HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

We present the case of a 58-year-old man with a history of smoking cessation, arterial hypertension, chronic bronchopathy, microcrystalline arthropathy, atrial fibrillation, mitral annuloplasty two years earlier for severe valvular insufficiency and last admission for decompensation of heart failure a few months earlier due to consumption of non-steroidal anti-inflammatory drugs and anaemia. Last transthoracic echocardiogram the previous year: non-dilated left ventricle, with slight hypertrophy and preserved ejection fraction.
Mitral annulopasty with residual insufficiency III-IV/IV. Moderate pulmonary hypertension. Bicuspid aortic valve.
On the other hand, at the end of last year a low anterior intestinal resection was performed for a colon carcinoma in the rectum-sigmoid junction, diagnosed as a result of an anaemia study.
Previous treatments: dabigatran 150 mg 1-0-1; allopurinol 300 mg 1-0-1; furosemide 40 mg 1-0-0; omeprazole 20 mg 1-0-0, tiotropium bromide 18 mcg 1-0-0; budesonide 200 mcg 1-0-1; ferrous sulphate 1-0-0; alendronic acid 70 mg 1 every 7 days; calcium carbonate 500 mg/400 IU 1-0-0.
The patient is currently attending the emergency department for a 2-month history of dyspnoea, predominantly nocturnal with 2-pillow orthopnoea, paroxysmal nocturnal dyspnoea, progressive deterioration of functional class and cough without expectoration. In addition, the previous 4 days he started a febrile condition with temperatures up to 38.2 oC.
In the ED he presented with acceptable general condition and mild tachypnoea, maintaining baseline oxygen saturations of 98%. Cardiopulmonary auscultation revealed a systolic murmur in mitral focus and bibasal crackles. No other findings of interest.

COMPLEMENTARY TESTS
Blood tests:
Biochemistry: glucose 162.5 mg/dl. Creatinine 1.17 mg/dl. Sodium 135.6 mEq/l. Potassium 4.52 mEq/l. Chlorine 98.6 mEq/litre. Total protein 6.27 g/dl. Albumin 3.29 g/dl. ALT (GPT) 12,3 U/l. AST (GOT) 14,4 U/l. Gamma-GT 18 U/l. Alkaline phosphatase 76 U/l. LDH 282 U/l.
Bilirubin .51 mg/dl. C-reactive protein 13.78 mg/dl. Iron 16 mcg/dl [59-158] * Ferritin 99 ng/ml [30-400]. Transferrin 233 mg/dl [200-360]. TIBC 329 mcg/dl [250-400] %. Transferrin saturation 4.9% [20.0-50.0 ] NT-proBNP 2729 pg/ml (X2 with respect to previous)*. Haemolysis index 1. Lipaemia index 12.
Haematology: leucocytes 9.4 x1000/μl. Red cells 3.87 xmill/μl. Haemoglobin 8.6 g/dl (previous 9.7). Haematocrit 27.3%. MCV 70.5 fl. MCH 22.2 pg. MCHC 31.5 g/dl. RDW 20%.
Platelets 240 x1000/μl. MPV 7.2 fl. Neutrophils 7.1 x1000/μl. Neutrophils % 75.6. Lymphocytes 1.2 x1000/μl. Lymphocytes % 12.3. Monocytes 1.1 x1000/μl Monocytes % 11.5. Eosinophils 0 x1000/μl. Eosinophils % .2 Basophils 0 x1000/μl Basophils % 0.
Haemostasis: prothrombin activity 70%. INR 1.28. TTPa 36.6 sec. Fibrinogen (derivative) 869 mg/dl. D-dimer 507 ng/ml.

Electrocardiogram: sinus rhythm at 86 beats, left axis, widened QRS with image compatible with complete left bundle branch block, without other relevant findings.
Similar to previous ones.
Chest X-ray: evidence of heart failure without clear consolidations.
Nasopharyngeal exudate (x2): negative for SARS-CoV-2.
Blood cultures (2 sets): isolation of ampicillin-resistant Enterococcus faecium, sensitive to linezolid, glycopeptides, daptomycin and synergy with gentamicin.
Transthoracic echocardiogram: biventricular dilatation. Mitral and aortic insufficiency at least moderate.
Transesophageal echocardiogram: bicuspid aortic valve with infiltration and destructuring of the entire fused leaflet that prolapses and causes severe insufficiency, with probable perforation of the leaflet. Thickening of the posterior wall of the aorta, surrounding the left coronary artery, which cannot be ruled out as abscessation at that level.
Holodiastolic inversion pattern in descending thoracic aorta.
Mitral annuloplasty with a 12 mm filiform and mobile image suggestive of vegetation, leading to severe valvular insufficiency.
Magnetic resonance imaging of the brain: no intracranial complications of interest were observed.

CLINICAL EVOLUTION
Initially, under the diagnosis of heart failure probably related to anaemia, the patient was transfused with red blood cell concentrate and depletive treatment was started, with substantial clinical improvement. However, although the patient's dyspnoea and non-productive cough could be attributed to his decompensation of heart failure, given the current epidemiological context, especially with the febrile peak, it was imperative to rule out SARS-CoV-2 infection, and the patient was transferred to the COVID-19 hospital and treatment with hydroxychloroquine was initiated. Two negative nasopharyngeal swabs were obtained, which, together with the positivity in the two sets of blood cultures for E. faecium, made it possible to reasonably rule out the diagnosis of coronavirus infection and direct the focus towards a diagnosis of heart failure in the context of infective endocarditis and exacerbation of chronic anaemia.
He was therefore transferred from the internal medicine ward of COVID-19 to the cardiology ward, starting empirical antibiotherapy with daptomycin at the time of positive blood cultures. Once the antibiogram was known, it was decided to extend coverage by adding ampicillin and gentamicin.
The case was presented to the cardiac surgery department, who accepted the patient for intervention. A brain MRI was performed which ruled out significant neurological complications. However, it was decided to take another exudate for SARS-CoV-2 PCR as a precautionary measure, and the result was positive. The patient was therefore transferred back to the COVID-19 internal medicine hospital for medical treatment until the nasopharyngeal exudate was negative, with the option of urgent surgery in the event of worsening resistant to medical treatment. The patient remained for several days with persistent fever and progressive clinical deterioration, with dyspnoea on minimal effort, intense orthopnoea that forced him to sleep sitting up and several episodes of paroxysmal nocturnal dyspnoea, requiring oxygen therapy with a reservoir, so that finally, taking into account the risk/benefit balance, it was decided to intervene, performing a double valve replacement with mechanical prostheses.
After surgery, the patient was transferred to intensive care, where he experienced a torpid initial evolution, developing mixed cardiogenic and vasoplegic shock in relation to extracorporeal circulation, requiring orotracheal intubation and support with dobutamine and noradrenaline. Echocardioscopy showed volume depletion and moderate deterioration of left ventricular contractility, with a favourable response to levosimendan.
He also developed an episode of atrial fibrillation with rapid ventricular response, which was adequately controlled with digoxin. Finally, in the following days he evolved satisfactorily, and vasoactive support was discontinued and extubation was performed, although he intermittently required non-invasive mechanical ventilation.

DIAGNOSIS
Decompensation of predominantly left-sided heart failure secondary to anaemia and infective aortic and mitral endocarditis due to E. faecium with severe failure of both valves.
Exacerbation of chronic microcytic hypochromic anaemia, requiring 1 red blood cell concentrate.
Mild respiratory infection due to SARS-CoV-2.
Mixed cardiogenic and vasoplegic shock in relation to extracorporeal circulation, requiring invasive mechanical ventilation and vasoactive support.
De novo atrial fibrillation with rapid ventricular response, controlled with digoxin.
