LV pseudo-aneurysm is an uncommon but critical condition. It forms when a cardiac rupture is contained by adherent pericardium or scar tissue without endocardium or myocardium (4). There are various etiologies of LV pseudoaneurysm formation, including myocardial infarction (MI), cardiac surgery, intervention, endocarditis, and chest trauma. Frances et al. reported that 55% of cases were due to MI, and of which 49% were inferior MI (4). Meng et al. reported that the most common location of LV pseudoaneurysm formation was the posterior LV (5). Inflammatory reactions and pericardium adhesion mainly occur in the posterior wall of the LV, because patients are usually in a recumbent position after myocardial infarction (4). In the present case, pseudo-aneurysm occurred after inferior myocardial infarction.

The pseudoaneurysm is a deleterious reaction process that begins within hours of follow transmural myocardial infarction and alter the geometry of the ventricle and its wall thickness. This remodeling not only interests the infarcted zone but also the normal cardiac segments by promoting ventricular dilation according to Franck Starling's law. In the infarcted zone, systolic expansion occurs which is defined as an acute dilation and thinning from the infarct zone. This can lead to complications mechanical by rupture of the free wall of the LV or stabilization and chronic fibrosis.

Wall rupture in the acute phase can be either complete resulting in tamponade and death or incomplete forming a pseudoaneurysm as in the case of our patient. The wall of the pseudo aneurysm is then formed only from pericardial and epicardial tissue. Unlike the true aneurysm, the main differential diagnosis, the wall of which keeps all its constituents. The risk of rupture of the pseudo aneurysm is in consequence greater than that of the true aneurysm. The pseudo aneurysm can remain asymptomatic for a long time or lead to a heart failure [6].

Cardiac arrhythmias are frequently noted and can reveal the disease [7]. The aneurysmal thrombosis is a possible complication [6], with a low embolic risk. The major progressive risk is spontaneous rupture with sudden death by tamponade [6].

Clinically, a double apex beat should be researched [8]. The aneurysmal deformation of the left inferior arch on the chest X-ray is a frequent image in the case of a false left ventricular aneurysm [9], also noted in our patient.

Doppler echocardiography is the first-line test [9]. It makes it possible to make the diagnosis with certainty and to eliminate a real aneurysm. Unlike true aneurysms, which have a wall resistant fibrosis and a wider neck, the pseudo aneurysms initially consist of loose tissue, a narrower neck [10,11]. Our case presented a narrower neck at 16 mm

Cardiac CT and magnetic resonance imaging (MRI) can help distinguish the two forms and better study the specifications and location of the pseudoaneurysm [12].

After the diagnosis of LV pseudo-aneurysm is made,treatment options should be discussed.In most of cases , surgical repair is required, because of the high risk of rupture.

A previous report noted that the mortality of LV pseudo-aneurysm is considered to be higher after conservative therapy, so it should be actively treated with surgery [13] which is typically based on patch repair under extracorporeal circulation (ECC) by median sternotomy.

On the other hand, some retrospective studies have reported that cases involving chronic small LV pseudo-aneurysms of < 3cm in size or patients with high surgical risk can be managed conservatively [14].

However, rapidly progressive LV pseudo-aneurysm has also been reported [15] even in the case of conservative therapy. Periodic follow up echocardiography is mandatory.