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Closure of Apical Access Site After Transapical, Transcatheter Paravalvular Leak Closure
Canadian Journal of Cardiology 28 (2012) 516.e5–516.e7 www.onlinecjc.ca
Case Report
Closure of Apical Access Site After Transapical, Transcatheter Paravalvular Leak Closure Fabian Nietlispach, MD,a,b Friedrich Eckstein, MD,c Manfred Seeberger, MD,d Stefan Osswald, MD,a Beat A. Kaufmann, MD,a and Oliver Reuthebuch, MDc c
a
Department of Cardiology, University Hospital Basel, Basel, Switzerland
b
Department of Cardiology, Bern University Hospital, Bern, Switzerland
Department of Cardiac Surgery, University Hospital Basel, Basel, Switzerland d
Department of Anaesthesia, University Hospital Basel, Basel, Switzerland
ABSTRACT
RÉSUMÉ
The safety of percutaneous transapical mitral paravalvular leak (PVL) closure could potentially be enhanced by device closure of the ventricular access site. Percutaneous transapical PVL closure was performed. The 9F delivery sheath was pulled back, and a 6-mm Amplatzer muscular ventricular septal defect occluder was deployed at the apical puncture site. Immediate hemostasis was achieved. Total hospitalization was 9 days. New York Heart Association functional class was improved, hemoglobin and haptoglobin rose, while lactate dehydrogenase fell. Follow-up fluoroscopy and transthoracic echocardiography revealed a good functional result. Closure of the apical access site by means of an Amplatzer muscular ventricular septal defect occluder is feasible.
La sécurité de la fermeture percutanée de fuite paravalvulaire (FPV) mitrale par voie transapicale pourrait être améliorée par un dispositif de fermeture du site d’accès ventriculaire. La fermeture percutanée de la FPV par voie transapicale a été réalisée. La gaine 9F a été retirée, et un dispositif d’occlusion de la communication interventriculaire musculaire Amplatzer de 6 mm a été déployé à la zone de ponction apicale. Une hémostase immédiate a été obtenue. L’hospitalisation a été de 9 jours. La classification fonctionnelle de la New York Heart Association a été améliorée, l’hémoglobine et l’haptoglobine ont augmenté, tandis que le lactate déhydrogénase a chuté. La fluoroscopie et l’échocardiographie transthoracique de suivi ont révélé un bon résultat fonctionnel. La fermeture de la zone d’accès apical au moyen d’un dispositif d’occlusion de la communication interventriculaire musculaire Amplatzer est réalisable.
The feasibility of transapical, transcatheter mitral paravalvular leak (PVL) closure has recently been shown.1 However, bleeding complications are the Achilles’ heel of the procedure. The left ventricular apex can be accessed either through a small intercostal incision or by direct percutaneous puncture. While the former technique has potentially a lower risk of bleeding, the latter technique is a simpler and less traumatic approach. Here we report the percutaneous device closure of the apical puncture site following transapical PVL closure.
chanical prostheses (On-X Life Technologies Inc, Austin, TX). The postoperative course was complicated by major bleeding, requiring a rethoracotomy and cardiopulmonary resuscitation. In addition, worsening symptoms of heart failure (New York Heart Association [NYHA] class III) despite maximal medical therapy, and significant hemolysis in the context of a moderate mitral PVL, led to the decision to proceed with PVL closure. Owing to the patient’s high surgical risk (frailty, prior complicated postoperative course, renal failure, polyneuropathy, chronic immunosuppressive therapy), a percutaneous transapical access was decided on, despite the lack of long-term data supporting such an approach.
Methods Patient A woman aged 56 years with previous aortic and mitral mechanical valve replacements in 1986 and redo double valve replacements in 2006 underwent implantation of On-X meReceived for publication December 5, 2011. Accepted January 31, 2012. Corresponding author: Dr Fabian Nietlispach, Department of Cardiology, Swiss Cardiovascular Centre, Bern University Hospital, CH-3010 Bern, Switzerland. E-mail: [email protected] See page 516.e7 for disclosure information.
Investigations Blood analysis revealed a low hemoglobin level (84 g/L) and haptoglobin level (⬍ 0.0583 g/L), and elevated lactate dehydrogenase level (431 U/L). Transesophageal echocardiography located the leak on the medial aspect of the mitral valve ring with a transvalvular gradient of 16/4 mm Hg (max/mean) and revealed a normal left ventricular systolic function.
0828-282X/$ – see front matter © 2012 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved. doi:10.1016/j.cjca.2012.01.023
516.e6
Canadian Journal of Cardiology Volume 28 2012
Figure 1. (A) Mitral leaflets fully open. (B) Leaflets in closed position. (C) Three-dimensional transesophageal echocardiography, left atrial view of the mitral prosthesis and the Amplatzer device (St Jude Medical, St Paul, MN) (asterisk) occluding the paravalvular leak.
Procedure After informed consent was obtained, the procedure was performed under general anaesthesia in a hybrid operating room (OR). It was guided by fluoroscopy, transesophageal echocardiography, and transthoracic echocardiography (TTE). PVL closure was performed as previously described,1 with the use of a direct transcutaneous needle puncture of the ventricular apex. A 12-mm Amplatzer muscular ventricular septal defect (VSD) occluder (St Jude Medical, St Paul, MN) was used. This device resulted in complete closure of the PVL (Fig. 1). The sheath was pulled back into the midventricle. Protamine (50 mg) was given to reverse the previously administered 5000 units of heparine. A 6-mm muscular VSD occluder was then advanced with the use of the same 9F Am-
platzer delivery sheath, and the distal disc was released into the midventricle. The sheath was subsequently pulled back into the myocardium. The second disc was released while the sheath was being pulled back. After a stable device position was achieved and hemostasis at the puncture site was confirmed by TTE, the device was released. Results Procedural time was 55 minutes, and the volume of contrast dye used was 35 mL. Repetitive TTE studies in the hybrid OR during the next 30 minutes confirmed hemostasis. The patient was extubated in the OR, transferred to the intensive care unit for 24 hours, fully mobilized on day 3, and discharged on day 9 (NYHA class I).
Figure 2. (A) Ventricular septal defect (VSD) occluder in paravalvular position (black arrow) and VSD occluder in apical position (red arrows). (B) Transthoracic echocardiography image showing the VSD occluder in the left ventricular apex (red arrows). Note the 2 discs of the apical device adjacent to the epi- and pericardium.
Nietlispach et al. Closure of Apical Access Site
Follow-up Control fluoroscopy was performed on days 1, 2, and 5 and confirmed the stable position of the 2 devices. The mitral valve leaflets were freely mobile. TTE showed a transvalvular gradient of 11/4 mm Hg (max/mean), no residual paravalvular leak, a trivial localized pericardial effusion, and a stable position of the apical device (Fig. 2). The hemoglobin level rose to 104 g/L and the haptoglobin level to 0.22 g/L, while the lactate dehydrogenase level fell to 309 U/L. Systolic pulmonary arterial pressure fell from 76 mm Hg before the intervention to 33 mm Hg at discharge. One month following the procedure, the patient was doing well and remained in NYHA class I heart failure. TTE revealed no residual mitral PVL, no pericardial effusion, and a stable position of the ventricular apical device.
Discussion We described the procedural steps of ventricular apical access closure by means of an Amplatzer muscular VSD occluder. Only recently has a series of successful device closures of the apical access site by means of predominantly Amplatzer duct occluders been published.2 We believe that direct transapical access facilitates a variety of structural heart procedures and that device closure of the access site enhances the safety of this
516.e7
technique. This may be particularly pertinent in patients with friable myocardial tissue, as in our patient. Whether this technique may play a role in transapical transcatheter aortic valve replacement3 merits further investigation. Acknowledgements We would like to thank Professor Bernhard Meier, MD, from the Bern University Hospital, for his invaluable advice and technical input. Disclosures The authors have no potential conflicts of interest to disclose. References 1. Nietlispach F, Johnson M, Moss RR, et al. Transcatheter closure of paravalvular defects using a purpose-specific occluder. JACC Cardiovasc Interv 2010;3:759-65. 2. Jelnin V, Dudiy Y, Einhorn BN, Kronzon I, Cohen HA, Ruiz CE. Clinical experience with percutaneous left ventricular transapical access for interventions in structural heart defects a safe access and secure exit. JACC Cardiovasc Interv 2011;4:868-74. 3. Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aorticvalve replacement in high-risk patients. N Engl J Med 2011;364:2187-98.
Case Report
Closure of Apical Access Site After Transapical, Transcatheter Paravalvular Leak Closure Fabian Nietlispach, MD,a,b Friedrich Eckstein, MD,c Manfred Seeberger, MD,d Stefan Osswald, MD,a Beat A. Kaufmann, MD,a and Oliver Reuthebuch, MDc c
a
Department of Cardiology, University Hospital Basel, Basel, Switzerland
b
Department of Cardiology, Bern University Hospital, Bern, Switzerland
Department of Cardiac Surgery, University Hospital Basel, Basel, Switzerland d
Department of Anaesthesia, University Hospital Basel, Basel, Switzerland
ABSTRACT
RÉSUMÉ
The safety of percutaneous transapical mitral paravalvular leak (PVL) closure could potentially be enhanced by device closure of the ventricular access site. Percutaneous transapical PVL closure was performed. The 9F delivery sheath was pulled back, and a 6-mm Amplatzer muscular ventricular septal defect occluder was deployed at the apical puncture site. Immediate hemostasis was achieved. Total hospitalization was 9 days. New York Heart Association functional class was improved, hemoglobin and haptoglobin rose, while lactate dehydrogenase fell. Follow-up fluoroscopy and transthoracic echocardiography revealed a good functional result. Closure of the apical access site by means of an Amplatzer muscular ventricular septal defect occluder is feasible.
La sécurité de la fermeture percutanée de fuite paravalvulaire (FPV) mitrale par voie transapicale pourrait être améliorée par un dispositif de fermeture du site d’accès ventriculaire. La fermeture percutanée de la FPV par voie transapicale a été réalisée. La gaine 9F a été retirée, et un dispositif d’occlusion de la communication interventriculaire musculaire Amplatzer de 6 mm a été déployé à la zone de ponction apicale. Une hémostase immédiate a été obtenue. L’hospitalisation a été de 9 jours. La classification fonctionnelle de la New York Heart Association a été améliorée, l’hémoglobine et l’haptoglobine ont augmenté, tandis que le lactate déhydrogénase a chuté. La fluoroscopie et l’échocardiographie transthoracique de suivi ont révélé un bon résultat fonctionnel. La fermeture de la zone d’accès apical au moyen d’un dispositif d’occlusion de la communication interventriculaire musculaire Amplatzer est réalisable.
The feasibility of transapical, transcatheter mitral paravalvular leak (PVL) closure has recently been shown.1 However, bleeding complications are the Achilles’ heel of the procedure. The left ventricular apex can be accessed either through a small intercostal incision or by direct percutaneous puncture. While the former technique has potentially a lower risk of bleeding, the latter technique is a simpler and less traumatic approach. Here we report the percutaneous device closure of the apical puncture site following transapical PVL closure.
chanical prostheses (On-X Life Technologies Inc, Austin, TX). The postoperative course was complicated by major bleeding, requiring a rethoracotomy and cardiopulmonary resuscitation. In addition, worsening symptoms of heart failure (New York Heart Association [NYHA] class III) despite maximal medical therapy, and significant hemolysis in the context of a moderate mitral PVL, led to the decision to proceed with PVL closure. Owing to the patient’s high surgical risk (frailty, prior complicated postoperative course, renal failure, polyneuropathy, chronic immunosuppressive therapy), a percutaneous transapical access was decided on, despite the lack of long-term data supporting such an approach.
Methods Patient A woman aged 56 years with previous aortic and mitral mechanical valve replacements in 1986 and redo double valve replacements in 2006 underwent implantation of On-X meReceived for publication December 5, 2011. Accepted January 31, 2012. Corresponding author: Dr Fabian Nietlispach, Department of Cardiology, Swiss Cardiovascular Centre, Bern University Hospital, CH-3010 Bern, Switzerland. E-mail: [email protected] See page 516.e7 for disclosure information.
Investigations Blood analysis revealed a low hemoglobin level (84 g/L) and haptoglobin level (⬍ 0.0583 g/L), and elevated lactate dehydrogenase level (431 U/L). Transesophageal echocardiography located the leak on the medial aspect of the mitral valve ring with a transvalvular gradient of 16/4 mm Hg (max/mean) and revealed a normal left ventricular systolic function.
0828-282X/$ – see front matter © 2012 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved. doi:10.1016/j.cjca.2012.01.023
516.e6
Canadian Journal of Cardiology Volume 28 2012
Figure 1. (A) Mitral leaflets fully open. (B) Leaflets in closed position. (C) Three-dimensional transesophageal echocardiography, left atrial view of the mitral prosthesis and the Amplatzer device (St Jude Medical, St Paul, MN) (asterisk) occluding the paravalvular leak.
Procedure After informed consent was obtained, the procedure was performed under general anaesthesia in a hybrid operating room (OR). It was guided by fluoroscopy, transesophageal echocardiography, and transthoracic echocardiography (TTE). PVL closure was performed as previously described,1 with the use of a direct transcutaneous needle puncture of the ventricular apex. A 12-mm Amplatzer muscular ventricular septal defect (VSD) occluder (St Jude Medical, St Paul, MN) was used. This device resulted in complete closure of the PVL (Fig. 1). The sheath was pulled back into the midventricle. Protamine (50 mg) was given to reverse the previously administered 5000 units of heparine. A 6-mm muscular VSD occluder was then advanced with the use of the same 9F Am-
platzer delivery sheath, and the distal disc was released into the midventricle. The sheath was subsequently pulled back into the myocardium. The second disc was released while the sheath was being pulled back. After a stable device position was achieved and hemostasis at the puncture site was confirmed by TTE, the device was released. Results Procedural time was 55 minutes, and the volume of contrast dye used was 35 mL. Repetitive TTE studies in the hybrid OR during the next 30 minutes confirmed hemostasis. The patient was extubated in the OR, transferred to the intensive care unit for 24 hours, fully mobilized on day 3, and discharged on day 9 (NYHA class I).
Figure 2. (A) Ventricular septal defect (VSD) occluder in paravalvular position (black arrow) and VSD occluder in apical position (red arrows). (B) Transthoracic echocardiography image showing the VSD occluder in the left ventricular apex (red arrows). Note the 2 discs of the apical device adjacent to the epi- and pericardium.
Nietlispach et al. Closure of Apical Access Site
Follow-up Control fluoroscopy was performed on days 1, 2, and 5 and confirmed the stable position of the 2 devices. The mitral valve leaflets were freely mobile. TTE showed a transvalvular gradient of 11/4 mm Hg (max/mean), no residual paravalvular leak, a trivial localized pericardial effusion, and a stable position of the apical device (Fig. 2). The hemoglobin level rose to 104 g/L and the haptoglobin level to 0.22 g/L, while the lactate dehydrogenase level fell to 309 U/L. Systolic pulmonary arterial pressure fell from 76 mm Hg before the intervention to 33 mm Hg at discharge. One month following the procedure, the patient was doing well and remained in NYHA class I heart failure. TTE revealed no residual mitral PVL, no pericardial effusion, and a stable position of the ventricular apical device.
Discussion We described the procedural steps of ventricular apical access closure by means of an Amplatzer muscular VSD occluder. Only recently has a series of successful device closures of the apical access site by means of predominantly Amplatzer duct occluders been published.2 We believe that direct transapical access facilitates a variety of structural heart procedures and that device closure of the access site enhances the safety of this
516.e7
technique. This may be particularly pertinent in patients with friable myocardial tissue, as in our patient. Whether this technique may play a role in transapical transcatheter aortic valve replacement3 merits further investigation. Acknowledgements We would like to thank Professor Bernhard Meier, MD, from the Bern University Hospital, for his invaluable advice and technical input. Disclosures The authors have no potential conflicts of interest to disclose. References 1. Nietlispach F, Johnson M, Moss RR, et al. Transcatheter closure of paravalvular defects using a purpose-specific occluder. JACC Cardiovasc Interv 2010;3:759-65. 2. Jelnin V, Dudiy Y, Einhorn BN, Kronzon I, Cohen HA, Ruiz CE. Clinical experience with percutaneous left ventricular transapical access for interventions in structural heart defects a safe access and secure exit. JACC Cardiovasc Interv 2011;4:868-74. 3. Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aorticvalve replacement in high-risk patients. N Engl J Med 2011;364:2187-98.