Cenk Erdal

Early protective effects of iloprost, a stable prostacyclin analog, during spinal cord ischemia in a rabbit model

Spinal cord ischemia may develop into paraplegia in some cases during operation of the thoracoabdominal aorta. This is attributable to the vulnerability of spinal motor neurons to ischemia. In this study, iloprost was used as an agent to decrease the severity of ischemia and reperfusion injury to the spinal cord motor neurons. Twenty-one rabbits were randomized into three groups of seven animals each: group A (iloprost not administered), group B (25 ng/kg per minute iloprost), and group S (sham-operated). The spinal cord ischemia model was created by a 15-min occlusion of the aorta just caudal to the renal artery with a balloon catheter. Administration of iloprost began 10 min before occlusion of the aorta, and continued thereafter for 60 min. The pre- and postocclusion arterial pressure and heart rate recordings, results of blood gas analyses, and hematocrit and glucose levels were recorded. The spinal cords were removed after 8-h monitoring of neurologic function. Viable and nonviable motor neurons in the anterior horn of the spinal cord were counted under light microscopy. Any significant alteration in hemodynamics, blood gases, and other physiologic parameters could not be detected within the groups. Iloprost had a moderately hypotensive effect. Neurologic function in terms of Johnson scoring was significantly better in the iloprost group (P < 0.05). The number of viable cells was higher, whereas the number of nonviable cells was lower in iloprost group, when compared with the control group (P < 0.05). Higher numbers of viable motor neurons were consistent with the neurological findings. As a result of this study we concluded that iloprost infused during clamping of the aorta mitigates the spinal cord injury due to ischemia and reperfusion, and has a significant protective effect.

Treatment of an unusual complication of transfemoral TAVI with a new technique : successful occlusion of ventricular septal defect by opening the closure device in the ascending aorta : case report

Ventricular septal defect (VSD) is a rare complication of transcatheter aortic valve implantation (TAVI) via the transfemoral approach. Aetiological factors leading to VSD have been reported as post-balloon dilatation, oversized prosthesis implantation, and severe calcification of the aorta. However, we present a case of VSD occurring after TAVI with an Edwards Sapien XT prosthesis without any distinct aetiological factors. We used a new technique for closure of the significant VSD; opening the left ventricular disc of the closure device in the ascending aorta and successfully implanting the device without any damage to the bioprosthetic valve.

Mutation Analysis of the Vangl2 Coding Region Revealed No Common Cause for Tetralogy of Fallot

Vangl2 (Van Gogh-like 2) protein acts via non-canonical Wnt signalling to regulate polarized cell movements during development of the proximal outflow tract in vertebrate embryos. Recently, it has been shown that mutations of the Vangl2 gene cause aortic arch defects that are characteristic of the loop-tail (Lp) mouse and they have also became a strong candidate for causing congenital outflow tract defects in humans. Thus, in this study Tetralogy of Fallot (ToF), which comprises a group of syndromes that constitutes the most frequent cause of congenital cardiac outflow abnormalities in humans, was analysed for mutations within all coding regions of the Vangl2 gene. Based on direct sequencing data from a combination of 20 patients with ToF and 22 healthy people, three polymorphisms have been identified in exon 6 and exon 7 which do not change the amino acid sequence. It was concluded, therefore, that there is no specific mutation responsible for the ToF phenotype in the Vangl2 gene.