An experimental study to determine the optimal access route for renal artery interventions.

OBJECTIVE: The standard approach for endovascular treatment of the renal artery is access via the common femoral artery. However, approximately one in eight patients have a renal artery take-off angle that is less than 50°. In these patients approaching via a femoral access site can be technically challenging. The goal of this study was to design and implement a set of experiments that could empirically determine the critical renal artery take-off angle at which a superior approach would be employed. METHODS: An experimental model of the abdominal aorta, iliac arteries and the renal arteries was constructed using averaged CT angiography data from 10 patients. A number of guide catheter and guide wire combinations were advanced into this model and the force/displacement response was established. RESULTS: Our results demonstrate that a renal artery take-off angle less than 30° has a reduced probability of achieving stable guide wire placement in comparison with the base 90° anatomy (p ≤ .0001). Additionally, our results indicate that the probability of achieving stable guide wire access is increased if the stiffness mismatch between the guide catheter and guide wire is minimised. CONCLUSIONS: In conclusion, we recommend a superior approach to the renal artery if the renal artery take-off angle is within the range of 33-38° and a stiff guide wire platform (e.g. an Amplatz stiff) is required to complete the procedure. Finally, we report an equation that can be used to determine the difficulty associated with accessing the renal artery in comparison to the base 90° anatomy.

Novel localization of CD38 in perivascular sympathetic nerve terminals.

Using high performance liquid chromatography fraction analysis we have recently established that numerous smooth muscle preparations, including the canine mesenteric artery and vein, release beta-nicotinamide adenine dinucleotide upon short-pulse electrical field stimulation in tetrodotoxin- and omega-conotoxin GVIA-sensitive manners [ Release of beta-nicotinamide adenine dinucleotide upon stimulation of postganglionic nerve terminals in blood vessels and urinary bladder. J Biol Chem 279:48893-48903.]. The beta-nicotinamide adenine dinucleotide metabolites ADP-ribose and cyclic ADP-ribose are also present in the tissue superfusates. CD38 is a multifunctional enzyme involved in the degradation of beta-nicotinamide adenine dinucleotide to ADP-ribose and cyclic ADP-ribose. Western immunoblot analysis revealed that CD38 is expressed in both artery and vein. Confocal laser scanning microscopy established colocalization of CD38 with tyrosine hydroxylase, synaptotagmin and synaptic vesicle protein in both blood vessels. High performance liquid chromatography with fluorescence detection demonstrated that whole tissue segments metabolize 1,N(6)-etheno-nicotinamide adenine dinucleotide to 1,N(6)-etheno-ADP-ribose and nicotinamide-guanine dinucleotide to cyclic GDP-ribose, suggesting the presence of both nicotinamide adenine dinucleotide-glycohydrolase and ADP-ribosyl cyclase activities in these blood vessels. Both enzymes appear to be associated with the membrane fraction, and therefore might be attributed to CD38. These data demonstrate a previously uncharacterized localization of CD38 in perivascular autonomic nerve terminals. Therefore, the beta-nicotinamide adenine dinucleotide/CD38 system may provide new mechanisms in autonomic neurovascular control.