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Correction: Kim et al. Neuroprotective Effect of Statins in a Rat Model of Chronic Ocular Hypertension. Int. J. Mol. Sci. 2021, 22, 12500
In the original publication [...]
Journal Article
The HOPE Asia Network consensus on blood pressure measurements corresponding to office measurements: Automated office, home, and ambulatory blood pressures
For adopting recently introduced hypertension phenotypes categorized using office and out of office blood pressure (BP) for the diagnosis of hypertension and antihypertension drug therapy, it is mandatory to define the corresponding out of office BP with the specific target BP recommended by the major guidelines. Such conditions include white‐coat hypertension (WCH), masked hypertension (MH), white‐coat uncontrolled hypertension (WUCH), and masked uncontrolled hypertension (MUCH). Here, the authors review the relevant literature and discuss the related issue to facilitate the use of corresponding BPs for proper diagnosis of WCH, MH, WUCH, and MUCH in the setting of standard target BP as well as intensive target BP. The methodology of deriving the corresponding BP has evolved from statistical methods such as standard deviation, percentile value, and regression to an outcome‐based approach using pooled international cohort study data and comparative analysis in randomized clinical trials for target BPs such as the SPRINT and STEP studies. Corresponding BPs to 140/90 and 130/80 mm Hg in office BP is important for safe and strict achievement of intensive BP targets. The corresponding home, daytime, and 24‐h BPs to 130/80 mm Hg in office BP are 130/80, 130/80, and 125/75 mm Hg, respectively. However, researchers have found some discrepancies among the home corresponding BPs. As tentative criterion for de‐escalation of antihypertensive therapy as shown in European guidelines was 120 mm Hg in office BP, corresponding home, daytime, and 24‐h systolic BPs to 120 mm Hg in office systolic BP are 120, 120, and 115 mm Hg, respectively.
Journal Article
SUN-228 Associations Between Aldosterone, Renin, and Arterial Stiffness in Indigenous and Non-Indigenous Australians
Abstract
Disclosure: E. Ng: None. S.M. Gwini: None. B. Davison: None. P.J. Fuller: None. G. Singh: None. J. Yang: None.
Background: Primary aldosteronism (PA), the most common endocrine cause of hypertension, is a modifiable risk factor for cardiovascular disease (CVD). Chronic aldosterone excess causes endothelial dysfunction and development of atherosclerosis and arterial stiffness. Indigenous Australians have a higher rate of hypertension and CVD, as well as higher rates of arterial stiffness, compared to the non-Indigenous population. However, the relationship between markers of PA and arterial stiffness has never been examined in Indigenous Australians. Aim: The aim of this study was to examine the relationship between markers of PA (aldosterone, renin and the aldosterone-to-renin ratio (ARR)) and arterial stiffness in participants of the Aboriginal Birth Cohort (ABC) (urban and remote) compared to age-matched non-Indigenous urban-residing participants of the Top End Cohort (TEC), at the age of 32-35 years. Methods: Arterial stiffness was measured non-invasively using a Cardio Wave Analyzer (SA-3000P) which provides information on several vascular parameters including arterial elasticity. Better vascular health is indicated by a higher value for arterial elasticity. Aldosterone and renin were measured by immunoassay. ARR > 50 or 70 pmol/L:mU/L (1.8 or 2.5 ng/dL:mU/L) were evaluated as thresholds for a positive screening test for PA. Results: There were 255 participants in the ABC (205 remote, 55 urban) and 76 in the TEC. Arterial elasticity was lower in the ABC compared to the TEC, with a median (P25, P75) value of -8 (-18, 6) in the urban ABC, -7 (-18, 8) in the remote ABC and 6 (-6, 16) in the TEC (p<0.001 for difference between groups). In the combined group, renin was inversely correlated with arterial elasticity, while ARR was positively associated with arterial elasticity, in both the unadjusted and adjusted analyses (accounting for BMI and eGFR). Evaluating the urban cohorts according to whether ARR was elevated or not did not identify significant differences in arterial elasticity. Discussion and Conclusion: Markers of PA did not correlate with a worse outcome in arterial elasticity. This may be a reflection of the young age of the cohort, given age is a major determinant of arterial stiffness. Even in the presence of aldosterone excess, chronicity is likely required before complications such as arterial stiffness occur. Follow-up of the vascular outcomes as the cohorts age may provide further insights into the relationship between markers of PA and vascular health, in both Indigenous and non-Indigenous Australians.
Presentation: Sunday, July 13, 2025
Journal Article
MON-287 Addressing Diagnostic Inequities In Primary Aldosteronism: Health Disparities, Precision Care Innovations, And Cardiovascular Risk Reduction In Resistant Hypertension
Abstract
Disclosure: P.D. Rupasinghe: None. S.N. Durrani: None. N.G. Abdelrahman: None.
Context: Primary aldosteronism (PA), the most common endocrine cause of secondary hypertension, affects 5-10% of hypertensive individuals and up to40% of hypertension. Despite its 4-12× higher cardiovascular risk, PA remains under diagnosed due to normokalemia (38% of cases), inconsistent aldosterone-renin ratio (ARR), and systemic disparities in confirmatory testing. Black patients face compounded barriers, including reduced confirmatory testing despite higher screening rates. CETO PET imaging offers precision care potential, though equitable implementation lags. Objective: This review assesses PA detection rates, identifies diagnostic gaps and inequities, and evaluates therapeutic innovations using large-scale data. Focus is in screening access, biologic/systemic diagnostic barriers, and emerging precision technologies. Method: A PRISMA-guided systematic review analyzed cohorts, meta-analyses, and trials (2010-2023) from ENSAT (n=3,812), AVIS-2 (n=1,506),NHANES 2017-2Biobank (n=502,490), and SPRINT (n=9,361). Inclusion criteria prioritized studies reporting PA prevalence, screening, diagnostic accuracy, or treatment outcomes odds ratios (ORs), and Area Under the (ROC) Curve (AUCs)were calculated; disparities were analyzed via multivariable regression. Study quality was assessed using the Newcastle-Ottawa scale. Results: PA prevalence was 16.1% in resistant hypertension (n=12,743)and 28.5% in hypokalemic hypertensives (n=3,890). NHANES data showed only 1.2%of hyper testing, with <0.3% undergoing confirmatory testing. Black patients had higher screening odds (OR 1.52, 95% CI 1.2-1.9) but 30% lower confirmatory test patients. ARR performance varied by race (AUC 0.68 in Black vs. 0.81 in White cohorts), reflecting biological and access disparities. 18F-CETO PET demonstrated with adrenal vein sampling (AVS), reducing reliance on invasive AVS. Adrenalectomy achieved biochemical cure in 94% of lateralized PA cases, while mineralocorticoid receptor antagonists (MRAs) decreased cardiovascular events by 34% (HR 0.66, 95% CI 0.54-0.79) in bilateral PA. Expanding screening under the American College of Cardiology (ACC) /American Heart Association (AHA)targets (<130/80 m∼8% of annual hypertension-related strokes. Conclusion: PA is a major, modifiable cardiovascular risk factor in resistant hypertension. Underdiagnosis persists due to systemic inequities, biological variability in fragmented care. Equitable adoption of advanced diagnostics (e.g., 18F-CETO PET), race-adjusted ARR cutoffs, and policy-driven screening expansion are critical. care and dismantling access barriers could prevent thousands of cardiovascular events annually.
Presentation: Monday, July 14, 2025
Journal Article
3598 Beyond the pressure threshold: Redefining the clinical spectrum of idiopathic intracranial hypertension (IIH)
BackgroundIdiopathic Intracranial Hypertension (IIH) is defined using the Friedman criteria, requiring papilloedema, cerebrospinal fluid (CSF) opening pressure >25cmH2O and exclusion of secondary causes of raised intracranial pressure. Those with CSF opening pressure <25cmH2O but consistent clinical features are classified with ‘probable’ IIH. The clinical and pathophysiological significance of this distinction remains unclear. This study compares phenotype, clinical features, and visual outcomes between subtypes.MethodsA multi-centre retrospective cohort study was performed on adults diagnosed with ‘probable’ or ‘definite’ IIH between 2019–2024. Longitudinal analyses assessed changes in visual and structural parameters over time.Results407 patients were included (338 definite, 69 probable). Both groups were predominantly female (92.0% vs. 89.9%), had comparable mean age at diagnosis and symptom profiles. Baseline visual acuity and Humphrey visual field measurements were comparable across disease definitions, with mixed-model regression analysis identifying significant improvements in both parameters across groups over time. A higher BMI was associated with worse acuity and visual field mean deviation. Though baseline retinal nerve fibre layer thickness, macular ganglion cell volume and papilloedema grade were higher in definite disease, longitudinal analysis found no significant differences in their rates of change over time.ConclusionOur findings challenge the distinction between ‘definite’ and ‘probable’ IIH, instead revealing an overlapping clinical spectrum with similar demographic and long-term visual outcomes despite differences in CSF opening pressure. These results question the reliance on pressure alone for diagnosis and management and underscores the need to redefine disease classification, consensus management guidelines and trial inclusion criteria.
Journal Article