Background Plasma 25 hydroxycholecalciferol (vit D) deficiency has been associated with adverse cardiovascular outcomes in epidemiological studies. Chronic kidney disease is associated with loss of 1-α-hydroxylase and consequently vit D deficiency. We hypothesized that vitamin D deficiency was associated with increased mortality and increased vascular access failure in patients undergoing permanent vascular access for end stage renal disease. Methods This retrospective cohort study analyzed 128 patients undergoing permanent vascular access surgery between 2003 and 2012 who also had concurrent plasma vit D levels. Levels were considered deficient at <20 ng/mL. Multivariable analysis was used to determine the association between vit D and mortality and vascular access outcomes. Results The mean age was 66.7; 96.8% were male and 32.0% African American; 60.9% had diabetes mellitus. In the entire cohort 55.5% were vitamin D (vit D) deficient, despite similar rates of repletion among the vit D deficient and non-deficient groups. During median follow up of 2.73 years there were 40 (31%) deaths. Vit D deficient patients tended to be younger (P=.01), have higher total cholesterol (P=.001), lower albumin levels (P=.017), and lower calcium levels (P=.007). Despite their younger age, mortality was significantly higher (P=.026) and vascular access failure was increased (P=.008) in the vit D deficient group. In multivariate logistic regression analysis vit D deficiency OR=3.64; (CI 1.12-11.79) P=.031, hemodialysis via central catheter OR=3.08; (CI 1.04-9.12) P=.042, coronary artery disease OR=3.08; (CI 1.06-8.94) P=.039, increased age OR=1.09; (CI 1.03-1.15) P=.001 and albumin OR=0.27 (CI 0.09-0.83) P=.023 remained independent predictors of mortality. Vit D deficiency HR=2.34 (CI 1.17-4.71) P=.02, synthetic graft HR=3.50 (CI 1.38-8.89) P=.009, , and hyperlipidemia HR=0.42 (CI .22-.81) P=.01 were independent predictors of vascular access failure in a Cox proportional harzardmodel. Conclusion Vit D deficiency is highly prevalent in patients undergoing vascular access procedures. Patients who are deficient have worse survival and worse vascular access outcomes. Further study is warranted to assess whether aggressive vitamin D repletion will improve outcomes in this population.
A 42-year-old man sustained a stroke secondary to malignant hypertension and was found to have complete aortic interruption. We report a case of real-time image-guided endovascular repair to highlight the value of preprocedural planning and intraprocedural cone beam computed tomography. Two-dimensional fluoroscopy enhanced with three-dimensional landmarks from cone beam computed tomography was used to direct a Nykanen radiofrequency wire (Baylis Medical, Montreal, Quebec, Canada) through the interruption, avoiding critical adjacent structures. A covered Cheatham-Platinum stent (NuMED, Inc, Hopkinton, NY) was deployed successfully, recanalizing the thoracic aorta. The pressure gradient normalized, and the patient was discharged on postoperative day 1. At 10-month follow-up, the patient was on an antihypertensive regimen of two minimum-dose drugs.
Total symptom score was higher for patients without deep reflux both pre (median, 14, [IQR,(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)] vs median 13.5 [IQR, 9.5-18.0]; P ¼ .005) and postprocedurally (median, 4 [IQR,(1)(2)(3)(4)(5)(6)(7)(8)(9) vs median 3.25 [IQR, 1-7]; P < .001) but no difference was seen in change in symptom score (median, 8 [IQR,(4)(5)(6)(7)(8)(9)(10)(11)(12)(13) vs median 9 [IQR, 4-13]; P ¼ .172). Patients with deep reflux had substantially higher rates of complications (10.4% vs 3.0%; P < .001) with a particular increase in proximal thrombus extension (3.1% vs 1.1%; P < .001). After controlling for confounding, this estimate of effect size for any complication increased (OR, 5.72; 95% CI, 2.21-14.81; P < .001).Conclusions: No significant difference is seen in total symptom improvement when patients undergo truncal endovenous ablation with concomitant deep venous reflux, although a greater improvement was seen in VCSS score in these patients. Patients with deep venous reflux had a significantly increased rate of complications independent of confounding variables and should be counseled appropriately before the decision for treatment.
Aim To investigate whether vertebrobasilar geometry contributes to the presence, severity, and laterality of white matter hyperintensities (WMH). Methods We retrospectively reviewed 290 cerebral scans of patients who underwent time-of-flight and fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) between 2017 and 2018. WMH were counted, localized, and grouped according to laterality on the FLAIR sequence. A 3D mesh of the posterior circulation was reconstructed (with ITK SNAP software) and the morphology of the vertebrobasilar system analyzed with an in-house software written in Python. Results Patients were assigned into a group with WMH (n = 204) and a group without WMH (n = 86). The severity of WMH burden was mainly affected by age and hypertension, while the localization of the WMH (or laterality) was mainly affected by the vertebrobasilar system morphology. Basilar artery morphology only affected the parieto-occipital region significantly if both posterior communicating arteries were hypoplastic or absent. The dominant vertebral artery and basilar artery curve had an opposite directional relationship. Conclusions An unequal vertebral artery flow is an important hemodynamic contributor to basilar bending. Increased basilar artery curvature and increased infratentorial WMH burden may signal inadequate blood flow and predict cerebrovascular events.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.