Case Report: Atrial Septal Defects

An Unusual Thrombotic Complication during Percutaneous Closure of Atrial Septal Defect

S. Bijulal, MD, DM, Sivasubramanian Sivasankaran, MD, DM, V. K. Ajitkumar, MD, DM
S. Bijulal, MD, DM, Sivasubramanian Sivasankaran, MD, DM, V. K. Ajitkumar, MD, DM
From the Department of Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India. The authors report no conflicts of interest regarding the content herein. Manuscript submitted March 3, 2008, provisional acceptance given May 8, 2008, and final version accepted May 12, 2008. Address for correspondence: S. Bijulal, MD, DM, Consultant, Department of Cardiology, SCTIMST, Trivandrum, Kerala, India 695 011. E-mail:

_____________________________________ ABSTRACT: A case is described where intracardiac thrombus was observed at the junction of the superior vena cava and the right atrium during attempted closure of an atrial septal defect (ASD) using a device similar in design to the Amplatzer septal occluder (Heart R atrial septal occluder). Thrombosis was likely related to the multiple attempts required when deploying the device and the attendant prolonged procedural time. The patient underwent subsequent urgent surgical closure of the ASD.

J INVASIVE CARDIOL 2009;21:83–85

Percutaneous closure using a double-umbrella device is a well-established and standardized modality of treatment for atrial septal defects (ASD).1,2 The procedure is usually performed under transesophageal echocardiographic (TEE) guidance. Patients receive antiplatelet drugs before the procedure. After femoral venous access, heparin is administered to achieve a therapeutic anticoagulant level (activated clotting time [ACT] > 250 seconds). An appropriate-sized delivery sheath for the selected device is then advanced to the left atrium and the device is delivered and positioned across the defect. Associated complications are infrequent and include device embolization, air embolism and cardiac tamponade.3 Thrombotic complications are generally related to insufficient anticoagulation and are rare.4–6 We describe the case of a female patient who was noted during her procedure to have thrombus at an extremely uncommon intracardiac location and discuss the circumstances and the probable mechanism. Case Report. A 22-year-old female with a 22 mm ostium secundum type of ASD was taken to the catheterization laboratory for percutaneous closure. Cardiac catheterization revealed normal pulmonary artery pressure, and TEE showed a 22 mm defect with adequate rims for device closure, except for the fact that the inferior vena caval rim was only 5 mm. Since the rims were firm, balloon sizing was not contemplated. A dose of 100 units/kg body weight of unfractionated heparin was administered after venous access. Next, a 12 Fr Mullins sheath (Cook Inc., Bloomington, Indiana) was placed in left atrium and a 26 mm Heart R (Lifetech Scientific Inc., Shenzhen, China) ASD occluder was advanced and attempts were made to deploy the device across the defect. However, the device was not aligning with the septum easily and multiple attempts at deployment and consequent withdrawal into the sheath became necessary. After five attempts, including a right pulmonary venous deployment technique, it was determined that the device was too small for the defect and we decided to use a larger size. At that point, TEE showed a new 15 x 10 mm mobile structure, which was not present at the beginning of the procedure. The structure was attached to the interatrial septum at the junction of the superior vena cava with the right atrium (Figures 1–3). It was concluded that the structure was intracardiac thrombus. The patient’s ACT at that point was 276 seconds. As further manipulation in the right atrium during continued attempts at device deployment may dislodge and embolize the thrombus, no other attempts were made and the patient was subjected to urgent surgery with high cannulation of the superior vena cava for cardiopulmonary bypass. Perioperatively, no thrombus was identified at that particular location, however, intraoperative TEE before cardiac decompression showed the thrombus. No endothelial damage was identified at that region. It was assumed that the thrombus embolized during superior vena caval cannulation. She underwent pericardial patch closure of the defect. Post-operative TEE showed no thrombus. The patient had no clinical evidence of systemic embolization and had an uneventful recovery. Discussion. The incidence of thrombosis on an Amplatzer septal occluder was noted to be nil in the elegant TEE study reported by Krumsdorf et al. 4 However, a few case reports of immediate formation of thrombus over an Amplatzer device have been reported, most of which were thrombus formation over the left atrial disc managed by anticoagulation, abciximab, thrombolytic therapy and surgery.7,8 However, this is the first report of thrombus formation in the peculiar location of the right atrium with an Amplatzer-like device. The reason for thrombus formation in this patient is obscure, but is very likely to be procedure-related. She had no clinical or laboratory evidence to suggest thrombophilia. She attained a therapeutic anticoagulant level with heparin. The probability of endothelial damage and consequent thrombosis at the junction between the superior vena cava and the right atrium during device closure is remote, as manipulation in this region is not required for the procedure and endothelial injury was not identified at surgery. It is likely that during several unsuccessful attempts at deployment, which required multiple withdrawals into the sheath, and prolonged procedure time, thrombus formation occurred inside the sheath and was pushed out of the sheath during the subsequent attempts and adhered to that particular site. The large size of the sheath might have contributed to thrombus formation due to stasis. It is worth noting that several attempts at device positioning were required in the case of left atrial disc thrombosis reported by Wilcoxson et al.7 What caused propagation of the thrombus to this particular site? If thrombus forms at the tip of the sheath, it will become displaced into the left atrium or will be attached to the left atrial disc during subsequent deployment. However, in this patient, thrombus was noted inside the right atrium. It is likely that thrombus formed inside the sheath in the small space between the collapsed left atrial and right atrial discs (waist of the device) and was released into the right atrium during deployment of the right atrial disc after deployment of the left atrial disc (Figure 4). Another question arises regarding the thrombogenecity with the type of device used. Our experience with more than 75 implantations of the Heart R ASD occluder produced neither increased thrombogenicity nor immediate or delayed thrombotic complications. The literature also does not report on added thrombotic risk with the Heart R ASD occluder.9 What is the optimal method to manage this problem? It is obvious that with further manipulation inside the atria, which is required for proceeding with device closure, thrombus may get dislodged. Thus this situation would require surgical treatment or therapy aimed at clot dissolution followed by percutaneous closure in a separate procedure. As the thrombus was mobile, we felt the patient might develop systemic embolization during the recovery period from general anesthesia related to dynamic pressure changes in the right atria associated with changes in intrathoracic pressure during endotracheal extubation. Hence, we sent the patient on for urgent surgery. One surgical hazard, which happened in this case, is the dislodgement of thrombus during cannulation of the superior vena cava, which can be prevented by high cannulation or, alternatively, systemic embolization can be avoided by keeping an inflated sizing balloon across the defect. Conclusion. Development of a right atrial thrombus during attempts at positioning an atrial septal occluder device across a secundum ASD requiring surgical correction and the likely mechanisms were discussed in this case report. We report this unusual complication to bring the attention of the readers to the excellent clinical utility of TEE in the timely recognition and management of this complication and the close observation required to identify and manage uncommon problems. Note: The Heart R atrial septal defect occluder is made of nitinol and is similar in shape to the Amplatzer septal occluder, character and deployment technique, but costs only half the price.


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