HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

BACKGROUND:
61-year-old woman.
No known drug allergies.
No cardiovascular risk factors or toxic habits. No family history of early ischaemic heart disease or sudden death.
No previous cardiological history.
Vitiligo.
No other diseases of interest. No hospital admissions or surgical interventions
No usual treatment.

CURRENT ILLNESS:
Previously asymptomatic cardiovascular until the week prior to admission, which begins with pseudo-flu-like symptoms of myalgia, asthenia and dysthermic sensation with febrile fever. On the day of admission, she had two episodes of dizziness with associated vegetative cortex and subsequent syncope, with complete recovery within seconds. There was no associated chest pain or palpitations. She had not had previous syncopal episodes, nor did she present dyspnoea, orthopnoea, oliguria or oedema.

PHYSICAL EXAMINATION:
Arterial hypotension of 50/70 mmHg and tachycardia at 110 bpm were observed, together with signs of poor peripheral perfusion, with coldness and sweating. Afebrile. Cardiopulmonary auscultation with rhythmic heart sounds, without murmurs and preserved vesicular murmur without pathological sounds.
Pulses present and symmetrical in all four extremities. No oedema or evidence of venous thrombosis in the lower limbs.

COMPLEMENTARY TESTS
ELECTROCARDIOGRAM (ECG): sinus rhythm at 90 bpm, PR 140 ms, narrow QRS, with discrete J point elevation especially in inferior face and V5-V6, with slow progression of R in precordials and generalised decreased voltages.
THORAX RADIOGRAPHY (admission): normal cardiothoracic index. No evidence of heart failure or visible condensation.
THORAX RADIOGRAPHY (evolution): acute pulmonary oedema.
ANALYSIS:
CBC: leukocytes 6600/μl (70% neutrophils), Hb 13.6 g/dl, platelets 140,000/μl.
Coagulation: INR 1, PT 96 %.
Biochemistry: at baseline: glucose 145 mg/dl, urea 52 mg/dl, creatinine 1.03 mg/dl, glomerular filtration rate 52 ml/min (CKD-EPI) [>60], K 4.5 mmol/l, Na 140 mmol/l, CK 151 U/l, ultrasensitive Troponin 24.4 ng/l. ProBNP 414 pg/ml. In the evolution: GOT 1.322 U/l, GPT 1.050 U/l, CK 3578 U/l, ultrasensitive troponin 5.001 ng/l, ProBNP 3.229 pg/ml, CRP 8,7 mg/dl.
Transthoracic echocardiogram: hypertrophic left ventricle (interventricular septum 15 mm) with echodensity suggestive of infiltrative disease or inflammation, not dilated (end-systolic diameter 40 mm), with very severe depression of ejection fraction (LVEF 10-15 %) at the expense of global hypokinesia. Normal sized right ventricle with severe ventricular dysfunction (TAPSE 7). Normal sized left atrium. No significant valvular heart disease. Mild pericardial effusion. Ascending aorta of normal size.
CARDIAC NUCLEAR MAGNETIC RESONANCE (MRI): very artifactual study due to inadequate cooperation of the patient. Both ventricles are normal size with severe global hypokinesia and significant oedema and diffuse hyperemia, compatible with acute inflammatory pathology. There are no areas of late gadolinium uptake. No pericardial effusion. Minimal bilateral pleural effusions.

CLINICAL EVOLUTION
In a situation of arterial hypotension and poor peripheral perfusion with initial suspicion of acute myocarditis in cardiogenic shock, he was admitted to the coronary unit and haemodynamic support was started with dobutamine and noradrenaline. The day after admission, cardiac MRI was performed, confirming the suspected diagnosis. Progressive worsening in the following hours despite treatment with vasoactive amines at maximum tolerated doses, with clinical deterioration and onset of multi-organ failure, with oligoanuria, lactidemia greater than 6 nmol/l and increased liver damage enzymes. It was decided to place an aortic balloon pump and ECMO type veno-arterial circulatory support.
In the following hours, there were persistent signs of poor distal perfusion and poor ventilation with pinkish expectoration through an orotracheal tube compatible with acute pulmonary oedema.
He presented an episode of severe bradycardia and asystole, advanced cardiopulmonary resuscitation manoeuvres were performed, and he died on the third day of admission.

DIAGNOSIS
Fulminant myocarditis.
Very severe biventricular dysfunction (LVEF 10-15%).
Cardiogenic shock with circulatory support with veno-arterial ECMO.
Death.
