Delayed Amplatzer Occluder Device Closure of Postinfarction Ventricular Septal Defect: A Case Report

Postinfarction ventricular septal defect (VSD) is a rare complication after acute myocardial infarction, with an incidence rate of 1-2% of all myocardial infarcts (Hutchins, 1979). It is a medical emergency with sobering survival numbers, having a mortality rate of 70–80% within two weeks of the incident event (Bouchart et al., 1998). Cardiac surgery is considered the gold standard in the management of these defects; however, its main limitation is that it carries a high risk of perioperative mortality and postoperative sequelae. Percutaneous transcatheter closure of VSD is a relatively new method of repair. Due to scarcity of reports in the literature, there is limited data regarding survival data; however, noninferiority to surgery has been demonstrated in one case series (Papalexopoulou et al., 2013). Long-term follow-up studies are lacking, and thus long-term mortality has yet to be discerned. We present a case of an 87-year-old female who, following postmyocardial infarction VSD, developed clinically significant heart failure. The patient was reluctant to undergo open repair given her age and comorbidities and she underwent successful percutaneous repair of her VSD using a 16？mm Amplatzer occluder device 18 months after her initial presentation. 1. Introduction Percutaneous transcatheter closure of ventricular septal defect (VSD) is a relatively new technique. Particularly, in patients precluded from open cardiac surgery given their age or comorbidities, percutaneous closure is a viable option. We present a case report of an Amplatzer device closure of postinfarct VSD in a clinically contextual manner highlighting considerations of patient age and comorbidities, type of presentation, timing of procedure, and also device sizing. 2. Case Report An 87-year-old woman presented to a tertiary referral hospital with progressive dyspnoea and decreased exercise tolerance following a fall. She denied chest pain, palpitations, or syncope. She had a past history of hypertension, hypercholesterolemia, and impaired glucose tolerance. Physical examination revealed a regular pulse of 110 beats per minute. Her supine blood pressure was 120/50？mmHg and there was a harsh grade III holosystolic murmur heard best at the apex. She had clinical and radiological signs of congestive cardiac failure. The 12-lead electrocardiograph (ECG) revealed sinus tachycardia (110 beats per minute), with 2？mm ST elevation in the anteroseptal leads ( ) and a left anterior fascicular block. Serum troponin T level at admission was elevated (163？ng/L). Transthoracic echocardiography