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Transcatheter implantation of pulmonary balloon-expandable stent-valves requires pre-stenting of the right ventricular outflow tract with large calibre stents. To increase awareness of the associated risks of this part of transcatheter pulmonary valve replacement therapy, we report potential fatal complications during the implantation of AndraStents® in the right ventricular outflow tract in six cases from five different European institutions and their management.
Method and result:
We present a retrospective case series analysis looking at the time period from 2013 to 2018. Of 127 AndraStents® implanted in the right ventricular outflow tract, in six patients, age from 13 to 71 years, a misconfiguration of the AndraStent® occurred forming a “diabolo”-configuration. During inflation of the balloon, the stent showed extreme “dog-boning”, an expansion of the stent at both ends with the middle part remaining unexpanded. This led to rupture of the balloon and loss of manoeuvrability in four patients. Out of the total six cases, in four patients the stent was eventually expanded with high-pressure balloons, and in one case the stent was surgically retrieved. In one patient, in whom a percutaneous retrieval of the embolised stent was attempted, a fatal bleeding occurred.
Pre-stenting of the right ventricular outflow tract by AndraStents® can lead to misconfiguration of the stent with potentially fatal complications. Rescue strategies of misconfigured stents include stent inflation and placement with high pressure non-compliant balloons or surgical backup. Interventional retrieval measures of AndraStents® cannot be advised.
Although the right jugular vein approach for percutaneous pulmonary valve implantation is well described, there are no reports that describe a percutaneous pulmonary valve implantation through a left superior caval vein to coronary sinus pathway.
A 14-year-old female with tetralogy of Fallot, mesocardia, left superior caval vein draining into the coronary sinus, and hemiazygos continuation of the inferior caval vein underwent ventricular septal defect closure, with homograft insertion from the right ventricle to the pulmonary artery, patch augmentation of the left pulmonary artery, and creation of an atrial communication. Thereafter followed numerous catheterisations and interventions with stent implantation for stenosis of the left pulmonary artery and the homograft, as did device closure of the atrial communication. When she was a 12-year-old, the indications for a percutaneous pulmonary valve implantation were fulfilled and she underwent implantation of a 22 mm Melody® valve through the left superior caval vein. The extra-stiff exchange wire was pre-formed into a “U-spiral”-type configuration, according to the underlying anatomy, in order to provide a smooth route for the delivery of stents, to create the landing zone, and for the implantation of the Melody “ensemble”. The procedure was performed under deep sedation according to our standard protocol. The duration of the procedure was 172 min and the radiation time was 24.9 min.
On the basis of this unique experience, percutaneous pulmonary valve implantation is safe and feasible even in patients with unusual anatomy. Crucial is the “U-spiral” shaped configuration of the guide wire.
Arterial thrombosis in neonates and children is a rare event and is often associated with external risk factors such as asphyxia or sepsis. We report our experiences with two neonates with spontaneous aortic arch thrombosis mimicking aortic coarctation. Despite single case reports until now, no data exist for the underlying thrombophilic risk factors and prognosis of this rare event. Both patients were carriers of a heterozygous factor V Leiden mutation, which has been reported once before as a risk factor for aortic arch thrombosis. One of our patients was operated upon successfully and is alive. The second patient suffered a large infarction of the right medial cerebral artery and had a thrombotic occlusion of the inferior caval vein. The patient obtained palliative care and died at the age of 6 days. In the literature, we identified 19 patients with neonatal aortic arch thrombosis. Of the 19 patients, 11 (58%) died. Including the two reported patients, the mortality rate of patients with multiple thromboses was 80% (8/10) compared with 18% (2/11) for patients with isolated aortic arch thrombosis; this difference reached statistical significance (p = 0.009). The analysis of thrombophilic disorders revealed that factor V Leiden mutation and protein C deficiency seem to be the most common risk factors for aortic arch thrombosis. Conclusion: Neonatal aortic arch thrombosis is a very rare but life-threatening event, with a high rate of mortality, especially if additional thrombotic complications are present. Factor V Leiden mutation seems to be one important risk factor in the pathogenesis of this fatal disease.
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