Outcomes of Hypogastric Coverage and Occlusion during Endovascular Treatment of Aortoiliac Occlusive Disease.

BACKGROUND: The risk of hypogastric occlusion (HO) following bare-metal stent (BMS) coverage of the hypogastric origin during endovascular treatment of aortoiliac occlusive disease (AIOD) is unclear. This study sought to determine the rate and clinical significance of HO following BMS coverage during iliac stenting for complex AIOD. METHODS: Consecutive patients undergoing elective iliac stenting for AIOD from 2010-2018 at Cleveland Clinic were reviewed. Patients with BMS coverage of a patent hypogastric origin were included. Rate of HO were determined by review of intraoperative angiography and follow up imaging. Predictors of HO were identified by univariable and multivariable logistic regression. Outcomes were compared between those who did and did not develop HO. RESULTS: There were 251 patients (338 limbs) with BMS coverage of the hypogastric origin during treatment of AIOD. Lesion severity was classified as TASC C/D in 249/338 (73.7%) of cases. Bilateral hypogastric coverage occurred in 93/251 (37.1%) patients. Hypogastric patency was 78.1% at 24-months following coverage. Recanalization of an ipsilateral external iliac artery (EIA) occlusion was predictive of HO (HR 3.12, 95% CI: 1.33, 7.34; P= 0.009). Increased luminal diameter of the hypogastric origin protected against HO (HR 0.64; 95% CI: 0.47, 0.88; P= 0.006). Perioperative outcomes were no different between patients with and without HO. There were no cases of gluteal necrosis, spinal cord ischemia, or pelvic organ ischemia. Four-year mortality and limb salvage were not affected by HO. HO was associated with decreased primary patency of ipsilateral iliac stents and increased risk of ipsilateral reintervention (HR 5.49; 95% CI: 1.82, 16.58; P= 0.002). CONCLUSIONS: HO is relatively infrequent following BMS coverage during treatment of AIOD. Luminal diameter of the hypogastric origin and ipsilateral EIA occlusion are associated with occlusion. HO is well tolerated in AIOD, though it is potentially associated with increased risk iliac stent occlusion and reintervention.

Computer-based video training is effective in teaching basic surgical skills to novices without faculty involvement using a self-directed, sequential and incremental program.

INTRODUCTION: Computer-based video training (CBVT) of surgical skills overcomes limitations of 1:1 instruction. We hypothesized that a self-directed CBVT program could teach novices by dividing basic surgical skills into sequential, easily-mastered steps. METHODS: We developed a 12 video program teaching basic knot tying and suturing skills introduced in discrete, incremental steps. Students were evaluated pre- and post-course with a self-assessment, a written exam and a skill assessment. RESULTS: Students (n = 221) who completed the course demonstrated significant improvement. Their average pre-course product quality score and assessment of technique using standard Global Rating Scale (GRS) were <0.4 for 6 measured skills (scale 0-5) and increased post-course to ≥3.25 except for the skill tying on tension whose GRS = 2.51. Average speed increased for all skills. Students' self-ratings (scale 1-5) increased from an average of 1.4 ± 0.7 pre-elective to 3.9 ± 0.9 post-elective across all skills (P < 0.01). CONCLUSION: Self-directed, incremental and sequential video training is effective teaching basic surgical skills and may be a model to teach other skills or to play a larger role in remote learning.

Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury.

OBJECTIVE: Previous studies showed the benefit of canonical transient receptor potential 6 (TRPC6) channel deficiency in promoting endothelial healing of arterial injuries in hypercholesterolemic animals. Long-term studies utilizing a carotid wire-injury model were undertaken in wild-type (WT) and TRPC6-/- mice to determine the effects of TRPC6 on phenotypic modulation of vascular smooth muscle cells (SMC) and neointimal hyperplasia. We hypothesized that TRPC6 was essential in the maintenance or reexpression of a differentiated SMC phenotype and minimized luminal stenosis following arterial injury. METHODS: The common carotid arteries (CCA) of WT and TRPC6-/- mice were evaluated at baseline and 4 weeks after wire injury. At baseline, CCA of TRPC6-/- mice had reduced staining of MYH11 and SM22, fewer elastin lamina, luminal dilation, and wall thinning. After carotid wire injury, TRPC6-/- mice developed significantly more pronounced luminal stenosis compared with WT mice. Injured TRPC6-/- CCA demonstrated increased medial/intimal cell number and active cell proliferation when compared with WT CCA. Immunohistochemistry suggested that expression of contractile biomarkers in medial SMC were essentially at baseline levels in WT CCA at 28 days after wire injury. By contrast, at 28 days after injury medial SMC from TRPC6-/- CCA showed a significant decrease in the expression of contractile biomarkers relative to baseline levels. To assess the role of TRPC6 in systemic arterial SMC phenotype modulation, SMC were harvested from thoracic aortae of WT and TRPC6-/- mice and were characterized. TRPC6-/- SMC showed enhanced proliferation and migration in response to serum stimulation. Expression of contractile phenotype biomarkers, MYH11 and SM22, was attenuated in TRPC6-/- SMC. siRNA-mediated TRPC6 deficiency inhibited contractile biomarker expression in a mouse SMC line. CONCLUSIONS: These results suggest that TRPC6 contributes to the restoration or maintenance of arterial SMC contractile phenotype following injury. Understanding the role of TRPC6 in phenotypic modulation may lead to mechanism-based therapies for attenuation of IH.