HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
A 58-year-old male patient, smoker of one pack of cigarettes/day, with no other medical history of interest, who is referred to the cardiology department for a routine ECG requested by his primary care physician, which turns out to be pathological.
In the detailed anamnesis, the patient reported no previous episodes of chest pain, although he did report dyspnoea on moderate exertion, without progression in recent weeks.
He also reported that a few days prior to admission he had a sudden episode of loss of strength in the right upper limb and facial paralysis, with subsequent complete recovery, going to his health centre from where he was discharged, citing the cervical origin of the symptoms.
Physical examination revealed no findings of interest.
An echocardiogram was performed in the consultation room and, in view of the findings, it was decided to admit him to the ward to complete the diagnostic study with cardiac magnetic resonance (CMR). Initially, given the structural cardiac pathology of the patient and the neurological symptoms that he presented days prior to admission, a transient ischaemic attack (TIA) was suspected, so a CT scan of the brain was performed, which was found to be normal. While the patient was on the ward, CMR was performed which confirmed the diagnosis of ventricular pseudoaneurysm with abundant thrombus.
He was considered a candidate for surgery and coronary angiography was performed, finding a severe lesion of the mid-distal left main coronary artery (LMCA) and the 3 vessels.

COMPLEMENTARY TESTS
Transthoracic echocardiography: left ventricle (LV) moderately dilated, with moderate global systolic dysfunction (LVEF by Simpson biplanar 35%), thinning and inferolateral and inferior akinesia and large inferobasal and inferoseptal basal aneurysm, 44 mm neck and 40 mm deep, with an oval mass of 8 x 7 mm hyperechogenic inside suggestive of thrombus.
CHEST X-RAY: showing slight cardiomegaly.
ECG: Q waves and negative T waves in inferior leads.
Complete ANALYSIS:
Haemogram: 14.1 g/dl. Leukocytes 13,500 10^3/μl. Platelets 207,000 10^3/μl.
Biochemistry: glucose 134 mg/dl. Creatinine 0.86 mg/dl. Na 139 mM/l. K 4.7 mM/l.
Lipid profile: total cholesterol 149 mg/dl. HDL 33.7 mg/dl. LDL 208U/l. Triglycerides 82 mg/dl.
Liver profile: bilirubin 0.42 mg/dl. GOT 17.7 U/l. GPT 29.3 U/l. GGT 29.3 U/l. GGT 49.6 U/l. Alkaline phosphatase 128 U/l.
Glycated Hb 6.1.
Cardiac MRI: ventricular pseudoaneurysm, with image of abundant thrombus in the cul-de-sac, without compromise of mitral valve function, with ventricular remodelling and moderate systolic dysfunction.
CORONARYGRAPHY: left coronary trunk: with severe lesion in the distal middle third affecting the ostium of the anterior descending and circumflex arteries. Anterior descending: with severe stenosis in the proximal third, good distal vessel. Circumflex: significant ostial stenosis, occluded at the level of bifurcation with first obtuse marginal which has severe stenosis at the level of bifurcation with subdivision, both vessels of good diameter. Right coronary: dominant, ostial occluded, filled by heterocoronary collateral circulation, regular distal vessel.

CLINICAL EVOLUTION
The patient remained asymptomatic during his stay on the ward, wandering around, without presenting arrhythmic events on telemetry.
Subsequently, and despite maintaining the patient on correct levels of anticoagulation, he again presented motor deficit in the left middle cerebral artery (MCA) and right anterior cerebral artery territory of cardioembolic cause and with recovery without subsequent deficit, with no sequelae in the control CT scan performed. The transcranial Doppler study showed significant stenosis in MCA I.
Finally, he was transferred to the reference hospital for surgery: by means of median sternotomy and with the aid of extracorporeal circulation, the aneurysmal area was resected, the intraventricular thrombus was removed and the lower wall was reconstructed with a Dacron patch. Subsequent sequential AMI-DA and AMI-OM aortocoronary bypass was performed. Although myocardial protection with antegrade and retrograde cardioplegia was performed, removal of extracorporeal circulation proved difficult, requiring high doses of vasoactive amines (dobutamine + noradrenaline). He was subsequently admitted to the intensive care unit, where he had a torpid evolution, and died 24 hours after admission due to refractory cardiogenic shock.

DIAGNOSIS
Silent infarction complicated by inferior ventricular pseudoaneurysm (with mural thrombus inside).
Coronary artery disease of LMCA and three vessels.
Moderate left ventricular dysfunction.
Surgery for resection of the aneurysmal area + AMI-DA and AMI-OM bypass, with torpid postoperative course and death.
