We present the case of a 59-year-old male patient who was referred to our hospital from the cardiology outpatient department after reviewing the images of a cardiac magnetic resonance imaging (CMR) performed on an outpatient basis and requested due to a pathological electrocardiogram (ECG).

HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION

History
No known allergic reactions to drugs.
Toxic habits: smoker of 1 pack a day (cumulative exposure of 40 packs/year).
Cardiovascular risk factors (CVRF): hypercholesterolemia.
No family history of early ischaemic heart disease.
Surgical history: laparoscopic Nissen fundoplication in 2011.
Usual treatment: omeprazole 20 mg/day, atorvastatin 20 mg/day.

Current disease
A 59-year-old male patient came to the cardiology outpatient clinic referred from primary care for evaluation after a casual finding of a pathological electrocardiographic tracing in a health check-up at his company.
The patient brought to the consultation an ECG showing Q waves in the inferior aspect and an echocardiographic study performed in a private clinic describing alterations of contractility in the inferior aspect at mid-basal level with a moderately depressed left ventricular ejection fraction. In view of these findings, magnetic resonance imaging (MRI) was requested, which showed chronic necrosis of 4 segments of the territory belonging to the right coronary artery and a pseudoaneurysm in the inferior face of the middle segment, so it was decided to admit the patient to hospital to complete the study and present the case at the medical-surgical session.
In the anamnesis, the patient denied any previous episodes of chest pain. Nor did he report cardinal symptoms of heart failure or suggestive of systemic embolism. NYHA functional class I.

Physical examination
Good general condition, normohydrated, normal colour. Eupneic at rest without use of accessory muscles. Conscious, oriented and cooperative, without apparent neurological focality.
Blood pressure (BP) 136/67 mmHg, heart rate (HR) 72 bpm, oxygen saturation (SatO2) 99% (ambient air).
Cardiac auscultation: regular sounds, no audible murmurs.
Pulmonary auscultation: preserved vesicular murmur, no rales.
No oedema in the lower limbs. Radial and femoral pulses present.

COMPLEMENTARY TESTS
The following complementary tests were performed on an outpatient basis:
ECG: sinus rhythm at 80 bpm, PR 160 ms, narrow QRS with axis at +30°, Q wave in II, III and aVF, flattened T wave V4-V6.
CMR: normal left ventricular volumes with moderately depressed systolic function (LVEF 37%). Hypokinesia of inferoseptal, inferior and inferolateral basal segments. Severe dyskinesia and thinning (< 2 mm) located in the lower middle segment, with rupture of the wall and image of pseudoaneurysm contained by the pericardium (neck 7 mm; width 28 mm; depth 18 mm). Partial thrombosis is observed lining its inner wall. Absence of myocardial oedema. Normal right ventricular volumes, with normal systolic function (RVEF 63%). Normal sized atria. Normal sized great vessels.
First-pass hypoperfusion at rest in the dysfunctioning segments. Intravenous gadolinium (meglumine gadoterate 0.15 mmol/kg) is administered. Late gadolinium enhancement suggestive of transmural necrosis in mid inferior segment and subendocardial necrosis in inferoseptal, inferior and inferolateral basal segments. In summary: chronic necrosis of 4 segments of the RCA, pseudoaneurysm in inferior inferior mid-segment and moderately depressed left ventricular systolic function.

After admission, the study was completed with the following examinations:
Chest X-ray: mediastinal silhouette of normal size. No areas of alveolar consolidation or pleural effusion were observed.
Laboratory tests: glucose 81 mg/dl, creatinine 0.85 mg/dl, urea 39 mg/dl, sodium 138 mmol/l, potassium 4 mmol/l, total cholesterol 188 mg/dl, LDL cholesterol 113 mg/dl, HDL cholesterol 56 mg/dl, triglycerides 99 mg/dl, leucocytes 6.05 x 109/l, haemoglobin 14.6 g/dl, platelets 226 x 109/l, glycated haemoglobin 5.4%, ultrasensitive troponin T 26 pg/ml (normal < 14 pg/ml), NT-proBNP 1.780 pg/ml.
Transthoracic echocardiography: non-dilated left ventricle, with slight septal hypertrophy and akinesia of the basal and mid inferior and inferoseptal wall (thinned and echorefringent wall suggestive of chronic necrosis), with presence of a defect in the mid segment inferior wall (wall rupture) and image of saccular pseudoaneurysm, narrow neck (ostium 7-8 mm), visible in parasternal short axis and mainly in apical planes of 2C and 3C. Moderately depressed LV global systolic function (biplane Simpson LVEF 40%).
Severely dilated left atrium. Mitral valve with good opening and minimal valve regurgitation. Aortic valve with normal transvalvular gradients, without valvular regurgitation. Right ventricle not dilated, with good contractility. Absence of pericardial effusion.

Diagnostic coronary catheterisation (videos 1 and 2): left main coronary artery (LMCA) without lesions.
Long anterior descending artery (ADA), good calibre, with severe lesion (80%) in proximal segment, very calcified and significant lesion (60%) in middle segment (with feasible percutaneous revascularisation). Circumflex artery (ACx) non-dominant, with non-significant wall irregularities. Dominant right coronary artery (RCA), with long ostial chronic total occlusion, with coin stack image in proximal cap, and distal vessel of good calibre and visible development by epicardial and septal heterocoronary circulation (Rentrop 3) with poor profile for percutaneous revascularisation. Conclusions: two-vessel coronary artery disease with severe lesion in proximal and significant medial LAD and chronic total occlusion of ostial RCA.
Transthoracic echocardiography (postoperative control): left ventricle with akinesia of the inferior wall and basal and medial inferoseptal wall, with thinned and echorefringent wall, with no pseudoaneurysmal cavity observed in the inferior face. Moderately reduced global systolic function of the left ventricle. Rest of the study unchanged with respect to previous. Absence of pericardial effusion.

CLINICAL EVOLUTION
During admission, the preoperative study was completed with the complementary tests described above. Transthoracic echocardiography confirmed the findings described in the CMR, while coronary catheterisation showed two-vessel coronary artery disease consisting of a severe lesion in the proximal LAD and significant mid LAD, and a chronic ostial occlusion of the RCA.
During surgery, a left ventricular pseudoaneurysm was visualised on the inferior aspect of approximately 3 cm in diameter with thickened and calcified walls, with thrombotic content inside and an ostium communicating with the left ventricle of approximately 1 cm2. A posterior descending artery of small calibre and located in the scar territory of the pseudoaneurysm was also visualised and was therefore ruled out as a tributary vessel for aortocoronary bypass.
Finally, resection of the aneurysmal area and reconstruction of the lower wall with an autologous pericardial patch were performed. Subsequently, a double aortocoronary bypass was performed to the middle ADA with the left mammary artery and to the first diagonal with the saphenous artery, both of them end-to-side.
The patient's stay in the resuscitation unit was uneventful with early extubation and discharge to the hospital ward 48 hours after surgery. A control transthoracic echocardiography was performed, which did not show the pseudoaneurysmal cavity and ruled out early postoperative complications. Postoperative evolution was satisfactory with clinical and haemodynamic stability, and he was discharged from hospital for outpatient follow-up in cardiology and cardiac surgery outpatient clinics.

DIAGNOSIS
Silent myocardial infarction complicated by left inferior ventricular pseudoaneurysm. 2-vessel coronary artery disease (proximal and middle LAD and ostial LAD).
Moderate left ventricular dysfunction. Aneurysm resection surgery and coronary revascularisation of LAD.
Hypercholesterolemia. Smoking.
