A 43-year-old man presented to the Emergency Department with ischaemic chest pain of more than a week's duration.

History, current illness and physical examination
Personal history: NAMC. Former cocaine user. Smoker and heavy drinker. Nodal tuberculosis (diagnosed in July 2011) with necrotizing granulomatous lymphadenitis with tuberculous profile. Syphilis. Deep vein thrombosis of DID and portomesenteric thrombosis. Recent anterior AMI. Usual treatment: Sintrom, pantecta, rifampicin/isoniazid, ethambutol, ASA, atorvastatin, coropres, acovil, omeprazole. BFS: Higher functions preserved, autonomous for ABVD.
Current illness: Admitted to the Coronary Unit on 11/10/2012 for previous AMI, requesting voluntary discharge without catheterisation or medical treatment. Since then, he has presented recurrent chest pains and so he came to the emergency department again on 20/10/2012 for another episode of pain, referred by his primary care physician. With a diagnosis of advanced AMI, she was again transferred to the Coronary Care Unit.
Examination: BP 134/91 mm Hg; HR 100 bpm; Ta 36.2 oC. Conscious and oriented, cooperative. Good peripheral perfusion. Adequate muco-cutaneous colouring. Eupneic at rest. Head and neck: No IY. AC: rhythmic at 100 bpm, systolic murmur in mitral focus. AP: VCM. Abdomen: soft, depressible, not painful on palpation. No evidence of peritoneal irritation. Sounds present. Hepatomegaly. Lower extremities: No oedema or evidence of DVT.

Complementary tests
- ECG: Sinus rhythm at 100 bpm, QRS axis at 0o, Q waves in inferior face, ST segment elevation in anteroseptal face and negative T waves in all precordial leads.
- Echocardiogram: LV slightly dilated (LVEDD 56 mm) with normal wall thickness. Moderately depressed systolic function (LVED 40%) due to apical aneurysm, akinesia of the mid-apical segments of the septum, inferior and anterior face, hypokinesia of the posterior face, maintaining only the contractility of the lateral face and basal segments of the rest of the faces. A large thrombus is observed adhered to the apex. Pseudonormalised diastolic pattern. Mitral valve with moderate central regurgitation. Aortic root not dilated (35 mm). Aortic valve without detectable functional alterations. Slight biauricular dilatation. RV not dilated and without signs of dysfunction. Moderate tricuspid regurgitation with a RV-AD gradient of 35 mmHg. No pericardial effusion.
- Chest X-ray: Cardiomegaly, no pulmonary condensation images, free costophrenic sinuses.  Given that it was an AMI of more than a week's evolution, with necrosis in the ECG and development of apical aneurysm and an intracavitary thrombus in the echocardiogram, urgent catheterisation was not performed and medical treatment was prescribed with antiplatelet therapy, anticoagulation at full doses, lipid-lowering agents, beta-blockers and ACE inhibitors, maintaining his tuberculostatic treatment.
The study was completed with: Catheterisation: Left coronary angiography: The common trunk shows no lesions. The anterior descending artery is occluded in its distal segment after the birth of a large diagonal branch. The circumflex artery is of medium development without lesions. Right coronary angiography: It is the dominant vessel and of great extension. Mild atheromatosis in the middle third.
Conclusions: Severe single-vessel coronary artery disease due to distal occlusion of the LAD. Cardiac MRI: dilated LV with severe systolic dysfunction. LVEF: 28%. Saccular dilatation at the level of the apex with akinesia of the apical segments of all the faces with heterogeneous density content with liquid areas inside that in the perfusion sequences do not seem to be related to the ventricular cavity. Likewise, the lateral aspect does not show continuity of the myocardium with the saccular area described. Late enhancement sequences show 50% subendocardial enhancement in mid-apical segments of the inferior face and septum, with transmural enhancement in the rest of the apical segments.
The patient had a torpid evolution with heart failure that was difficult to manage and systemic embolisation despite anticoagulation, so in view of this clinical picture and given the findings described (anterior AMI evolved with apical aneurysm and thrombus inside, together with doubtful rupture of the LV wall with some associated pericardial effusion), cardiac surgery was consulted and surgery was scheduled. He underwent surgery on 17/11/2012 and left ventricular aneurysm resection and thrombus extraction, with subsequent closure with a pericardial patch. No rupture of the LV free wall was visualised. In the immediate postoperative period he required vasoactive drugs due to haemodynamic instability, which could be suspended on the 2nd day post IQ. He was extubated and the rest of the postoperative period was uneventful. He was discharged to the ward after 3 days in the Coronary Unit and home a week later.

Diagnosis
- Evolved Killip II/IV anterior infarction with severe systolic dysfunction.
- Apical aneurysm with intraventricular thrombosis.
- Surgical intervention with resection of the LV aneurysm and extraction of the intraventricular thrombus.
