HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

PERSONAL HISTORY
Cardiovascular risk factors: hypertension (HT), smoker. No diabetes mellitus (DM), no dyslipidaemia (DL).

Cardiological history:
2006: out-of-hospital cardiorespiratory arrest (CRA) recovered. First rhythm detected: ventricular fibrillation. The output electrocardiogram (ECG) showed ST elevation in precordial leads. Catheterisation: non-significant lesion in AMD. Positive acetylcholine test. Transthoracic echocardiogram: normal LVEF, apical septal dyskinesia. She was discharged with a diagnosis of coronary vasospasm and treatment was started with nitrates and calcium antagonists.
Subsequent follow-up in cardiology outpatient clinics, she remained stable. It was not possible to increase the dose of diltiazem to maximum doses due to poor tolerance.
2009: admitted for non-ST-segment elevation acute coronary syndrome (NSTEACS). On arrival he reported chest pain, the ECG showed ST-segment depression in V1-V2 and I,aVL; he presented peak Tn I of 0.14. Catheterisation: coronary arteries without lesions. Transthoracic echocardiogram: normal LVEF. No segmental alterations.
Baseline: independent for basic activities of daily living. New York Heart Association (NYHA) functional class I.
Usual treatment: acetylsalicylic acid (ASA) 100 mg/d, atorvastatin 20 mg/d, isosorbide mononitrate 60 mg/d, diltiazem retard 120 mg/12h, valsartan 320 mg/12h.
Pregabalin, tramadol, naproxen.

CURRENT ILLNESS
50-year-old woman brought to the emergency department by SUMMA after recovered out-of-hospital CRA. Her daughter reported that she woke up this morning with general malaise and chest discomfort. At 8 o'clock in the morning she presented with witnessed CPR and basic CPR manoeuvres were started immediately. The police arrived after a few minutes and continued with basic CPR. On arrival of SUMMA, ventricular fibrillation was observed and sinus rhythm was recovered after a 200 J shock. The basic and advanced CPR manoeuvres lasted 15-20 minutes. The emergency services proceeded with orotracheal intubation, sedation and transfer to our centre.

PHYSICAL EXAMINATION
Intubated, sedated under midazolam perfusion.
Blood pressure (BP) 113/83 mmHg without inotropics. Heart rate (HR) 74 bpm. Sat 100% with VMI with FiO2 100%, VT 500, FR 17.
Well hydrated, nourished and perfused. Normal colour. No jugular ingurgitation.
Cardiac auscultation: rhythmic, no murmurs.
Pulmonary auscultation: preserved vesicular murmur without over-additions.
No oedema in the lower limbs. Pulses present and symmetrical.

COMPLEMENTARY TESTS
ECG performed by the emergency services during transfer to our centre: atrial fibrillation at 130 bpm with normal axis (+60) narrow QRS (100 ms), diffuse repolarisation alterations. Normal QTc (430 ms).
Chest X-ray on arrival: technically limited plaque, rotated and tilted (no right costophrenic sinus). Aortic elongation. Mediastinum difficult to assess due to the limitations of the X-ray. Cardiothoracic index within the normal range. Unspecific alterations of the pulmonary parenchyma. No left pleural effusion was observed.
Analysis and blood gases on arrival: Hb 13.1 g/dl. Leukocytes 23.1 x 103/ul. Platelets 265 000/ul. INR 1. Creatinine 0.97 mg/dl. Na 143 mmol/l. K 3.7 mmol/l. Tn I 3.55 ng/ml. CRP < 2.9 mg/l. pH 7.32, pCO2 49 mm Hg, pO2 87 mm Hg, HCO3 25 mmol/l, lactate 1.8 mmol/l.
Transthoracic echocardiogram in the resuscitation room: left ventricle not dilated, not hypertrophic, with normal global systolic function. Apical akinesia. Right ventricle of normal size and function. Atria of normal size. No significant valvular heart disease. No pericardial effusion.
Catheterisation: epicardial coronary arteries without significant lesions.
Normal ventriculography and aortography.

CLINICAL EVOLUTION
At 10:00 hours the patient was admitted to the coronary unit, following catheterisation in which coronary arteries were observed without significant lesions and a transthoracic echocardiogram showed normal ventricular function with apical akinesia. The patient was monitored and a therapeutic hypothermia protocol was started. In addition, treatment was started with verapamil via nasogastric tube. Target temperature of 32 ̊C was reached at 16:00 hours. He remained stable until 6:58 am the following day when he presented with new ventricular fibrillation.
Advanced CPR manoeuvres were started and the patient received multiple unsuccessful defibrillations.
The cardiac rhythm became asystole/agonal rhythm with no recovery of spontaneous circulation at any time. The manoeuvres were prolonged for more than 60 minutes without success, and the patient received > 10 mg of adrenaline, two boluses of 300 mg of amiodarone, 2 ampoules of lidocaine and 1 ampoule of magnesium.
Death was certified at 8:18 hours.
On reviewing the patient's telemetry, ST-segment depression (lead aVF) was observed in the previous minutes, with the appearance of increasingly frequent ventricular extrasystoles that progressively led to ST-segment elevation in this lead and finally an extrasystole with R-over-T phenomenon generated an episode of ventricular fibrillation.

DIAGNOSIS
Out-of-hospital cardiorespiratory arrest with first ventricular fibrillation rhythm in the context of MINOCA (acute myocardial infarction with coronary arteries without significant obstructive lesions), possibly related to coronary vasospasm.
In-hospital cardiorespiratory arrest and death in a patient under therapeutic hypothermia with first ventricular fibrillation rhythm.
