HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
A 15-year-old male patient with no known pathological history came to the emergency department with epigastralgia, anorexia, weight loss and asthenia of one month's duration, with slight swelling of the lower limbs. No fever or other associated symptoms, no chest pain. The anamnesis revealed that he had been practising sport regularly until 2 months ago, when he began to experience fatigue that forced him to reduce his exercise load, nausea with abdominal pain, and loss of up to 6 kg in the last two months.

Physical examination
BP 96/61 mmHg, HR 120 bpm, RR 24 rmp, Sat 95%. Regular general condition, tachypneic, afebrile, hydrated. Neurological: no pathological findings.

Cardiorespiratory: rhythmic heart tones, systolic murmur II/VI in mitral focus. Bibasal crackles. Positive hepatojugular reflux. Abdomen: hepatomegaly of 2 fingers under the costal ridge. Pain on palpation in the epigastrium. Extremities: peripheral pulses present and symmetrical. Minimal bimalleolar oedema.  COMPLEMENTARY TESTS Emergency analytical tests: Hb 12.6 g/d. Leukocytes 14,000 u/L. Cr 1.37 mg/d. Urea 69 mg/dl. GOT 1145 U/L. GTP 1590 U/L. TnTUs 1,722 pg/ml. Venous blood gas Ph 7.44, PCO2 35 mmHg. HCO3 26 mmol/L. Lactate 2,4 mmol/L. ECG on arrival: sinus tachycardia at 115 bpm, normal PR narrow QRS with inverted T wave on lateral side. Echocardiogram: dilated left ventricle (DTD 59 mm) with thinned walls. Severely depressed systolic function at the expense of global hypokinesia, LVEF 19%. Moderate MI of functional profile. Trivalve aortic valve with normal transvalvular gradients. RV slightly dilated, with TAPSE of 9 mm. Trivial TR allowing estimation of PAPs of 45 mmHg. Slight pericardial effusion. IVC of 19 mm with little inspiratory collapse. Cardiac magnetic resonance (CMR): dilated left ventricle (LVEDV 139 ml/m2) with decreased wall thickness, and very severe depression of ventricular function, LVEF 14%. Right ventricle with slightly increased volumes (RVOTV115 ml/m2) and severely decreased systolic function, RVEF 22%. Absence of oedema in STIR sequences. First-pass perfusion (dimeglumine gadobenate) at rest normal. Late multifocal contrast uptake, intramyocardial and epicardial, circumferential throughout the LV. In conclusion DCM with very severe depression of biventricular function secondary to extensive myocardial fibrosis.

EVOLUTION
After initial examinations in the emergency department and bedside echocardiography, the patient was admitted to the Intensive Care Unit for further study and treatment, where CMR was requested, confirming the echocardiographic findings, showing no myocardial oedema and extensive fibrosis with absence of viability. In view of these results, and with the suspicion of possible evolved myocarditis, under optimal medical treatment, which included ACE inhibitors, beta-blockers, loop diuretics and antialdosterone drugs, the referral hospital was contacted to assess cardiac transplantation. Simultaneously, the patient presented progressive haemodynamic deterioration, with symptoms of persistent heart failure, increased lactate and other signs of peripheral hypoperfusion, so vasoactive drugs were started, which were regularly tolerated, with episodes of SMVT from the start of treatment, as well as levosimendan perfusion, without satisfactory response, so a Levitronix Centrimag type ventricular assist device was implanted via the left subclavian artery, pending cardiac transplantation. Finally, orthotopic transplantation was performed using the bicava technique, with adequate graft functioning during the postoperative period. Extubated during the first 24 hours after surgery. Post-transplant echocardiogram showed good LV function (LVEF 66%), slightly decreased TAPSE (15 mm), absence of valve disease and minimal pericardial effusion. Currently, 6 months post-transplant, the patient has remained asymptomatic, since discharge with immunosuppressive treatment with corticosteroids, mycophenolate mofetil, tacrolimus, atorvastatin and valganciclovir (after detection of CMV+ in controls). Coronary angiography with OCT showed no intimal proliferation, and endomyocardial biopsies showed no rejection.

DIAGNOSIS
Non-ischemic DCM, with very severe depression of biventricular function. Cardiogenic shock. Cardiac transplantation.
