HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
75-year-old male patient.
No known allergic reactions to medication.
Ex-smoker of 12 pack-years. Arterial hypertension. No enolic habit.
Cardiological history: advanced heart failure. Severe left ventricular systolic dysfunction (left ventricular ejection fraction 20% in last echocardiographic study in November 2019). Right ventricular dysfunction with severe tricuspid regurgitation and severe pulmonary hypertension. Transposition of great vessels congenitally corrected, not intervened. Last coronary angiography in 2017 without angiographically significant coronary lesions. Primary prevention with a resynchronised defibrillator. NYHA functional class III-IV. Discarded for cardiac transplant or ventricular assistance by his reference unit due to age and associated comorbidity.
Other antecedents: hyperuricaemia. Stage 3aA1 chronic kidney disease. Urothelial carcinoma operated on in 2019 by transurethral resection. Anxiosodepressive syndrome.
Family history: no history of sudden cardiac death, cardiac surgery or heart transplant. Denies cases of early cardiovascular disease in the family.
On regular treatment with: furosemide 80 mg daily; bisoprolol 5 mg daily; sacubitril/valsartan 24/26 mg /12 hours; eplerenone 25 mg daily; allopurinol 100 mg daily; sertraline 50 mg daily; omeprazole 40 mg daily.

Present illness
Patient who was admitted to our centre on a scheduled basis to start outpatient cycles of levosimendan. The patient was referred from his reference centre (in the Community of Madrid) due to the overload of the system due to the onset of the SARS-CoV-2 viral pandemic. On admission, he denied an increase in basal oedema in the lower limbs and an increase in basal dyspnoea (which persisted on minimal exertion, although not at rest). However, he reported an increase in the use of a pillow in the last week to achieve a good night's rest.

Physical examination
Temperature 36.7 oC; blood pressure 108/69 mmHg; heart rate 60 bpm; O2 saturation 93% with no oxygen intake. Weight on admission 72 kg. No signs of tachypnoea at rest.
Neurological examination without alterations. Cardiac auscultation was rhythmic, with a low intensity systolic murmur in the aortic focus, non-radiated, and pulmonary auscultation with fine crackles in the right base. On abdominal examination, no organomegaly was palpable; hepatojugular reflux was positive. The lower limbs showed oedema in the distal third and no signs of deep vein thrombosis. Pulses were palpable and symmetrical.

COMPLEMENTARY TESTS
Electrocardiogram on admission: sinus rhythm at 65 bpm with ventricular stimulation by resynchroniser. No significant artefacts or signs of acute ischaemia.
Laboratory tests on admission: haemoglobin 11.8 g/dl, MCV 91 fl, MCHC 33.5 g/dl, leukocytes 2400/μl (1900 segmented/ 300 lymphocytes/ 200 monocytes), platelets 130000/μl; glycaemia: 92 mg/dl, urea 94 mg/dl, creatinine 2.2 mg/dl, estimated glomerular filtration rate (MDRD) 26 ml/min/1.73, total bilirubin 1, GOT 39, GPT 26, sodium 131 mmol/l, potassium 4.8 mol/l, calcium 8 mg/dl, magnesium 2.3 mg/dl.
Urgent chest X-ray: increased cardiothoracic index with discrete signs of vascular redistribution. Parenchymal infiltrate in the right lower lung lobe. There was minimal associated pleural effusion. The patient had a resynchronisation device, with normally positioned three-chamber electrodes.
Microbiological study: rapid influenza A and B test: negative; antigenuria for pneumococcus: negative; antigenuria for Legionella (serogroup 1): negative; PCR for SARS-CoV2 coronavirus: positive.
Control analytical study: haemoglobin 11.5 g/dl, MCV 93 fl, MCHC 32 g/dl, Leukocytes 4700/μl (3600 segmented/ 900 lymphocytes/ 150 monocytes), platelets 237000/μl; glycaemia: 109 mg/dl, urea 67 mg/dl, creatinine 1.7 mg/dl, estimated glomerular filtration rate (MDRD) 37 ml/min/1.73, total bilirubin 1.3, GOT 29, GPT 25, sodium 136 mmol/l, potassium 4.2 mol/l, calcium 8.3 mg/dl, magnesium 1.8 mg/dl. Cardiac biomarkers: ultrasensitive troponin I 78 μg/l (reference limit < 20 μg/l) CPK 121 IU, ProBNP 4325 pg/ml.
Anaemia profile: iron 147 μg/dl (ref < 175), ferritin 94 μg/ml, transferrin 187 mg/dl, IST 7%, folic acid > 24 ng/ml.
Chest X-ray prior to discharge: the right pulmonary infiltrate practically disappeared.

CLINICAL EVOLUTION
The patient had been seen in outpatient cardiology consultations at our centre the previous week for re-evaluation of the case, in which he reported an absence of symptoms suggestive of COVID-19 infection. However, he did describe the symptoms described previously, compatible with an increase in his usual orthopnoea.
A blood test drawn by protocol prior to the first cycle with levosimendan showed lymphopenia and thrombocytopenia with an increase in acute phase reactants. The patient was re-evaluated in a targeted manner, on this occasion referring to the existence of a diarrhoeal syndrome with stools without pathological products in the last 4 days, which he had not previously described. His temperature had not been taken, although he did not describe fever or chills. She did report intense asthenia, which she had attributed to her cardiac pathology. A chest X-ray was requested, which revealed the presence of a right pneumonic infiltrate. In this context, the COVID-19 suspicion protocol was activated and the patient was transferred to an isolation area, where microbiological samples were taken.
Treatment was started with hydroxychloroquine and lopinavir/ritonavir, given the high suspicion in a patient at risk with pulmonary infiltrate, and diuretic treatment was reinforced by adding intravenous furosemide 80 mg daily to his usual treatment.
During admission, serial electrocardiographic and analytical determinations were performed. At the last check-up after finishing the hydroxychloroquine regimen, an iron profile study was performed and ferropenia was detected, so it was proposed to start treatment with 1 gram of hierrocarboxymaltose prior to discharge. Administration was carried out without incident.
The patient had a favourable clinical evolution, remaining afebrile and with minimal oxygen intake throughout admission. He showed a weight reduction of 5.5 kg.
He completed the treatment regimen with hydroxychloroquine and, after consultation with the patient, it was decided to administer the first course of levosimendan, with good haemodynamic tolerance and no notable complications.
Three weeks after discharge, the patient received the second cycle of levosimendan with excellent tolerance. When contacted by telephone, the patient reported symptomatic improvement with a reduction in the number of pillows and a decrease in dyspnoea to NYHA functional class II. The asthenia had disappeared.

DIAGNOSIS
Advanced chronic heart failure with severely depressed ejection fraction.
Congenitally corrected transposition of great vessels.
Right lower pneumonia due to SARS-CoV-2/COVID-19.
Re-exacerbated chronic kidney disease.
Iron deficiency treated with intravenous administration of iron-carboxymaltose.
