HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
55-year-old male patient with the following personal history:
No known adverse drug reactions.
Cardiovascular risk factors: smoker.
No family history of interest.

Cardiological history: chronic ischaemic heart disease:
2004: ACS. Conservative management.
October 2018: assessed in cardiology outpatient clinic for angina. The patient had no signs of heart failure and the electrocardiogram (ECG) showed no alterations of interest. The following complementary tests were requested:
Transthoracic echocardiography: non-dilated left ventricle, with a slight increase in septal wall thickness. Slight hypokinesia at the septal level in the basal and middle segments with adequate contractility of the remaining segments, with overall preserved LV systolic function. No aortic and left atrial root dilatation. Right chambers not dilated with preserved right ventricular systolic function. No significant organic valvular pathology. Vena cava not dilated with adequate respiratory collapse. No pericardial effusion.
Diagnostic coronary angiography:
Coronary trunk with non-significant angiographic lesions.
Anterior descending artery with severe stenosis from its origin to the middle segment and in the distal third with thin distal bed and TIMI 2 flow. Recanalisation of septal branches by heterocoronary circulation.
Circumflex artery (Cx) with non-significant angiographic lesions.
Dominant right coronary artery, diffusely diseased, with non-significant focal lesion.
In view of these findings, it was decided to assess myocardial viability in order to decide on the approach to revascularisation. Stress echocardiography was requested: a stress test was performed with dobutamine, until reaching 15 mcg/kg/min and doubling the baseline heart rate (HR), showing an improvement until almost normalisation of the motility of the septal segments described with hyperdynamic systolic function. Absence of complications.
Clinically asymptomatic and without electrical changes. Preserved LVEF, viable myocardium.
November 2018: patient placed on waiting list for surgical revascularisation
Usual treatment: ramipril 5 mg (1 tablet every 12 hours), nitroglycerin patch 10 mg (1 tablet every 24 hours), omeprazole 20 mg (1 tablet every 24 hours), fluvastatin 80 mg (1 tablet every 24 hours), acetylsalicylic acid (ASA) 100 mg (1 tablet every 24 hours) and bisoprolol 2.5 mg (1 tablet every 24 hours).
On 6 December, while the patient was out for a walk, he began to feel generally unwell and then suffered syncope. Witnesses tried unsuccessfully to wake him up and called the emergency services. The emergency team took approximately 10 minutes to arrive, finding cardiorespiratory arrest, with bradycardia at 45 bpm and no pulse (electromechanical dissociation). In this context, advanced cardiopulmonary resuscitation (CPR) manoeuvres were started, a total of 3 ampoules of adrenaline were administered and the patient was intubated orotracheally.
After 20 minutes of performing these manoeuvres, a ventricular fibrillation rhythm was observed, from which the patient was defibrillated with a shock at 360 Joules. An ECG was then performed showing: irregular tachycardia at 130 bpm, QRS at 120 ms, ST-segment elevation in inferior leads and V1. QS pattern in V2 and V3 with ST elevation of 2-3 mm in V2-V4 and aVR.
On-call cardiology was contacted, the haemodynamics service was activated and the patient was transferred to our centre. On arrival at the emergency department, an urgent echocardiogram was performed, documenting severe left ventricular (LV) dysfunction with severe hypokinesia in the territory of the anterior descending artery (LAD). The patient was haemodynamically unstable and noradrenaline and dobutamine perfusion was started. Primary angioplasty is then performed.

COMPLEMENTARY TESTS
First ECG after recovery of spontaneous circulation: irregular tachycardia at about 130 bpm, QRS at 120 ms, ST-segment elevation in inferior leads and V1. QS pattern in V2 and V3 with ST elevation of 2-3 mm in V2-V4 and aVR.
Transthoracic echocardiography in the emergency department: limited study due to poor echocardiographic window but showing severe left ventricular dysfunction, with severe hypokinesia in the territory of the anterior descending artery.
Primary percutaneous coronary intervention: diseased left main trunk with significant ostial involvement. Diffusely diseased LAD with severe proximal plaque and no visualisation of the distal bed. Cx with significant proximal plaque; rest of vessel without lesions. Right coronary artery with diffuse lesions not amenable to revascularisation.
Percutaneous coronary intervention (PCI) on the left main coronary artery (LMCA), CX and ADA: given the situation observed, it was decided to pass the guidewire to the ADA and the CX, implant a drug-eluting stent (Resolute Onyx 3.5 x 8 mm) ostial and a "V" stent towards the Cx (Resolute Onyx 3 x 22 mm) and towards the ADA (Resolute Onyx 3 x 26 mm). Balloon angioplasty (2.25 and 2.5 mm) was then performed to the LAD and a stent was implanted overlapping the previous one (Resolute Onyx 2.75 x 18 mm), with a good final angiographic result.
Laboratory tests on admission to the coronary unit: Hb 13.7 g/dl, haematocrit 44%. Normal white blood count but with lymphocytosis of 7,140. Platelets 232,000. Blood glucose 261 mg/dl. Cr 1.40 mg/dl, urea 34 mg/dl. Na 133, K 3.8. NT-proBNP 4623 pg/ml. CPK 180 - 3824 - 1266 - 464 - 1181 - 2959 - 1373 - 408; and TnT 20 - 4518 - 5207 - 3664 - 4535 - 3483 - 3809 - 1472. GSV pH 6.8; Lactic 12.9; pCO2 74 mm Hg. Total cholesterol 95 mg/dl; HDL cholesterol 30 mg/dl; LDL cholesterol 22 mg/dl; triglycerides 241. Neuro-specific enolase 28.1.
Transthoracic echocardiography at discharge: left ventricle neither dilated nor hypertrophic with hypokinesia of mid and apical antero-septal segments, without other segmental contractility disorders. Left ventricular ejection fraction (LVEF) of 51% by Simpson biplane. Left atrium not dilated. Right chambers of normal size and function with preserved right ventricular ejection fraction (RVEF). Mild degenerative mitro-aortic signs without significant associated valvulopathies. No pericardial effusion. Inferior vena cava not dilated with adequate inspiratory collapse.

CLINICAL EVOLUTION
After the intervention, the patient was transferred to the coronary unit and on arrival a neurological window was performed, showing a motor Glasgow of 5 points, so it was decided to perform therapeutic hypothermia, with a target temperature of 33 ̊C, using the Artic-Sun device.
He was sedated with propofol, relaxed with rocuronium and analgesia with fentanyl for 24 hours. During this period, haemodynamic improvement was observed, which allowed for the progressive withdrawal of amine support. After 24 hours, rewarming is started.
Once the protocol is completed, sedoanalgesia and relaxation medication is withdrawn. The patient awoke slowly and, during this process, an electroencephalographic study was carried out, which described: "Abnormal electroencephalographic tracing due to the absence of normal rhythms and generalised slowing of baseline activity, with no clear EEG response to stimuli, reflecting mild-moderate diffuse brain damage. No epileptiform activity or significant asymmetries were recorded".
The evolution was slow and he presented several complications: aspiration pneumonia, acute renal failure, moderate neurogenic oropharyngeal dysphagia. Finally, after a total of 17 days in the coronary unit, he was transferred to the cardiology ward. His evolution on the ward was very good; he started to ambulate progressively and was finally discharged home.

DIAGNOSIS
Out-of-hospital cardiorespiratory arrest recovered; pulseless electrical activity.
Acute ST-segment elevation myocardial infarction (STEMI) KK IV. Multivessel coronary artery disease. PCI with DES implantation in LMCA, ADA and Cx.
Therapeutic hypothermia. Post-arrest anoxic-ischaemic encephalopathy.
Slightly depressed left ventricular systolic function.
