ABSTRACT NUMBER: ESOC2026A513 BLOOD PRESSURE PARAMETERS AND COGNITIVE DECLINE AND DEMENTIA AFTER STROKE OR TRANSIENT ISCHAEMIC ATTACK: RESULTS FROM THE PROGRESS TRIAL

Abstract Background and aims Aside from elevated mean systolic blood pressure (BP), additional measures such as variability, pulse pressure (PP), or mean-arterial pressure (MAP), could be important targets for dementia prevention. This study aimed to investigate these associations in participants with stroke or transient ischaemic attack from the Perindopril Protection Against Recurrent Stroke Study (PROGRESS) trial. Methods Logistic regression models were used to estimate associations of BP parameters with a composite of cognitive decline according to Mini-Mental State Examination scores and/or adjudicated dementia outcomes. Subgroup analysis was conducted by mild cognitive impairment (MCI) at baseline, sex and stroke subtype. Results After 4 (median) years of follow-up of 5,128 participants, 567 (11.1%) developed cognitive decline/dementia. For systolic BP (SBP), the mean, maximum, cumulative load and last measure were associated with higher odds of cognitive decline/dementia. Higher mean SBP conferred the highest odds (odds ratio [OR] 1.23, 95% confidence intervals [CI] 1.08-1.39). For diastolic BP, higher mean, maximum, variability, cumulative load, slope and last measure were associated, but the strongest association was for load (OR 1.29, 95% CI 1.15-1.45). Only the mean PP was associated (OR 1.14, 95% CI 1.00-1.30). For MAP, MAP load showed the strongest association (OR 1.26, 95% 1.13-1.41). Finally, systolic, diastolic and MAP variability showed higher odds in those without MCI (p interaction <0.001). Conclusions Besides higher mean SBP, alternative measures such as variability, cumulative load, slope and last measures of diastolic BP, PP and MAP were associated with cognitive decline/dementia and need further consideration in cognitive decline/dementia prevention. Conflict of interest Sultana Shajahan: nothing to disclose. Mark Woodward: nothing to disclose. Craig S Anderson has received grants from the NHMRC, the Medical Research Foundation (MRF) of the UK, and AstraZeneca paid to his institution; is a consultant to Auzone BioTech Shanghai; reports membership of data and safety monitoring boards for several investigator-initiated clinical trials, and is the Editor-in-Chief of Cerebrovascular Diseases and President-elect of the World Stroke Organisation. Cheryl Carcel is supported by an NHMRC Investigator Grant, Emerging Leadership 1 (APP2009726), Heart Foundation Vanguard grant, and receives research support from Bayer. Linan Chen: nothing to disclose. Ruth Peters is supported by funding from NHMRC paid to her institution. Karin Rådholm: nothing to disclose. Stephen Harrap: nothing to disclose. John Chalmers: nothing to disclose. Katie Harris: nothing to disclose.