

PHYSICAL EXAMINATION:
Conscious, oriented and cooperative. Good general condition. Blood pressure (BP) 120/70.
Heart rate (HR) 65 bpm. Oxygen saturation (SatO2) 96% basal. Cardiac auscultation: rhythmic with systolic murmur in the apex. Pulmonary auscultation: preserved vesicular murmur without added noises. Abdomen: nondescript. Lower limbs: no oedema. Pedial pulses present.

COMPLEMENTARY TESTS
ANALYSIS: haemoglobin 13.7 g/dl. Leukocytes 10,800/mm3. Neutrophils 69.9%. Platelets 246,000/mm3. INR 1.26. Creatinine 0.90 mg/dl. Sodium 138 meq/l. Potassium 4.8 meq/l. Total bilirubin 1.9 mg/dl. Indirect bilirubin 1.40 mg/dl. GOT 51 U/l. GPT 49 U/l. Troponin I < 0.012 ng/ml, NT-proBNP 5270 pg/ml. CRP 24.50 mg/l. Sideremia 28 ug/dl. Transferrin 264 mg/dl. CTFH 372 ug/dl. Ferritin 74 ng/ml. IST 7.5%.
THORAX RADIOGRAPHY: standing upright, posteroanterior. Cardiothoracic index in the high limit. Normopositioned LAD. No infiltrates or condensation.
ELECTROCARDIOGRAM (ECG): pacemaker rhythm with biventricular stimulation.
QRS 150 ms with BCRDHH morphology.
Transthoracic echocardiography: dilated LV with severe systolic dysfunction.
Severe functional MI. IVT 12. Pseudonormalised filling pattern. Right ventricle (RV) not dilated, normocontractile. Electrode in RV, with mild triscuspid insufficiency. RVAD gradient 41 mmHg.

CLINICAL EVOLUTION
74-year-old female patient, with a history of dilated cardiomyopathy, admitted for chronic HF with no clear trigger. Given the signs of poor peripheral perfusion and haemodynamic deterioration, it was decided to administer a pulse of levosimendan as positive inotropic support to achieve early recovery from acute HF. This was carried out with good haemodynamic tolerance and good clinical response, achieving stabilisation with diuretic support 72 hours after admission following decompensation.
Likewise, the resynchronisation therapy of the ICD-CRT device was optimised, presenting a QRS of 150 ms on admission, and after optimisation and adjustment of the interventricular delay, a reduction to 132 ms was achieved.
After compensation of the acute HF condition and prior to discharge, medication for the treatment of chronic HF was optimised in order to plan a transition after the decompensation and subsequent follow-up in outpatient clinics, for which the previous home treatment was reinstated and an analysis of the iron deposits was carried out.
The patient was discharged from hospital and followed up in the HF outpatient clinic, where the continuation of medication titration, correction of the functional iron deficiency and inclusion in a treatment programme with repeated doses of levosimendan on an outpatient basis were considered.

DIAGNOSIS
Non-ischemic dilated cardiomyopathy with severe left ventricular dysfunction.
Severe functional mitral regurgitation.
Chronic heart failure stage C. NYHA functional class III.
