Clin Res Cardiol DOI 10.1007/s00392-015-0829-0

LETTER TO THE EDITORS

Very late cardiac tamponade following successful transcatheter closure of an atrial septal defect with the Amplatzer septal occluder Thomas Herren • Michael Schwanda Michele Genoni • Franz R. Eberli



Received: 3 January 2015 / Accepted: 17 February 2015 Ó Springer-Verlag Berlin Heidelberg 2015

Sirs: To avoid late complications, ASDs should be closed even when detected in adults, an endeavor that may be performed surgically or via the transcatheter approach, as is done for secundum-type ASDs that possess suitable anatomy and no associated lesions. Surgical ASD closure carries a higher periprocedural risk compared with transcatheter closure, but has an excellent long-term prognosis. We report the occurrence of a rare but life-threatening long-term complication following transcatheter ASD closure, cardiac perforation with cardiac tamponade, and its successful surgical treatment. Secundum-type ASD was diagnosed in a 30-year-old woman by cardiac catheterization in 1982. Paroxysmal atrial fibrillation (AF) developed at an age of 56. Both transthoracic (TTE) and transesophageal echocardiography (TEE, see Online Resource ESM Fig. 1) demonstrated biatrial enlargement, the volume-overloaded right ventricle appeared dilated and had a reduced function. All pulmonary veins were connected to the LA. Coronary

Electronic supplementary material The online version of this article (doi:10.1007/s00392-015-0829-0) contains supplementary material, which is available to authorized users. T. Herren (&)  M. Schwanda Department of Medicine, Limmattal Hospital, Urdorferstrasse 100, 8952 Schlieren, Switzerland e-mail: [email protected] M. Genoni Department of Cardiac Surgery, Triemli Hospital, Birmensdorferstrasse 497, 8063 Zurich, Switzerland F. R. Eberli Department of Cardiology, Triemli Hospital, Birmensdorferstrasse 497, 8063 Zurich, Switzerland

angiography was normal. Cardiac catheterization demonstrated mildly elevated pulmonary artery pressures. Oxymetric analysis confirmed the presence of a predominant left-to-right (67 %) shunt and a small right-to-left shunt (7 %). The balloon-stretched ASD diameter measured 25 mm by angiography, and 26 mm by intracardiac echocardiography (ICE). The ASD was closed with a 28 mm Amplatzer Septal Occluder (ASO, St. Jude Medical, Inc., St. Paul, MN) in 2008. Antiplatelet therapy was prescribed for 6 months, and then TEE documented correct positioning of the ASO with no residual shunts. The sizes of the atria decreased, and the RV function improved. Symptomatic paroxysmal atrial fibrillation necessitated treatment with flecainide and bisoprolol. The patient remained on aspirin. Acute chest pain and shortness of breath required urgent hospitalization three years after transcatheter ASD occlusion. On admission, the patient was in cardiogenic shock due to a large pericardial effusion with tamponade physiology (Fig. 1a). The removal of 350 ml of nonclotting blood (hematocrit = 42 %, identical to peripheral blood) via pericardiocentesis resulted in immediate hemodynamic improvement. The patient was transferred to a tertiary-care hospital. Correct positioning of the ASO, as well as a residual pericardial effusion was shown by TEE. An ECGtriggered cardiac CT scan indicated that the ASO impinged the left atrial dorsal wall (Fig. 1b), causing its erosion. The intact ASO (see Online Resource ESM Fig. 2) was removed, the ASD was closed with a patch, and the left atrial roof was surgically reconstructed 10 days later (Fig. 2). Additionally, a bipolar maze procedure was performed, and the left atrial appendage was ligated. Symptomatic bradycardia required the implantation of a DDDR pacemaker postoperatively. Follow-up exams confirmed excellent long-term operative results.

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Fig. 1 A subcostal view obtained during TTE on admission (a). The pericardial effusion (PE) led to diastolic right atrial wall collapse (*) and Doppler evidence of tamponade physiology (not shown). The arrow points to the ASO (a and b). An ECG-triggered cardiac CT scan showing a horizontal plane (b). The ASO’s larger left atrial disk

erodes the atrial wall posteriorly (LA left atrium, RA right atrium). The ASO covers the full anteroposterior dimension of the interatrial septum. There is minimal PE left: the tip of the pericardial catheter is located near the left atrial appendage (**)

Fig. 2 Intraoperative views following right atriotomy. Shown are the ASO in situ (a) and the patch-amended interatrial septum following removal of the device (b)

A metaanalysis of 13 observational, retrospective studies comparing surgical with transcatheter ASD closure suggests that surgically treated patients have 3.6 times more major periprocedural complications (including death) compared with patients undergoing transcatheter closure [128/1272 (10.1 %) vs. 50/1795 (2.8 %)] [1]. Specifically, pericardial effusions requiring removal occurred in 1.3 % of surgically treated patients versus 0.2 % of patients treated with the transcatheter approach [1]. In the latter, technique-related perforation of the left atrial appendage or a pulmonary vein are often causative [2, 3], but periprocedural device-related cardiac perforations have been reported [3]. Both approaches to ASD closure have high rates of success (surgical 97.8 % vs. percutaneous 93.6 %) [1]. According to the European guidelines, device closure is the method of choice for the treatment of secundum ASD and carries a class IC recommendation [4]. After successful surgical ASD closure, there is almost no need for re-intervention [5]. However, device-related erosion and pericardial effusion each occur at a rate of

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0.1 % [6] following transcatheter ASD closure. These findings are consistent with registry data, which report the occurrence of late ([30 days) cardiac perforation, erosion or rupture by an ASO in 0.1–0.3 % of patients [2]. Forty percent of all device-related cardiac perforations develop late, and may occur as long as 8.5 years following the index hospitalization [7]. Most of these patients require surgery. The rescue surgical mortality rate is 15–20 times higher than the surgical risk of primary ASD closure (5.4 vs. 0.36 %, and 2.6 vs. 0.13 %) [2, 8]. Nevertheless, the complication and mortality rate following percutaneous ASD closure compares favorably with the higher perioperative risk of surgical ASD closure [1]. The perforation site is most often the atrium (usually the left, most likely due to the larger size of the left atrial disk of the ASO), but may involve the aorta [2, 3]. Following successful ASD occlusion, atrial sizes invariably decrease and thus, make the device to increasingly impinge the atrial wall [9]. As a result, hemopericardium (or aorto-atrial fistulae) may develop. Following percutaneous closure of

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even large ASDs in children, erosions or late perforations are exceedingly rare. As children grow, the ratio of device to atrial septal diameter decreases, whereas this ratio increases over time in adults. Therefore, oversizing ASD closure devices in adults with dilated atria should be avoided. Device size selection should be the same size or 1 size larger than the diameter of the defect according to the instructions for use [10]. However, as many as one-third of cardiac perforations develop in patients in whom the ASO was not oversized [3]. In these, impingement of the ASO on the aortic wall due to insufficient (\5 mm) anterior or superior anchoring rims, or undersized, sharp-edged devices which move relative to contiguous cardiac structures may lead to perforations [11, 12]. The implantation should be guided by (3D)-TEE or ICE to allow correct positioning of the ASO and to avoid its contact with the aortic root or the atrial wall [11]; the ASD closure can even be performed without fluoroscopy [13]. To minimize the risk of perforation, use of the Gore Helex Septal Occluder may be considered in small to moderate ASD’s. However, wire frame fractures, risk of device embolization, and residual shunts limit its widespread use [14]. Biodegradable devices carry the promise to eliminate the erosion risk, but long-term safety data are lacking [15]. Post-interventional clinical and echocardiographic follow-up exams are recommended at 1 week, 1 month, 6 and 12 months [11], even though the abrupt cardiac tamponade due to late device erosion cannot be anticipated. The detection of a pericardial effusion, however small, must be carefully evaluated and is a sign of erosion until proven otherwise. In conclusion, if a patient develops chest pain, shortness of breath or faints following transcatheter ASD closure, pericardial effusion must be ruled out by emergent sonography, even if the event occurs several years following device implantation. Immediate pericardiocentesis must be performed if the pericardial effusion exhibits tamponade physiology. Treatment for device-related cardiac erosions often entails surgery [8].

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10. Acknowledgments We thank S. Ullrich, Institute of Radiology, Triemli Hospital Zurich, Switzerland for providing the CT image shown in Fig. 1b, and F. Osann for expert patient care in the emergency room. Integrity of research and reporting The patient was consented to publish this report. The authors declare that they have no conflict of interest.

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Very late cardiac tamponade following successful transcatheter closure of an atrial septal defect with the Amplatzer septal occluder.

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