HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
Cardiovascular risk factors: ex-smoker for 11 years, hypertension and dyslipidaemia. No other known cardiovascular risk factors. Benign prostatic hyperplasia. Cardiological history: Lateral ischaemic heart disease type STEMI in April 2016, 2-vessel coronary artery disease with primary percutaneous coronary intervention on diagonal branch. Second time on right coronary artery. Complete revascularisation. In 2020, repeat cardiac catheterisation during admission for chest pain, with epicardial coronary arteries without angiographic lesions. Congenital valvular heart disease: bicuspid aortic valve. Transthoracic echocardiogram in 2020: left ventricle (LV) slightly dilated. Mild left ventricular dysfunction (EF 45%) with altered contractility in the inferior and apical territory. Moderate aortic stenosis and mild aortic insufficiency. Usual NYHA functional class II/IV. Ascending aortic aneurysm with a maximum diameter of 46 mm. Baseline electrocardiogram (ECG) in sinus with LBBB.   On regular treatment with acetylsalicylic acid, atorvastatin, ramipril, bisoprolol, spironolactone, tamsulosin and dutasteride.

Present illness
The patient was transferred to the hospital emergency room by the emergency service for an episode of chest pain lasting more than one hour, which began with minimal exertion at home. It was oppressive central chest pain, with concomitant vegetative cortex, which in the initial assessment presented arterial hypotension and rhythm disturbances with second-degree atrioventricular block (AVB) Mobitz I. During the transfer, powerful analgesic treatment was started, with no symptomatic improvement. He arrived at the emergency department with pain. Given the high suspicion of acute aortic syndrome, angio-CT was requested and ruled it out. At that time, cardiology was requested to collaborate.

Physical examination
On arrival at the ED, still with central thoracic pain, blood pressure persisted at 87/50 mmHg and heart rate of 55 bpm. On evaluation by cardiology after angio-CT which ruled out acute aortic syndrome, he showed signs of distal hypoperfusion and marked tendency to arterial hypotension with 80/40 mmHg, heart rate of 40 bpm, baseline oxygen saturation of 97%. Elevation of central venous pressure, jugular ingurgitation +. Cardiac auscultation: rhythmic, pan-focal systolic murmur with associated Gallavardin phenomenon. Pulmonary auscultation: normonophonesis in all fields. Abdomen without semiology of ascites, soft, depressible, not painful on palpation. No masses or visceromegaly palpable. Lower limbs without oedema, with signs of poor distal perfusion.

COMPLEMENTARY TESTS
ECG: his previous baseline ECG with LBBB showed repolarisation alterations compatible with acute myocardial ischaemia and advanced AV conduction disorder. Thoracic CT angiography: bicuspid aorta, calcified. Fusiform dilatation of the ascending aorta, with a maximum diameter of 52 mm. No aortic flap, intramural haematoma or other acute aortic parietal lesions are identified. Absence of coronary calcium. There was no opacification of the anterior descending artery from D1, with progressive narrowing of its calibre, suggestive of non-atherogenic occlusion of the anterior descending artery. Left ventricular dilatation with diffuse myocardial thinning, more accentuated in the anterior wall. Signs of cardiogenic interstitial pulmonary oedema and mild bilateral pleural effusion. No pericardial effusion. Emergency transthoracic echocardiogram: dilated left ventricle (LV). Severely depressed left ventricular function (LVEF 10% by Simpson) with anteroseptal, anterior and apical segment akinesia. CBC: troponin I US 101.2 ng/l -> 306,540.8 ng/l (normal <18 ng/l), creatinine 0.94 mg/dl, sodium 136 mEq/l, potassium 4.8 mEq/l. Haemogram: leucocytes 30,400/mm3 (N 28,600/mm3; L 700/mm3), haemoglobin 13.4 g/dl.

Urgent cardiac catheterisation: transient pacemaker via the right femoral vein, positioned in the apex of the left ventricle (LV). Acute thrombotic occlusion in proximal anterior descending (LAD) with TIMI 0 flow. Thromboaspiration and angioplasty with conventional 2.5 mm balloon achieved flow in the anterior descending and, subsequently, in the diagonal branch, leaving TIMI 3 flow in both arteries.

CLINICAL EVOLUTION
Given the high suspicion of acute coronary syndrome with ST-segment elevation Killip-Kimball IV, the infarction code was activated and a central venous line was channelled for the infusion of vasoactive drugs prior to transfer to the haemodynamics room (dobutamine and noradrenaline). During the transfer he presented cardiorespiratory arrest in ventricular fibrillation, so advanced cardiopulmonary resuscitation manoeuvres were started, and he recovered a pulse after defibrillation at 200J. Orotracheal intubation was performed and the patient was transferred with a transcutaneous pacemaker and sedorelaxed, finally arriving at the haemodynamics room. There, a transient pacemaker was implanted via the right femoral vein and continuous perfusion of noradrenaline and dobutamine was maintained at 0.9 and 8 μgr/kg/min, respectively. Embolic occlusion of the proximal LAD and diagonal branch was revascularised. Admitted to the intensive care unit. Initially, favourable evolution. Recovery of atrioventricular conduction after revascularisation, but temporary safety pacemaker is maintained at 50 bpm. Echocardiogram showed severely depressed ventricular function, LVEF by Simpson around 15%, with anteroseptal akinesia, anterior mid-apical and all apical segments, asynchronous septal movement, as well as a RV of normal size and function. Given the haemodynamic improvement, noradrenaline was started and the patient was extubated without incident, maintaining oxygen saturation with low-flow nasal cannulae and negative water balance. However, 24 hours after admission, he began to experience unstable angina that became refractory, together with haemodynamic deterioration. Given the severity of the condition and the lack of response, it was decided, together with the family, to limit the therapeutic effort and, finally, he died.

DIAGNOSIS
Ischaemic heart disease.
Acute anterior myocardial infarction, Killip IV.
Acute embolic occlusion of the anterior descending artery.
Severely depressed left ventricular function.
Primary ventricular fibrillation.
Complete ischaemic atrioventricular block.
Cardiogenic shock.
Exitus.
Valvular heart disease: bicuspid aortic valve disease with moderate stenosis and dilatation of the ascending aorta.
