Search

Objective: The study was conducted to evaluate the safety and efficacy of mild internal jugular (IJV) compression via an FDA approved compression collar for symptomatic treatment of venous pulsatile tinnitus. Methods: This is a prospective study that recruited 20 adult patients with venous pulsatile tinnitus. Participants completed the Tinnitus Handicap Inventory (THI), were fitted with the collar, and rated symptom intensity on a 10‐point tinnitus intensity scale before and during collar use. Once weekly for 4 weeks, they answered a survey quantifying days used, average tinnitus intensity before and after wearing the collar each day of use, and any safety concerns. Lastly, they completed an exit interview. The primary outcome was symptomatic relief, with secondary outcomes of safety, effect of treatment setting, effect of time, and quality of life assessed via nonparametric testing. Results: 18 participants completed the study, and 276 paired daily before use/during use intensity scores were submitted. The median symptom intensity without the collar was 6 (IQR 4, 7), whereas with the collar it was 3 (IQR 2, 5), for a median symptomatic relief of 50%. The collar had a significant effect in reducing symptom intensity (p < 0.0001) and burden of illness via the THI (p < 0.0001). There was no effect of setting, frequency, or time on symptomatic relief with the collar. There were no adverse safety events reported aside from minor discomfort upon initial application. Conclusions: Venous compression collars offer acute symptom relief for patients with venous pulsatile tinnitus. Further study is needed to assess safety and efficacy of longitudinal use. Level of Evidence: 4 Laryngoscope, 134:3342–3348, 2024 [ABSTRACT FROM AUTHOR]

Although expansive remodeling of the maternal uterine circulation during pregnancy is essential for maintaining uteroplacental perfusion and normal fetal growth, the underlying physiological mechanisms are not well understood. Using a rat model, surgical approaches were used to alter uterine hemodynamics and wall shear stress (WSS) to evaluate the effects of WSS and venoarterial communication (e.g., transfer of placentally derived growth signals from postplacental veins to preplacental arteries) on gestational uterine vascular remodeling. Changes in WSS secondary to ligation of the cervical but not the ovarian end of the main uterine artery and vein provoked significant expansive remodeling at the opposite end of both vessels, but only in pregnant animals. The ≈50% increase in lumen diameter (relative to the contralateral horn) was associated with an upregulation of total endothelial nitric oxide (NO) synthase expression and was abolished by in vivo NO synthase inhibition with N-nitro-L-arginine methyl ester. Complete removal of a venous segment adjacent to the uterine artery to eliminate local venous influences significantly attenuated the WSS-induced remodeling by about one-half (P < 0.05). These findings indicate that, during pregnancy, 1) increased WSS stimulates uterine artery growth via NO signaling and 2) the presence of an adjacent vein is required for arterial remodeling to fully occur. [ABSTRACT FROM AUTHOR]

Although expansive remodeling of the maternal uterine circulation during pregnancy is essential for maintaining uteroplacental perfusion and normal fetal growth, the underlying physiological mechanisms are not well understood. Using a rat model, surgical approaches were used to alter uterine hemodynamics and wall shear stress (WSS) to evaluate the effects of WSS and venoarterial communication (e.g., transfer of placentally derived growth signals from postplacental veins to preplacental arteries) on gestational uterine vascular remodeling. Changes in WSS secondary to ligation of the cervical but not the ovarian end of the main uterine artery and vein provoked significant expansive remodeling at the opposite end of both vessels, but only in pregnant animals. The ≈50% increase in lumen diameter (relative to the contralateral horn) was associated with an upregulation of total endothelial nitric oxide (NO) synthase expression and was abolished by in vivo NO synthase inhibition with N-nitro-l-arginine methyl ester. Complete removal of a venous segment adjacent to the uterine artery to eliminate local venous influences significantly attenuated the WSS-induced remodeling by about one-half ( P < 0.05). These findings indicate that, during pregnancy, 1) increased WSS stimulates uterine artery growth via NO signaling and 2) the presence of an adjacent vein is required for arterial remodeling to fully occur. NEW & NOTEWORTHY This study provides the first in vivo evidence for the importance of venous influences on arterial growth within the uteroplacental circulation.