Use Of Contrast During Echocardiography To Diagnose Cardiac Perforation After Device Closure Of Atrial Septal Defect

Transcatheter closure of select ostium secundum atrial septal defects (ASD) is now considered a safe and effective alternative to surgical closure [1]. Cardiac perforation (CP) or erosion after transcatheter ASD and patent foramen ovale (PFO) closure has been described with the incidence ranging between 0.1% and 4% [2–4]. Although CP is known to occur with most of the devices, it has been reported more commonly with the Amplatzer septal occluder (ASO, St Jude, Plymouth, MA). In a review of registry of complications associated with the ASO, Amin et al. noted that most of the CPs or erosions occurred near the dome of the atria near the aortic root [2]. A majority of these patients had deficient aortic margin and their device to unstretched ASD ratio was significantly larger. This led them to conclude that those with a deficient aortic/superior margin and those with an oversized ASO were at higher risk of erosion. In a data review provided by the US and Canadian drug agencies, 66% of the 29 CPs reported were late (postdischarge), 24% occurred 1–6 months later, and only 1 occurred more than a year later (3 years) [5]. Patients with CP may present with pericardial effusion, chest pain, dyspnea, syncope, hemodynamic collapse, or even sudden death [6]. Pericardial effusion in a patient with ASD device closure may be secondary to erosion or due to multiple other causes such as viral infection, inflammation associated with collagen vascular disease, secondary to renal dysfunction, hypothyroidism, idiopathic, and many other less common etiologies. Sometimes, after device closure one sees a small echo-free space posteriorly which was not very evident pre-procedure. This is more often associated with the use of large devices measuring more than 30 mm and is probably due to stenting of the interatrial septum tending to lift up the heart anteriorly. A 30-year-old lady underwent transcatheter closure of a 28 mm ASD with a 34 mm ASO. The procedure was uneventful and she was discharged after 24 hr with no evidence of pericardial effusion on the predischarge echo. At a routine 1-month follow-up, she was asymptomatic with stable vital parameters. Her blood pressure was 110/70 mm Hg with no evidence of pulsus paradoxus and her jugular venous pressure was not elevated. There was no hepatomegaly or pedal edema. Her respiratory examination was unremarkable. On 2D echocardiography, the device was noted to be in position with no residual flow across the defect. The mitral and tricuspid valves were functioning normally. There was pericardial effusion noted predominantly posterior to the left ventricle. An intravenous line was secured and ultrasound contrast agent (SonoVue; Bracco Imaging, Genève, Switzerland) was injected intravenously to opacify the right (Fig. 1) and subsequently the left sided cardiac chambers (Fig. 2). There was no contrast visualized in the pericardial space thus ruling out any erosion of the cardiac walls. The patient was managed conservatively and kept on a close follow-up with regular echocardiographic screening to rule out any increase in the amount of effusion. The