Abstract
A patient with porcelain aorta underwent transcatheter aortic valve implantation with a self-expandable prosthesis for severe aortic stenosis. After postdilatation trace paravalvular regurgitation was accepted. 10 weeks later the patient returned with complete heart block and underwent pacemaker implantation. A new heart murmur prompted further investigation. A ventricular septal defect from the left ventricular outflow tract into the right ventricle was detected. It was successfully closed under direct surgical visualization and total cardiopulmonary bypass in an aortic no touch approach. Closure was accomplished with a percutaneous Amplatzer-PFO-occluder. Functional result was excellent.
INTRODUCTION
Development of a ventricular septal defect (VSD) is a rare complication in transcatheter aortic valve implantations (TAVI). Therefore experience is limited even in large centers. Treatment options range from complete surgical repair to conservative treatment in this elderly patient population.
CASE REPORT
A 69-year-old female with symptomatic (NYHA III) severe aortic stenosis (valve area: 0.5 cm2, mean gradient 44 mmHg) was evaluated for TAVI. The patient had heavy circumferential calcifications of the ascending aorta after mediastinal radiation for non-Hodgkin lymphoma 50 years earlier.
(A) Calcifications in computed tomography. (B) Angiographic VSD (→) 12 weeks after TAVI (*). (C) TOE color Doppler flow between LVOT and RV within prosthesis stent struts (*).
Initial angiographic result of TAVI.
The Heart Team decided for a VSD closure to prevent right heart failure. We chose a percutaneous PFO closure device with a thin waist and a diameter large enough to cover the tear and small enough to avoid interference with prosthesis leaflets on the LVOT side and the septal tricuspid leaflet on the right ventricular side. A percutaneous approach appeared difficult since the VSD was covered by the subvalvular stent-struts.
(A) Structure of Symetis ACCURATE TA (Courtesy of Symetis S.A.). (B) Lateral x-ray showing occluder (→) within prosthesis stent. (C) Postoperative TOE color Doppler with occluder (→).
Angiographic VSD.
DISCUSSION
Iatrogenic VSD after TAVI is associated with heavy calcifications of the LVOT and post-dilatation. The VSD is not always immediately apparent. Reports of weeks to months until the appearance of symptoms exist [1, 2]. Small tears may increase with time when a self-expandable prosthesis causes further protrusion of calcifications.
The common treatment option for VSD after TAVI is SAVR with patch-closure of the VSD. In our case the porcelain aorta precluded a standard surgical approach including cross clamping of the aorta.
Anecdotally percutaneous approaches were successful with an antegrade arterio-venous loop technique using interventional occluders [1, 2]. The VSDs were located on the lower edges of Edwards Sapien 3- and CoreValve®-prosthesis. In our case the VSD was located within the prosthesis cage possibly impeding passage of percutaneous delivery sheaths.
A valve-in-valve solution with coverage of the VSD was judged hazardous because of the degree and location of calcification in the LVOT.
We combined the experiences of cardiology and cardiac surgery to an individualized hybrid strategy with enhanced probability of closure success at reduced surgical risk. The Symetis valve allowed for insertion of an occluder without leaflet interference. The nadir of its native porcine leaflets is attached to a self-expanding nitinol stent 8 mm above its lower edge (Fig. 2A) [3]. It cannot be assumed that such devices will generally work well in different prosthesis or VSD-locations.
CONCLUSION
Closure by means of a PFO-occluder with surgical visualization is a feasible treatment option for iatrogenic VSD after TAVI. Individualized bail-out strategies are a particular treasure of an experienced interdisciplinary Heart Team.
Conflict of interest: none declared.
