Paradoxical embolism is considered the major cause of cerebral ischemic events in young patients. The most common cause of paradoxical embolism, which has been widely described, is right-to-left shunting (RLS) at cardiac level through a patent foramen ovale (PFO). Rarely paradoxical embolism can also be caused by RLS at pulmonary level due to pulmonary arteriovenous fistula (PAVF). Herein, we present a case of a young man, who experienced transient ischemic attack (TIA) due to paradoxical embolism, in whom both abovementioned abnormalities coexisted. This coincidence is very rare (noted in only 1% of patients with cryptogenic stroke or TIA), but it highlights the importance of searching for extracardiac RLS in patients with cryptogenic stroke, even if a PFO has been detected.
A 46-year-old male with a history of arterial hypertension and obesity was referred to our hospital due to symptoms of congestive heart failure (NYHA class III). Physical examination revealed a diastolic heart murmur. Transthoracic echocardiogram showed a fistula from the right aortic sinus to the right ventricle. Invasive angiography visualised a ruptured sinus of Valsalva aneurysm (SVA) (Fig. 1). The defect measured 6 mm in diameter at the aorta. The patient was qualified for transcatheter closure of the SVA. Occlusion of the SVA was performed using a 12 × 16 mm Nit-Occlud Lê VSD Occluder (Pfm Medical) under local anaesthesia. The procedure was conducted under transoesophageal echocardiography guidance. The device was delivered from the venous side after the formation of an arteriovenous loop (Fig. 2). The procedure and further hospitalisation was uneventful. The patient experienced gradual symptom reduction, and an echocardiography performed after three months did not reveal a residual shunt. SVAs constitute rare cardiac anomalies, which can be of congenital or acquired origin. Commonly they involve the right coronary sinus (70%) and the non-coronary sinus (29%). Congenital SVAs are caused by weakness at the junction between the aortic media and the aortic ring. Acquired aneurysms are caused by conditions affecting the aortic wall, such as endocarditis, trauma, or connective tissue disease. Unruptured SVAs usually remain asymptomatic. In most cases rupture occurs at the age of 20-40 years. Usually SVAs rupture into the right ventricle and the right atrium, or less frequently into the pulmonary artery, left ventricle, left atrium, or pericardial cavity. This most commonly manifests as exercise intolerance, dyspnoea, or chest pain. Surgery is considered the gold standard treatment for SVA. However, percutaneous closure appears to be a feasible alternative to surgical repair. The first transcatheter closure of SVA was reported in 1994. Since then, a significant number of such procedures have been performed using various devices, most commonly patent ductus arteriosus occluders or atrial septal defects occluders. We chose the Nit-Occlud Lê VSD Occluder, which was originally designed for ventricular septal defect (VSD) closure (Fig. 3). The implant is constructed of a single coil. The coil is made of nitinol, an alloy with shape memory characteristics, and in its relaxed state it adopts the form of a pair of cones nested one inside the other. This implant is distinguished by a gentle and refined structure, which minimises its interference with neighbouring tissues. This is substantiated by the lower rate of atrio-ventricular conduction disturbances after VSD closure with the Nit-Occlud Lê VSD Occluder in comparison with other devices (0% vs. 5-7%, respectively). We believe that the above-mentioned occluder should be considered for transcatheter SVA closure. Of note, to the best of our knowledge this is the first closure of an SVA with a Nit-Occlud Lê VSD device.
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