HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

BACKGROUND:
Hypercholesterolemia.
Diabetes mellitus (DM) type 2 of 15 years of evolution with good metabolic control, currently with oral antidiabetic drugs (ADO) and insulin.
Obesity grade I.
Ex-smoker for 9 years (IPA 56).
Absence of arterial hypertension. Sedentary.
Leriche syndrome operated with aortobifemoral bypass.
Advanced non-ischaemic HF with reduced LVEF and pulmonary arterial hypertension (LVEF according to magnetic resonance imaging [MRI] 2014) 34%.
Permanent atrial fibrillation (AF) and left bundle branch block (LBBB). Implantable cardioverter defibrillator (ICD) in primary prevention implanted in 2015.
Stage IIIb chronic kidney disease.
Thrombophilia with mutation of the prothrombin gene 20210A.
Chronic obstructive pulmonary disease (COPD) GOLD B with forced expiratory volume in the first second (FEV1) 67%, non-acute.
T1bN0M0 right upper lobe lung adenocarcinoma (LSD), treated with surgery and radiotherapy in 2016, currently disease free.
Seropositive polyarthritis with carpal involvement. Gout.
Subclinical hyperthyroidism with multinodular thyroid.
Allergies. Not known.

Previous treatment: chronic home oxygen therapy, acenocoumarol 10 mg weekly, insulin lantus 26 IU, insulin glulisine 12-10-8, metformin 850 mg (0-1-0), empaglifozin 10 mg (0-1-0), ezetimibe 10 mg/simvastatin 40 mg (0-1-0), furosemide 40 mg (1-1-0) (changing doses according to clinical situation), carvedilol 6.25 mg (1-0-1/2), eplerenone 25 mg (0-1/2-0), sacubitrilo-valsartan 97/103 mg (1-0-1), lansoprazole 30 mg (1-0-0), allopurinol 100 mg (0-1-0), escitalopram 15 mg, indacaterol/glycopyrronium bromide.

CURRENT ILLNESS:
79-year-old male with the history described, under follow-up by the advanced HF unit and on treatment with intermittent doses of levosimendan, who consults for progressive worsening of functional class, currently IIIb/IV. He denies palpitations, chest pain or syncope.
No cough, no expectoration, no increase in sputum purulence. No dysthermic sensation or infectious semiology.

PHYSICAL EXAMINATION:
Blood pressure (BP) 100/60, heart rate (HR) 64 bpm, oxygen saturation (SatO2) 97%, respiratory rate (RF) 20 rpm. Afebrile. Cardiac auscultation: arrhythmic, no audible murmurs. Abdomen soft, depressible, non-painful. Extremities with discrete oedema with fovea, without signs of deep vein thrombosis (DVT).

COMPLEMENTARY TESTS
ANALYTICS: biochemistry: glucose 83 mg/dl, creatinine 1.60 mg/dl, GFR (MDRD) 38.56 ml/min, urea 62 mg/dl, sodium 131 mm/l, potassium 4.5 mm/l, chlorine 100 mm/l, calcium 7.9 mg/dl, phosphorus 2.5 mg/dl, albumin 2.8 g/dl, total protein 5.5 g/dl, total bilirubin 0.99 mg/dl, creatine kinase (CK) 50 U/l, BNP 401 pg/ml. Haemoglobin 16.6 g/dl, haematocrit 53.5%, platelets 150,000/μl, leukocytes 8430/μl, neutrophils 66.20%. Coagulation: prothrombin time 13.70 sg, prothrombin activity 69.40%, international normalised ratio (INR) 1.23, cephalin time 35.70 sg.
Chest X-ray: cardiomegaly, signs of redistribution, increased bronchovascular tract. Device in the pectoral region, access through the subclavian vein and tipped in the right cavities.
ELECTROCARDIOGRAM: atrial fibrillation at 66 bpm. QRS of 120 ms with LBBB morphology. QTc (Bazett, V4) 440 ms. The 8th QRS represents an isolated ventricular extrasystole.
ECHO-CARDIOGRAM (video1): moderate-severe global LV systolic dysfunction (LVEF 37%). The s e p t a l m o v e m e n t m o v e m e n t i s c o m p a t i b l e w i t h a n o m a l y a n o m a l y o f t h e c o n d u c t i o n .
Abnormal apical motion may reflect pacemaker activation. ICD lead in right chambers. Mild mitral insufficiency (MI) and tricuspid insufficiency (TI). Mild pulmonary arterial hypertension (PAH).

CLINICAL EVOLUTION
Given the patient's progressive dyspnoea and poor response to pharmacological treatments for HF (not escalated to evidence-based doses due to the appearance of adverse effects), the implantation of a carotid baroreceptor stimulator was proposed as a therapeutic complement. Previously, cardiac resynchronisation therapy (CRT) was ruled out due to QRS 110-120 ms and ivabradine due to permanent AF.
On the other hand, it was decided to change therapy to direct-acting anticoagulants due to INR lability.
The patient was admitted on a scheduled basis and the Barostim neo device was implanted without complications (control X-ray). The patient was discharged 24 hours later. 45 days later, the patient reports improvement in his functional class, currently II/IV, with a decrease in daily furosemide doses and no need, for the time being, for intermittent therapy with levosimendan. Pre-implantation brain natriuretic peptide (BNP) values 401.2 pg/ml; BNP 45 days post-implantation 371.3 pg/ml.

DIAGNOSIS
HF with reduced LVEF (HFrEF) of non-ischaemic aetiology, stage D and functional class II in treatment with carotid baroreceptor stimulator.
Hypercholesterolemia. Type II DM for 15 years with good metabolic control, currently insulin-dependent. Grade I obesity. Ex-smoker for 9 years (IPA 56). No arterial hypertension. Sedentary.
Leriche syndrome operated with aortobifemoral bypass. Advanced non-ischemic HF with reduced LVEF and pulmonary hypertension (LVEF according to MRI 2014) 34%. AF and LBBB. ICD in primary prevention implanted in 2015. Stage IIIb CKD.
Thrombophilia with mutation of the prothrombin gene 20210A.
COPD GOLD B with FEV1 67%, non-acute. LSD T1bN0M0 lung adenocarcinoma, treated with surgery and radiotherapy in 2016, currently disease free.
Seropositive polyarthritis with carpal involvement. Gout.
Subclinical hyperthyroidism with multinodular thyroid.
