The Pathophysiological Role of Arterial Stiffness in Underactive Bladder among Women: Insights from Blood Pressure Pulse Wave Testing

Niimi A1, Watanabe D1, Kamei J1, Fujii Y1, Kakutani S1, Miyakawa J1, Taguchi S1, Yamada Y1, Sato Y2, Kume H1

Research Type

Clinical

Abstract Category

Female Lower Urinary Tract Symptoms (LUTS) / Voiding Dysfunction

Abstract 211
Female LUTS, SUI and Imaging 2
Scientific Podium Short Oral Session 24
Friday 9th October 2026
09:45 - 09:52
Parallel Hall 3
0.4 Brussels / 0.5 Paris
Capacity: 356
Underactive Bladder Female Voiding Dysfunction
1. Department of Urology, Graduate School of Medicine, The University of Tokyo, 2. Department of Urology, New Tokyo Hospital
Presenter
Links

Abstract

Hypothesis / aims of study
Underactive bladder (UAB) is one of the lower urinary tract conditions that commonly affects older adults, but its pathophysiology remains unclear. Animal studies have shown that arterial stiffness affects detrusor underactivity, yet clinical evidence in humans is scarce. Among vascular markers, brachial-ankle pulse wave velocity (baPWV) reflects arterial stiffness, whereas the ankle-brachial index (ABI) indicates arterial narrowing. We therefore examined the association between UAB and these vascular function tests.
Study design, materials and methods
92 patients aged ≥40 years who visited both urology and cardiology department between 2022 and 2024 were included in this study. Patients were divided into those without LUTS (non-UAB) and those with UAB, based on the 2018 ICS definition. Patient background, comorbidities, and the presence of arterial stiffness were evaluated using non-invasive vascular assessment. Exclusions were pelvic organ prolapse, urethral stricture, spinal cord disease, neurodegenerative disorders, and acute or severe stroke. Both baPWV (brachial-ankle pulse wave velocity) and ABI were measured to assess vascular status; a prespecified high-risk cutoff for baPWV was ≥1800 cm/s.
Results
86 patients were analyzed (UAB n=24, non-UAB n=62), the mean ages were 80.2 and 75.9 years, respectively (p=0.07). Mean baPWV was higher in UAB than non-UAB patients (2605.5 vs 1855.0 cm/s). In logistic regression, baPWV ≥1800 cm/s was independently associated with UAB (adjusted OR 9.8, 95% CI 1.9–50.7, p<0.01), whereas age, BMI, hypertension, diabetes, dyslipidemia, LSCS, and ABI ≤0.9 were not significant.
Interpretation of results
These results suggest that, in older women, arterial stiffness is not just a bystander but a potential independent contributor to UAB pathophysiology. The strong association between elevated baPWV and UAB, even after adjustment for age and conventional cardiovascular risk factors, indicates that systemic atherosclerotic change may specifically impair detrusor function rather than simply reflecting overall frailty or aging. The lack of association with ABI supports the notion that diffuse arterial stiffening, rather than focal large-vessel narrowing, is the relevant vascular phenotype in UAB. Taken together, these findings raise the possibility that microvascular compromise due to increased arterial stiffness could underlie detrusor underactivity, and they highlight the need to consider vascular health assessment and possibly early vascular intervention as part of the comprehensive management and prevention strategy for UAB in elderly women.
Concluding message
In women, UAB was independently associated with arterial stiffness, irrespective of age. These findings suggest that systemic atherosclerosis may play an important role in the pathogenesis of UAB.
Figure 1
References
  1. Yang JH, Choi HP, Niu W, Azadzoi KM. Cellular Stress and Molecular Responses in Bladder Ischemia. Int J Mol Sci. 2021 Nov 1;22(21):11862. doi: 10.3390/ijms222111862. PMID: 34769293; PMCID: PMC8584445.
  2. Andersson KE, Boedtkjer DB, Forman A. The link between vascular dysfunction, bladder ischemia, and aging bladder dysfunction. Ther Adv Urol. 2017 Jan;9(1):11-27. doi: 10.1177/1756287216675778. Epub 2016 Nov 4. PMID: 28042309; PMCID: PMC5167073.
  3. Kim, M., Yu, H.Y., Ju, H. et al. Induction of detrusor underactivity by extensive vascular endothelial damages of iliac arteries in a rat model and its pathophysiology in the genetic levels. Sci Rep 9, 16328 (2019). https://doi.org/10.1038/s41598-019-52811-4
Disclosures
Funding JSPS KAKENHI Grant Number 25K12607 Clinical Trial No Subjects Human Ethics Committee New Tokyo Hospital Ethical Committee Helsinki Yes Informed Consent Yes AI Not at all
Citation

Continence 19S (2026) 102688
DOI: 10.1016/j.cont.2026.102688

08/09/2026 18:45:14