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Page 2 of 10                                                   Formica et al. Vessel Plus 2019;3:37  I  http://dx.doi.org/10.20517/2574-1209.2019.19

               depending on the coronary collateral circulation, the severity and the time of coronary vessel occlusion and
               the individual demand for oxygen and nutrients. Loss of myocardial vitality is complete after 6-12 h from the
               onset of coronary occlusion. Within one week, macrophagic phagocytosis and irreversible collagen damage
               begin, and tissue becomes less resistant; in that period, myocardial tissue becomes more vulnerable and
                                                     [1,2]
               weaker and heart ruptures are more frequent .

               For the purpose of this review we analysed one of the 5 categories of complications of acute myocardial
               infarction (AMI) named as mechanical complications after AMI, such as ventricular free wall rupture,
               ventricular septal defect, papillary muscle rupture of mitral valve. The other 4 categories (electrical
               complication, inflammatory, ischemic and embolic complication) were exclude from this article.

               Most of all mechanical complications of myocardial infarction require an urgent/emergent surgical therapy.
               Meanwhile, initial diagnosis should be rapid and initial medical therapy should be promptly started,
               to improve coronary perfusion, stabilise the haemodynamic condition and ameliorate the peripheral
               perfusion. Supplement oxygen, mechanical ventilatory support whether necessary, analgesic therapy,
               crystalloid infusion and inotropic agents represent usually the first medical approach. In very critical and
               challenging poor clinical and hemodynamic status, requirement of an intra-aortic balloon pump (IABP)
               or even a more advanced temporary circulatory support such as veno-arterial extracorporeal membrane
                                                                     [3]
               oxygenation are valid option to manage and stabilise the patient .

               LEFT VENTRICULAR FREE WALL RUPTURE
               Left ventricular free wall rupture (LVFWR) is account for 15% after AMI and it is more frequent than
                                            [4,5]
               septal or papillary muscle rupture . LVFWR may occur at any time after myocardial infarction, usually
                                                                [6]
               within the first 3-5 days but may happen up two 15 days . However, at least 25% of heart rupture occurs
               within the first 24 h. The short-term mortality remains very high even rapid diagnosis and surgery. Data
               from one of the largest multicentre trial, the Global Registry of Acute Coronary Events study, report an
                                                                        [7]
               incidence of LVFWR of 0.2% with an in-hospital mortality of 80% . In more recent retrospective studies
               and reviews, the early mortality was ranging between 14% to 35%, according the initial haemodynamic
               status, the type of LVFWR and the type of surgical repair [3,8-10] .

                                                                                                        [11]
               Three types of cardiac rupture of cardiac rupture were classified as follows: acute, subacute, and chronic .
               The acute rupture (also named “blow-out” rupture) is characterized by a massive haemopericardium
               [Figure 1] and most of patients presented with electro-mechanical dissociation and sudden cardiac death.
               When the rupture area is smaller, the bleeding is stopped by clot formation or pericardial adhesions. This
               type is called also “oozing” rupture, and patients presented with hypotension and arrhythmias and clinical
               signs of pericardial tamponade.

                                                                                          [12]
               The accuracy of diagnosis of subacute LVFWR requires a high degree of suspicion . Trans-thoracic
               echocardiogram is the first diagnostic tool as most of patients show pericardial effusion in addition to
               echogenic images, in an early period after AMI. Due to these findings, echocardiogram has a high level
                                                                            [13]
               of sensitivity and specificity (more than 95%) for the LVFWR diagnosis . Furthermore, when pericardial
               effusion is more than 10 mm in patients with a recent diagnosis of AMI with ST elevation, the probability
                                                [14]
               of 30-day mortality is as high as 43% . When pericardial effusion is associated with hypotension and
               bradycardia, rapid pericardiocentesis is useful to stabilize the patients before taking the patients for
               emergency surgical therapy.

               Surgical repair of the rupture site is the gold and definitive treatment. Surgery may be performed in
               different ways and different techniques according to the hemodynamic status and the types of cardiac
                                                    [10]
               rupture. In a recent review, Matteucci et al.  described the following surgical techniques: (1) linear closure
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