HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
This is a 72-year-old man with multiple cardiovascular risk factors (CVRF) (hypertension, type 2 diabetes mellitus, hypercholesterolemia, ex-smoker), permanent atrial fibrillation anticoagulated with warfarin (previously with acenocoumarol; the anticoagulant was changed in 2017 after finding a thrombus in the left atrial appendage despite correct INR levels) and rheumatic valve disease with valve replacement in 2004 with mechanical prostheses in mitral and aortic position, without significant lesions in pre-surgical coronary angiography and with a subsequent LVEF of 30%. During follow-up, he presented a tendency towards asymptomatic moderate hyperkalaemia (maximum figure of 6.3 mEq/l) that prevented correct titration of neurohormonal medication, remaining in NYHA functional class III/IV. In September 2019, he attended the emergency department due to worsening of his usual dyspnoea to minimal effort, orthopnoea, bendopnoea, decreased diuresis rate and the appearance of oedema in the lower limbs.

Physical examination
Blood pressure (BP) 110/55 mmHg, heart rate (HR) 90 bpm. Temperature 36.2 oC. Oxygen saturation 95% basal. Acceptable general condition. Conscious, oriented and cooperative. Normal colour, normohydrated and normoperfused. Discreetly tachypnoeic at rest, with intolerance to decubitus.

Cardiac auscultation: arrhythmic heart sounds. Prosthetic metallic clicks. No murmurs were heard. Pulmonary auscultation: bilateral crackles up to midfields, no other superimposed sounds. Lower extremities: symmetrical pulses present and symmetrical. Bilateral pitting oedema up to the knees. No signs of deep vein thrombosis. Current treatment: candesartan 4 mg (0-0-1), furosemide 40 mg (1-0-1), simvastatin 20 mg (0-0-1), bisoprolol 2.5 mg (1-0-1), warfarin 5 mg as prescribed, metformin 850 mg (0.5-0-0.5), pantoprazole 20 mg (1-0-0) Given that this was his first episode of decompensation of heart failure, admission to the conventional cardiology ward for depletive treatment and study was decided.

COMPLEMENTARY TESTS
Laboratory tests on admission: haemoglobin 15.1 g/dl (11.4-15.1 g/dl), creatinine 1.78 mg/dl (0.50-0.90 mg/dl), glomerular filtration rate (GFR) 41 ml/min/1.73 m2 (> 90 ml/min/1.73 m2), sodium 139 mEq/l (135-145 mEq/l), potassium 5.6 mEq/l (135-145 mEq/l), sodium 5.6 mEq/l (0.50-0.90 mg/dl), potassium 5.6 mEq/l (3.50-5.00 mEq/l), GPT 21 U/l (5-35 U/l), GOT 22 U/l (5-27 U/l), NT-proBNP 2651 pg/ml (<= 125 pg/ml), glycosylated haemoglobin 6.9% (4.0-6.0). Electrocardiogram (ECG) on admission: atrial fibrillation with ventricular response at 85 bpm. Wide QRS with right bundle branch block (RBBB) morphology. Chest X-ray on admission: mid-sternotomy cerclages. Mechanical prosthesis in mitral position. Signs of pulmonary congestion (vascular redistribution, bilateral pleural effusion). Transthoracic echocardiogram: left ventricle (LV) severely dilated (Dd 63 mm, VTD 201 ml, VTDi 118 ml/m2), with slight concentric hypertrophy. Global hypokinesia. Biplane Simpson LVEF 20%. Right ventricle of borderline size (Dd 40 mm), with severely depressed global systolic function. Mechanical prosthesis in mitral and aortic position well seated, with normal disc motion, no gradient elevation or periprosthetic insufficiency.

CLINICAL EVOLUTION
Intravenous diuretic treatment was started with an excellent response and clear improvement in the congestive signs and symptoms, which led to discharge home after 8 days of hospitalisation. Serial analyses showed normalisation of renal function. In this context, it was decided to start a potassium chelator (patiromer at a minimum dose, i.e. one 8.4 g sachet per day) with the aim of normalising serum potassaemia figures in order to be able to start neurohormonal treatment. Follow-up was initiated in the Transversal Heart Failure Programme of our centre. A blood test was performed one month later, which showed serum potassaemia of 4.1 mEq/l, so it was decided to increase the dose of ARA-II (candesartan 8 mg every 24 hours). On review in consultation (November 2019), the patient reported improvement in his functional class to NYHA II/IV, with potassium levels remaining in the normal range. Given the good tolerance, it was decided to change to sacubitril/valsartan at low doses (24/26 mg every 12 hours), with which the improvement in functional class progressed to NYHA I/IV (December 2019): the patient reported that he could walk 2-4 km on level ground, as well as climb slopes and several flights of stairs without having to stop.

As serum potassaemia remains in range, a mineralcorticoid receptor antagonist (low-dose spironolactone) is started. At the next check-up, a new blood test showed slight hyperkalaemia (5.58 mEq/l), so it was decided to increase the dose of patiromer to two sachets (16.8 g) per day. With this, serum portasium levels were again normalised; at this time (February 2020) the patient was taking sacubitril/valsartan 24/26 mg every 12 hours and spironolactone 25 mg every 24 hours, and it was decided to maintain this treatment unchanged. Due to the SARS-CoV-2 pandemic, he was seen again in September 2020, when he presented serum potassaemia of 6.30 mEq/l, so the patiromer was titrated up to the maximum dose (25.2 g every 24 hours) and the dose of spironolactone was reduced to 12.5 mg every 24 hours. Three months later, potassium levels were at the upper limit of normal (5.19 mEq/l), so the same treatment was maintained. In January 2021, a control transthoracic echocardiogram was performed, showing an increase in LVEF to 35% and a clear improvement in adverse remodelling with a decrease in ventricular volumes, as well as normalisation of right ventricular function, with the prostheses remaining normal. The patient remains in good functional class (NYHA I-II/IV), and analytically there was a clear decrease in NT-proBNP during follow-up, with no notable adverse effects.

DIAGNOSIS
Chronic heart failure with severely depressed LVEF of valvular origin.
Carrier of mechanical prosthetic aortic and mitral valves.
Asymptomatic moderate hyperkalaemia in the context of neurohormonal treatment for heart failure.
