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,