HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
No known drug allergies.
No known classical cardiovascular risk factors. Obesity type 1.
Toxic habits: ex-smoker since youth, until the debut of ischaemic heart disease, with an accumulated consumption of 30 packets/year. Non-drinker and non-consumer of other toxic substances. Chronic ischaemic heart disease with debut in 2011 with acute myocardial infarction with ST-segment elevation (STEMI) anteroseptal Killip III undergoing emergent angioplasty on proximal anterior descending artery (ADA) with a drug-eluting stent and observing chronic occlusion of distal circumflex artery (ACx). Currently in dilated phase with very severe ventricular dysfunction (LVEF 25-28% in 2012, 2013 and 2015, 20% in 2017 and 18% in the last control in 2019) in follow-up by the advanced heart failure and heart transplant unit. Carrier of a Medtronic Protecta single-chamber implantable cardioverter defibrillator (ICD) in primary prevention since 2012.
Peripheral artery disease with 70% stenosis in the left common iliac artery due to calcified plaque, asymptomatic.
Left kidney with abundant cysts (some of them calcified) in which no renal parenchyma can be seen, which appears non-functioning.
Current treatment: acetylsalicylic acid 100 mg/24 hours, carvedilol 6.25 mg/12 hours, atorvastatin 80 mg/24 hours, ezetimibe 10 mg/24 hours, sacubitril/valsartan 24/26 mg/12 hours, eplerenone 25 mg/24 hours, omeprazole 20 mg/24 hours.

Present illness
53-year-old male with the previously described history, including ischaemic heart disease in dilated phase with two-vessel disease (proximal LAD revascularised in 2011 and chronic occluded ACx at distal level) with very severe residual left ventricular dysfunction who was referred to the advanced heart failure and heart transplant unit for evaluation in 2017 as he was in NYHA functional class III.
At that time, a complete pre-transplant study was performed without finding any contraindication for transplantation, although given that after adjustment and optimisation of medical treatment the patient remained in good functional condition, it was decided not to include him on the transplant waiting list. He has been clinically monitored by this unit on an outpatient basis since then, with medication readjustments as required. In the 2017 analytical control, he presented absolute iron deficiency, which was treated with a cycle of intravenous iron carboxymaltose in a single dose of 1000 mg. At that visit, the patient maintained his usual physical activity, although with certain limitations to moderate efforts, which improved after the replenishment of iron deposits.

Physical examination
Good general condition. Conscious, oriented and cooperative. Well hydrated and perfused. Height 174 cm. Weight 100 kg. Body mass index (BMI) 33.
Blood pressure (BP) in range, in consultation 110/70 mmHg, and heart rate 60 bpm. Eupneic at rest and when speaking, with no semiology of heart failure.
On auscultation, rhythmic heart tones with mitral systolic murmur I-II/VI without third sound or gallop rhythm. Bladder murmur was preserved without crackles or other added sounds.
Abdominal examination was unremarkable. Lower limbs without oedema or signs of deep vein thrombosis (DVT).

COMPLEMENTARY TESTS
Electrocardiogram (ECG) in consultations: sinus rhythm at 60 bpm. Axis normopositioned at 0o. PR 200 msec. Wide QRS of 160 msec very variegated with morphology of complete left bundle branch block (LBBB) and secondary repolarisation disorders.
CBC (November 2019): blood glucose 106 mg/dl. Creatinine 1.07 mg/dl, urea 26 mg/dl, sodium 144 mEq/l, potassium 5.3 mEq/l. Lipid profile: total cholesterol 119 mg/dl, HDL-C 46 mg/dl, LDL-C 60 mg/dl, triglycerides 66 mg/dl. Normal liver and thyroid profiles. Glycated haemoglobin 5.9%. Glomerular filtration rate 77 ml/min (MDRD). NT-proBNP 198 pg/ml. Haemogram without leukocytosis with normal formula. Hb 142 g/l. Platelets 262,000. Normal coagulation study. Iron metabolism: ferritin 45 μg/l and saturation index of 20%.
Analysis control after treatment with intravenous carboxymaltose: ferritin 141 μg/l and saturation index of 23%. Other parameters were similar to those of the previous control.
Chest X-ray: cardio-thoracic index at the upper limit of normality with left hilum slightly blurred and vascular redistribution to the vertex, without evidence of pulmonary congestion. Single-chamber ICD with normal-positioned electrode in the right ventricular apex.
Transthoracic echocardiography (November 2019): slightly dilated left atrium (46 mm AP. LVOT 37 ml/m2). Mitral valve without organic involvement, preserved opening with symmetric tenting closure and central jet of mild insufficiency. Trivalve aortic valve, without organicity and with normal flows. Aortic root not dilated: SV of 33 mm. Severely dilated left ventricle: DTD 75 mm, DTS 68 ml, VTD 387 ml, VTS 258 ml. LVEF 20% with global hypokinesia more marked in mid and apical segments. Mitral E 85 cm/sec, A 36 cm/sec, E/A= 2.85, TDE 130 msec. Septal E' 4.8 cm/sec, lateral E' 9.6 cm/sec, average E/e' 11.8. Right cavities not dilated. ICD electrode. TAPSE 21 mm. Light IP. PAP m 20 mm Hg. Normal IVC. Absence of effusion. Conclusions: dilated cardiomyopathy with severe left ventricular dysfunction (LVD) and mild functional mitral regurgitation (MR).
Ergospirometry (November 2018): the test was performed according to the modified Bruce ramp protocol without complications. Exercise time 12:24 min, stopped due to fatigue. It reached 129 bpm, 77% of the FCMT. The RER at peak effort was 1.05 which confirms that this is a conclusive test. The test shows a slightly decreased functional capacity with respect to predicted (Weber Stage B, peak oxygen consumption 19.6 ml/kg/min, 76% with respect to theoretical), ventilatory class II (VE/VCO2 slope 30.6) having reached ventilatory threshold 2. Baseline CO2 PET 36 increasing to 40 mmHg. No EOV. No alteration of the ventilatory reserve, not suggesting concomitant ventilatory alteration. From the ECG point of view, there were no dynamic changes. Isolated EV in the recovery phase. Normal blood pressure behaviour (baseline 124/80 mmHg and at maximum effort 150/90 mmHg). Conclusions: slight decrease in functional capacity with no data of poor prognosis in ergospirometry.

CLINICAL EVOLUTION
Since the administration of intravenous iron carboxymaltose (in 2017), the patient has remained asymptomatic and without the need for medication readjustments, with only one admission for decompensation of heart failure in a period of 2 years. On an outpatient basis, being in a stable phase of heart failure, regular monitoring of iron metabolism has been carried out, as well as the state of the iron deposits, which at all times has maintained stable figures. In the last analytical control (November 2019), as we can see in PPCC, she again presented data of iron deficit with depleted deposits, without associated anaemia, and it was decided to prescribe a new cycle of intravenous iron carboxymaltose with a dose adjusted according to the patient's weight, and in the last outpatient review by the advanced heart failure and heart transplant unit of our centre she reported an improvement in her current functional situation (currently NYHA II).

DIAGNOSIS
Advanced chronic heart failure.
Severe LV systolic dysfunction in a patient with chronic ischaemic heart disease in NYHA functional class II.
Carrier of single-chamber ICD in primary prevention with no events during follow-up.
Iron deficiency treated with intravenous iron carboxymaltose.
