Background and Aim: Switching regular salt for potassium-enriched salt reduces sodium intake, increases potassium intake, lowers blood pressure (BP) and prevents cardiovascular disease (CVD). This study estimated the health impacts, the costs and the cost-effectiveness of different scenarios for switching regular salt for potassium-enriched salt in Australia.

Methods: We used a multiple cohort, proportional, multistate, lifetable model to estimate the health and cost impacts of switching all salt from regular salt (100% sodium chloride) to potassium-enriched salt (25% potassium chloride, 75% sodium chloride) in 1) all packaged and prepared foods, 2) packaged foods targeted by the Australian government’s voluntary sodium targets, and 3) discretionary salt. Analyses were conducted over a 10-year time horizon with an extended healthcare perspective including costs related to healthcare, the intervention and policy implementation. BP data were sourced from the 2022 Australian National Health Survey and disease burden estimates from the Global Burden of Disease 2021 Study. Model outputs included difference in disease incidence, mortality, healthcare costs, and health-adjusted life years (HALYs) from the status quo, and incremental cost-effectiveness ratios.

Results: Over 10 years, switching to potassium-enriched salt in all packaged and prepared foods was estimated to prevent 56,980 (95% UI 43,581-71,790) CVD events and 49,274 (95% UI 35,079-64,226) incident chronic kidney disease (CKD) cases, while averting over 5,000 CVD and CKD deaths. These health gains translated to 23,092 (95% UI 17,650-28,872) HALYs gained and $780M (95% UI 569-1015) saved in healthcare costs. The scenario targeting foods covered by Australia’s voluntary sodium reformulation targets achieved approximately half these benefits, while substitution in discretionary salt achieved around one-sixth of the benefits. Intervention and policy implementation costs were $432M, $50M and $183M for scenarios 1-3, respectively. All three scenarios were estimated to be cost-effective (all >99% probability), and scenarios 1-2 were estimated to be cost-saving.

Conclusions: Switching regular salt to potassium-enriched salt in packaged and prepared foods and discretionary salt could substantially prevent CVD and CKD burden in Australia while being cost-effective. Broad implementation, particularly within packaged and prepared foods, represents a feasible and effective strategy to improve population sodium and potassium intake and deliver meaningful health gains.

In essential hypertension, the baroreflex resets to defend a higher blood pressure (BP) rather than correct it, and currently, no antihypertensive specifically targets this resetting. Baroreflex activation therapy shows the pathway can be re-engaged directly: electrically stimulating the carotid sinus lowers BP by reducing sympathetic tone and increasing renal excretory function, partly via suppressed renin secretion, linking central autonomic drive to renal and RAAS activity. Less clear is whether changes in the brain precede, accompany, or follow such adjustments. In addition, the white-coat hypertension effect, a sympathetically-mediated "alerting reflex" present in 28-39% of patients labelled treatment-resistant, shows attentional/cortical states, not just the reflex arc, can drive apparent BP elevation, raising the question of whether higher brain centres shape sympathetic drive more broadly, independent of the baroreflex.

This study aimed to identify central brain activity preceding spontaneous bursts of muscle sympathetic nerve activity (MSNA) in healthy adults, the outflow that baroreflex activation therapy ultimately suppresses.

Nineteen healthy adults (age 30 ± 10 years; BP 109 ± 11 / 73 ± 8 mmHg) underwent simultaneous microneurography and whole-brain neuroimaging during 10 minutes of quiet rest. The cardiac cycle influencing beat-to-beat BP was arranged into epochs and classified as burst or no-burst conditions according to subsequent MSNA activity recorded. This accounted for the ~1-second brain-to-peripheral leg nerve conduction delay. Epochs were contrasted with brain activity across cortical, subcortical, and brainstem regions. Both conditions were anchored to the same cardiac cycle, so differences reflected central correlates of burst generation rather than baroreflex gating.

Mean MSNA burst incidence was 42 ± 16 bursts/100 heartbeats, with BP stable throughout. Activity preceding bursts localised to brainstem nuclei central to baroreflex integration, and to the frontal pole, in cortical areas implicated in attention. Activity in these regions, and the thalamus, rose together in the seconds before each burst.

These findings identify a central network operating upstream of spontaneous sympathetic bursts, independent of baroreflex gating. Whether this network is altered in hypertension remains untested, though it represents a candidate mechanism, and potential therapeutic target, for the baroreflex resetting that sustains chronically elevated BP, complementary to renal and RAAS-directed approaches.

Background and Aim: Carotid-femoral pulse wave velocity is the gold standard for assessing arterial stiffness. Although vascular changes begin in childhood, carotid-femoral pulse wave velocity is rarely used in children and adolescents, likely due to a number of challenges including difficulties associated with direct measurement. Equations exist for older adults to estimate carotid-femoral pulse wave velocity, but none for children, adolescents or young adults. This study aimed to 1) examine the correlation between measured carotid-femoral pulse wave velocity and estimated carotid-femoral pulse wave velocity using an existing adult equation in healthy children, adolescents and young adults and 2) develop new equations which more accurately estimate carotid-femoral pulse wave velocity in children, adolescents and young adults.

Methods: We analyzed data from healthy participants aged 1-40 years in the Youth Vascular Consortium. Estimated carotid-femoral pulse wave velocity was calculated using a previously established adult equation. Agreement between measured carotid-femoral pulse wave velocity and estimated carotid-femoral pulse wave velocity was assessed using Pearson correlation and Bland-Altman analysis. New equations were developed via multiple linear regression, with model selection guided by adjusted R² and Akaike Information Criterion.

Results: 4,771 healthy participants (51% female) were included. Agreement between measured carotid-femoral pulse wave velocity and estimated carotid-femoral pulse wave velocity was poor (≤19 years: r=0.08 and 0.09 for females and males; >19 years r=0.47 and 0.31 for females and males), with estimations up to 3 m/s higher than measured. New age- and sex-specific equations improved associations with measured carotid-femoral pulse wave velocity, particularly in children and adolescents (≤19 years; ∆r≈+0.34), with smaller gains observed in young adults (>19 years; ∆r≈+0.10).

Conclusions: Use of adult-based equations substantially overestimates carotid-femoral pulse wave velocity in youth. Our newly developed youth-specific equations may provide more accurate estimates of carotid-femoral pulse wave velocity for children, adolescents and young adults, offering a practical alternative when direct measurement is not feasible.

Background: Acute kidney injury (AKI) is a frequent and serious complication of cardiac surgery requiring cardiopulmonary bypass (CPB). However, clinical diagnosis relies largely on plasma creatinine, which has limited sensitivity and rises only after substantial loss of kidney function. Novel biomarkers, including cystatin C, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL), may enable earlier detection of kidney injury. However, their temporal profiles and diagnostic utility following CPB remain poorly characterised in clinically relevant large-animal models.

Aim: To investigate temporal changes in plasma and urinary cystatin C, KIM-1 and NGAL compared with plasma creatinine, and evaluate their potential as early biomarkers of AKI following CPB.

Methods: Eight female sheep were studied at baseline, during 2 h of CPB, and for 48 h postoperatively. Blood and urine samples were collected at baseline, 2 h of CPB, and 24 and 48 h postoperatively. Plasma and urinary concentrations of cystatin C, KIM-1 and NGAL, and plasma creatinine were measured. Kidney tissue was collected at 48 h for histopathological assessment.

Results: Compared with baseline, plasma cystatin C increased during CPB from 0.9 ± 0.1 to 1.4 ± 0.5 mg/L (p = 0.04). Urinary KIM-1 increased at 24 h postoperatively from 461.4 ± 107.1 to 609.0 ± 67.7 pg/mL (p = 0.01). In contrast, plasma creatinine decreased from 62.3 ± 14.2 µmol/L at baseline to 50.5 ± 7.8 µmol/L at 24 h (p = 0.02) and 43.4 ± 8.1 µmol/L at 48 h (p = 0.01) postoperatively. Acute tubular necrosis was observed in 50% of animals. Urinary cystatin C and plasma or urinary NGAL did not significantly change during CPB or postoperatively.

Conclusion: Despite histopathological evidence of kidney injury, plasma creatinine failed to identify AKI following CPB. In contrast, plasma cystatin C increased during CPB, while urinary KIM-1 increased postoperatively, suggesting that these biomarkers may provide earlier detection of kidney injury than creatinine following cardiac surgery.