Transcatheter closure of an inferior post infarction ventricular septal defect using a customised device

Abstract

Introduction: A ventricular septal defect (VSD) is a rare but devastating complication of a myocardial infarction in an era of early coronary revascularisation. Transcatheter closure of post-infarction VSD may offer an alternative to surgery for patients deemed too high risk. Accessibility to transcatheter closure has been limited by anatomy and available of devices. We present the first custom-made VSD device for an acute post-infarction VSD with a successful outcome. Case report description: An 85-year old female presented with an anterior ST elevation myocardial infarction (STEMI) with subtotal left anterior descending artery occlusion requiring primary balloon angioplasty. Day 3, the patient developed cardiogenic shock and a new holosystolic murmur. Transthoracic echocardiogram confirmed a post-infarction VSD. 3D transoesophageal echocardiography (3D TOE) demonstrated an inferiorly placed VSD, measuring 28/16mm with no inferior margins, as the septum had avulsed from the apex. The inferior defect position and haemodynamic instability made surgical closure extremely high-risk. When assessed for potential transcatheter VSD closure, the devices available were unsuitable due to the lack of inferior margins for attachment. 3D TOE measurements allowed manufacturers to mould an existing device to the exact configuration of our patients VSD. 9-days following original rupture, the VSD was closed by transcatheter route with a custom-made device. Within 15-minutes of device deployment, left ventricular pressure increased from 60mmHg to 120mmHg and inotropes were reduced. Day 7 post-procedure the patient was transferred to their local hospital for rehabilitation and discharged from hospital 1-month following admission. Discussion(s): Ventricular septal rupture typically presents within the first week after myocardial infarction. Medical management is associated with 94% mortality. Poor prognostic factors: cardiogenic shock, right ventricular dysfunction, and inferior infarct location. In our case, as the operative risk of cardiac surgery was deemed too high risk due to the inferior position of the VSD, the patient's age and progressive cardiogenic shock, only transcatheter closure could be offered. The morbidity and mortality of transcatheter repair of a post-infarction VSD in such a patient is significant albeit less than reported surgical risk. Conclusion(s): Current guidelines recommend immediate surgical closure but advances in 3D TOE allowing custom-made closure devices may allow primary transcatheter closure for post-infarction VSD closure and/or initial hemodynamic stabilisation.