LVP after replacement of the mitral valve complicates the post-operative course of this intervention at a percentage between 0.02% and 2.0% (1, 2). Several causes may determine a rupture in the posterior wall of left ventricle post-mitral surgery, such as the presence of endocarditis with or without abscess, the need for extensive decalcification of the annulus, and the placement of a valve oversized. From the few works in the literature on the subject, it emerges that the formation of LVP is facilitated by the presence of coronary heart disease with myocardial infarction (3). LPA after mitral valve replacement usually occurs from a few days to a few weeks after the surgery. In our case, two years have passed between the surgery and the diagnosis of LPA. The onset in our case may have been delayed due to the repeated stress of the mitral valve over a back ventricular wall already weakened. But the rupture may have occurred even shortly after the intervention and then with time the LPA has increased considerably. Due to a poor trans-thoracic echocardiographic window and the absence of symptoms, the diagnosis may have been delayed. The main symptoms in presence of LVP are dyspnea and chest pain, although in 10% of cases it can be asymptomatic and diagnosis occurs at a post-operative echo (4). There are also changes in electrocardiogram and widening of the cardiac shadow to the chest x-ray, but the instrumental investigations that best allow diagnosis are echocardiography, including trans-esophageal, cardiac tomography or magnetic resonance (MRI) and angiography. The last one represents a method that can be used after the echocardiographic suspect of LVP and allows for a good view of the size of the sac around the left ventricle, the size of the neck, and assess the presence of coronary occlusion. Cardiac tomography and MRI allow you to delimit the contours of LVP and relationships with other cardiac structures, as well as measuring the distance of the neck from the mitral prosthesis (MP). The only therapeutic solution for LVP is represented by surgery, since leaving this untreated would mean a volumetric increase and a 30 to 45% of rupture risk (5). Elective surgery is at high risk, with a mortality ranging from 10–23%, and requires optimal planning based on the characteristics of the pseudo-aneurysm. Sternotomy access allows better control of LVP, especially when by large size, and troubles derived from the presence of adhesions. Closure of LVP has been described without opening the cardiac cavities, but suturing the wall from the outside with teflon reinforced prolene points (6). Alternatively, access may be performed by left mini-thoracotomy at the fifth intercostal space, avoiding exposure of the lesion by retracting the heart (7). The planning of this operation was crucial, through the interpretation of cardiac tomography with three-dimensional reconstruction and angiography.