January 21, 2016Neurology137 citationsOpen Access

Association of arterial stiffness with progression of subclinical brain and cognitive disease

Q: What is the clinical evidence from this study?

Study design: Cohort. Population: Subclinical brain and cognitive disease (n=1223). Intervention: Arterial stiffness and pressure pulsatility (iCFPWV, CPP, MAP) vs. Lower arterial stiffness and pressure pulsatility. Primary outcome: Change in Trail Making Test, Parts B and A (ΔTrails B-A) performance (β 0.10, p=0.019).

CTConnie W. Tsao JHJayandra J. Himali ABAlexa Beiser

Key Result

Higher baseline arterial stiffness (iCFPWV) was associated with greater longitudinal progression of neurocognitive decline on the Trail Making Test (β 0.10, p=0.019).

Study Design

Type

Cohort (n=1,223)

Multicenter

PICO

Population

1,223 middle-aged and older adults from the community, free of prior stroke or dementia, followed for a mean of 6.4 years.

Exposure / Comparator

Arterial stiffness and pressure pulsatility (iCFPWV, CPP, MAP) vs Lower arterial stiffness and pressure pulsatility

Primary Outcome

Change in Trail Making Test, Parts B and A (ΔTrails B-A) performance — β 0.10, p=0.019

Main Result

Effect estimate: β 0.10

p-value: p=0.019

Limitations

The relatively healthy sample may have diminished some of the observed effect sizes and reduced sensitivity to detect associations.
Did not account for multiple testing to avoid overcorrection and false-negative bias.
Predominantly white participants of Western European ancestry, potentially limiting generalizability to other ethnicities.

Abstract

OBJECTIVE: We tested whether abnormal arterial stiffness and blood pressure would be associated with progression of brain aging measured by brain MRI and neurocognitive testing. METHODS: Framingham Offspring Cohort participants (n = 1,223, 61 ± 9 years, 56% women) without previous stroke or dementia underwent applanation tonometry, brain MRI, and neurocognitive testing at examination 7 (1998-2001). Follow-up brain MRI and neurocognitive testing was performed at examination 8 (2005-2008, mean interval 6.4 ± 1.3 years). We related examination 7 inverse-transformed carotid-femoral pulse wave velocity (iCFPWV), central pulse pressure (CPP), and mean arterial pressure to changes in the following variables between examinations 7 and 8: total cerebral brain volume, white matter hyperintensity volume, and performance on executive function and abstraction tasks, the Trail Making Test, Parts B and A (ΔTrails B-A), and Similarities tests. RESULTS: Higher baseline iCFPWV and CPP were associated with greater progression of neurocognitive decline (iCFPWV and ΔTrails B-A association: SD unit change in outcome variable per SD change in tonometry variable β ± SE = 0.10 ± 0.04, p = 0.019; CPP and ΔSimilarities association: -0.08 ± 0.03, p = 0.013). Higher mean arterial pressure, but not iCFPWV or CPP, was associated with increase in white matter hyperintensity volume (β ± SE 0.07 ± 0.03, p = 0.017). No tonometry measures were associated with change in cerebral brain volume. CONCLUSIONS: In middle-aged and older adults without evidence of clinical stroke or dementia, elevated arterial stiffness and pressure pulsatility are associated with longitudinal progression of subclinical vascular brain injury and greater neurocognitive decline. Treatments to reduce arterial stiffness may potentially reduce the progression of neurovascular disease and cognitive decline.

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