A 38 year old male presented to the Emergency Department for dyspnoea.

HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
No family history of interest, no known allergies. Smoker of 10 cigarettes/day, occasional weekend drinker and sporadic ex-consumer of cocaine and marijuana. Does not take regular treatment. Patient with an active life, asymptomatic from the cardiological point of view until two months prior to admission, who began with progressive deterioration of functional class with dyspnoea on moderate exertion until becoming resting. For this reason, he came to the hospital one week prior to admission, with a predominantly nocturnal cough and intermittent mild pain in the anterior chest region, and was diagnosed with a possible respiratory tract infection. Antibiotic and corticoid treatment was prescribed. Since then, clinical worsening with paroxysmal nocturnal dyspnoea, orthopnoea of up to two pillows associated with oedema up to 2/3 in the lower limbs and weight gain in the last week.
On arrival at the emergency department, BP 110/60. HR: 120 bpm. Basal SatO2: 97 %. Weight: 74 kg.
Good general condition: well hydrated, well nourished and perfused, normal colour. Neck: no palpable lymph nodes or evidence of jugular engorgement. Cardiac auscultation: gallop rhythm by R3. Pulmonary auscultation: bibasal crackles in the lower third of both lung fields. Abdomen: RHA +, soft, depressible, not painful on deep or superficial palpation. Lower limbs: oedema up to the lower third of both lower limbs without fovea, peripheral pulses (+). No signs of deep vein thrombosis (DVT).

COMPLEMENTARY TESTS
Complementary tests on admission ECG: sinus tachycardia at 120 bpm. Narrow QRS with unspecific repolarisation alterations (negative T waves in I, aVL and from V4 to V6).
Haemogram: leucocytes 8,000. Hb 14.7 g/dl. Platelets 217,000/ul.
Haemostasis: APTT: 31.3. PT: 12.8. INR: 1.11.
Biochemistry: glucose 121 mg/dl. Creatinine 0.9 mg/dl. Albumin 3.6 g/dl. Calcium 8.6 mg/dl. GOT 29 U/l. GPT 50 U/l. CK 111. Troponin 0.09 ng/ml. Bilirubin 0,4 mg/dl. Amylase 44. Lipase 37. Na 144. K 4,2 mmol/l. Chlorine 109 mmol/l. GOT: 20 U/I GPT: 32 U/I GGT: 117U/I 4. BNP: 405 pg/ml.
Arterial blood gases: pH 7.49, pCO2 27 mmHg, pO2 89 mmHg, HCO3 20 mmol/l.
Chest X-ray: cardiomegaly. No parenchymal infiltrates. Vascular redistribution with evidence of CHF.
Portable echocardiogram (Vscan): dilated LV with severe global systolic dysfunction with generalised hypokinesia and RV systolic dysfunction. Moderate MI. Severe TR. No pericardial effusion.
In view of the findings, it was decided to admit him to the ward for treatment and to complete the study.

Complementary tests on the ward ECG: dilatation and severe LV dysfunction with LVEF around 15%. Restrictive filling with mild MI. Dilatation and dysfunction of the RV with PSAP around 55 mmHg.
Biochemistry: TSH: 2.28. CRP: 3.4. Ferritin: 59 ng/ml. Vitamin B12: 464 ng /dl A.
Folic: 5. HDL: 32 mg/dl. LDL: 99.4 mg/dl.
Serology: anti HIV 1-2 (-). IgM anti CMV(-). EBV IgG(-). Toxoplasma IgG(-). IgG antiHBc(-). HCV(-).
Catheterisation: coronary arteries without significant lesions.
Chest X-ray (at discharge): cardiomegaly with no evidence of pulmonary congestion.
Walking test (prior to discharge): 6-minute test was performed, covering 426 metres, finishing at 100-110 bpm and with a baseline saturation of 95%.
Cardiac MRI (prior to discharge): dilated cardiomyopathy with severe LV and mild RV dysfunction. Mild MI and TR. No evidence of myocardial fibrosis.

EVOLUTION
Treatment with beta-blockers, antialdosterone and ACE inhibitors was started on the hospital ward, and the latter had to be discontinued due to symptomatic arterial hypotension of up to 85/40 mmHg. During the first days of admission he required inotropic support with levosimendan and intravenous depletive treatment with diuretics, losing approximately 8 kg of weight since admission.
He was monitored with telemetry during admission and only isolated ventricular extrasystoles were observed.
A regular echocardiogram confirmed the presence of dilated cardiomyopathy with severe LV dysfunction, with no significant valvulopathy to justify it. In order to rule out coronary artery disease, coronary angiography was performed, ruling out coronary artery disease.
Due to a tendency to sinus tachycardia with BP figures of 90-100/50-60 that prevented an increase in the dose of beta-blockers, it was decided to associate ivabradine, achieving a resting heart rate of around 70-80 bpm.
With the aim of prognostic stratification and with a view to assessing myocardial fibrosis, MRI was performed, ruling it out, showing a slight improvement in LV (LVEF 25%) and RV function with respect to the initial echocardiographic study.
Also for prognostic purposes, a walking test was performed prior to discharge, reaching more than 300 metres in 6 minutes and without desaturation.
Given the stability and good clinical evolution, he was discharged pending the optimisation of pharmacological treatment on an outpatient basis in consultations, as well as early re-evaluation with the aim of considering an ICD if ventricular function did not improve.

DIAGNOSIS
Congestive heart failure.
Idiopathic dilated cardiomyopathy. Severe LV dysfunction. Mild RV dysfunction.
Coronary arteries without significant lesions.
