Percutaneous Repair of Post-Myocardial Infarction Ventricular Septal Defect: Current Approaches and Future Perspectives

Abstract

Post-myocardial infarction ventricular septal defect is a devastating complication of STelevation myocardial infarction. Although surgical intervention isT he occurrence of a ventricular septal defect (VSD) after a myocardial infarction (MI) is an infrequent but serious sequela, which usually occurs within the first week.1 In the years before reperfusion became available, the incidence of VSD after an MI was between 1% and 2%, with an in-hospital mortality rate of 45% with surgery, and 90% with medical management alone.1-4 After the introduction of reperfusion therapy, the rate of post-MI VSD decreased to 0.2% to 0.34%. 4,5 However, mortality rates remain high after surgical intervention, ranging from 20% to 87%, depending on severity in the individual patient and on length of follow-up. 5-11Because surgery offers a better outcome than medical management alone, immediate surgical intervention is now a class I recommendation for post-MI VSD. 12,13 However, early surgical repair can be difficult because of the soft and friable tissue surrounding the area of infarction and the possibility of VSD expansion.14-16 In addition, a residual shunt persists in 10% to 37% of patients despite surgical repair; 11% of those residual defects need further surgical procedures. 7 An approach that would enable immediate hemodynamic stabilization and closure of the defect is desirable. Although transcatheter closure of a post-MI VSD is relatively new, investigators have shown that this procedure is well suited for treating residual shunts after surgical closure and for stabilizing critically ill patients as a bridge to future surgery. [17][18][19][20][21][22][23] We report our experience with 2 cases of the percutaneous closure of post-MI VSDs, which illustrate these principles. Case Reports Patient 1Transcatheter Closure of Recurrent Shunt after Surgical Repair. A 65-year-old man presented at our institution's emergency department with chest pain and shortness of breath. On physical examination, the patient exhibited signs of congestive heart failure, together with a grade 3/6 harsh holosystolic murmur. The patient was hypotensive, his cardiac enzymes were elevated, and electrocardiographic findings showed ST-elevation in the anterior leads. An echocardiogram revealed a VSD, an akinetic anterior wall, and a hyperdynamic posterior wall. Cardiac catheterization showed critical left main and multivessel coronary artery disease. The patient's pulmonary artery (PA) pressure was 42/22 mmHg, there was an oxygen elevation in the right ventricle (RV), and his PA oxygen saturation was 79%. The Qp/Qs was 2.2:1.The patient underwent successful coronary artery bypass grafting (CABG), together with Dacron-graft repair of the VSD. One week postoperatively, he developed increasing dyspnea and had a recurrent holosystolic murmur. He was found on echocardiography to have a residual VSD (Fig. 1). Repeat angiography showed 2 defects,

Cardiac rupture complicating acute myocardial infarction: the clinical features from an observational study and animal experiment

“…Therapeutically, studies on mice have revealed successful inhibition of CR by anti-in ammatory therapies 41 , or use of some currently routine medications like anti-platelet drugs, ARB or ACEI 36 . Collectively, our ndings on patients with CR are supported in part by studies in the mouse model of CR regarding signi cance of infarct size, age 42 , in ammation 39,41 and histopathology of type-III CR 9,23 . Further research is required to illustrate the mechanism of early CR and test therapeutic interventions.…”

“…A signi cant body of knowledge has been generated by preclinical studies on the mechanism and therapeutic intervention of CR. These studies were entirely conducted in the mouse as the only laboratory species that develop CR post transmural MI like human patients 9,23,36 . Mechanistically, CR occurred in mice within a single onset peak timing (days 3-5) together with wall thinning and ventricular dilatation 23 , simulating the human type-III rupture but without CR event within the rst 24 hours, which differs from our clinical nding.…”

“…These studies were entirely conducted in the mouse as the only laboratory species that develop CR post transmural MI like human patients 9,23,36 . Mechanistically, CR occurred in mice within a single onset peak timing (days 3-5) together with wall thinning and ventricular dilatation 23 , simulating the human type-III rupture but without CR event within the rst 24 hours, which differs from our clinical nding. In the mouse model of MI, the infarct size and scale of in ammatory response are pivotal determinants of CR, observations in keeping with the ndings from the present study 9,37 .…”

Cardiac rupture complicating acute myocardial infarction: the clinical features from an observational study and animal experiment

“…Management of CR patients is complex and might require a variety of therapeutic approaches, including pharmacologic (include ACEI, β-blocker, intravenous nitrates, and hydralazine) and device-based therapies to achieve afterload reduction and hemodynamic stabilization. Whilst medical therapy and non-pharmacologic methods may only stabilize CR patients, the treatment of choice is closure of rupture site by surgical and catheter-based means [ 25 , 26 ]. The outcome of operated CR patients is closely related to their hemodynamic state prior to the surgery.…”

Plugging the Hole: Diagnosis and Management of Post–Myocardial Infarction Ventricular Septal Defect

“…7 VA ECMO has been reported as a bridge to percutaneous closure and surgical repair. 8,9 Percutaneous VSD closure may be optimal in smaller VSDs (#15 mm), though larger defects, such as the one in this case, have been successfully repaired. 10 Some operators prefer to advance the occluder from the venous side via the internal jugular vein, as there may be less tension on the friable VSD borders through this method.…”