Larger studies with a well-defined PCOS population using rigorous methodology may be required to draw a more robust conclusion. However, these results suggest women with PCOS are at a greater risk of premature atherosclerosis, which emphasizes the importance of screening and monitoring CVD risk factors in women with PCOS.
Our findings indicate that cfPWV and faPWV reflect distinct aspects of segment-specific vascular stiffness and their associated profile of cardiovascular risk factors. Even among older adults, age is associated with higher cfPWV and baPWV, but not with faPWV. Understanding factors that ostensibly play a role in increasing arterial stiffness in different arterial territories can inform opportunities for cardiovascular disease (CVD) prevention and risk management.
Repeatability was acceptable for all PWV measures in a multicenter, population-based study of older adults and supports its use in epidemiologic studies. Quantifying PWV measurement variation is critical for applications to risk assessment and stratification and eventual translation to clinical practice.
Among older adults, diabetes is associated with higher central arterial stiffness and lower peripheral arterial stiffness, and prediabetes is associated with higher baPWV. Cross-sectionally, the magnitude of the effect of diabetes on central stiffness is equivalent to 6 years of arterial aging.
OH assessed in midlife was independently associated with incident dementia and ischemic stroke. Additional studies are needed to elucidate potential mechanisms for these associations and possible applications for prevention.
higher levels of social support were moderately associated with greater multi-dimensional cognitive function at mid-life, but mid-life social support was not associated with temporal change in global cognitive function over 20 years into late life. Prospective studies with time-dependent measures of social support and cognition are needed to better understand the role of social engagement in ageing-related cognitive functioning.
Background:
Vascular age is an emerging health indicator and predictor of end-organ damage to the heart, brain, and kidney. Although there have been many review publications concerning risk factors for vascular aging, most include cross-sectional epidemiological studies, limiting inferences about temporality. There is a need for a review of longitudinal epidemiological studies with repeat measures of vascular structure and function to allow for a systematic examination of determinants of vascular age and the association of vascular aging with outcomes.
Content:
Arterial stiffness is the most frequently used measure of vascular aging. We report here results of an extensive literature review of longitudinal cohort studies with repeat measures of arterial stiffness to characterize determinants of vascular age. Additionally, we summarize population-based studies which have focused on the association of arterial stiffness with end-organ damage and adverse cardiovascular outcomes.
Summary:
Changes in arterial stiffness are evident in early childhood. In adults, arterial stiffness has been observed to progress at the average rate of 0.2–0.7 meters per second for every five years of life. The state of the science is limited by the small number of studies with repeat measures of arterial stiffness and determinants of arterial stiffness progression, as well as limited studies in children and diverse race/ethnic groups. Several extant studies suggest that beyond age, cardiometabolic risk factors and adverse lifestyle behaviors contribute to arterial stiffening. Arterial stiffness is therefore, important in the assessment of healthy vascular aging and a possible target for the prevention of subclinical and clinical disease.
Background
Central arterial stiffening and increased pulsatility, with consequent cerebral hypoperfusion, may result in structural brain damage and cognitive impairment.
Methods and Results
We analyzed a cross‐sectional sample of
ARIC
‐
NCS
(Atherosclerosis Risk in Communities–Neurocognitive Study) participants (aged 67–90 years, 60% women) with measures of cognition (n=3703) and brain magnetic resonance imaging (n=1255). Central arterial hemodynamics were assessed as carotid‐femoral pulse wave velocity and pressure pulsatility (central pulse pressure). We derived factor scores for cognitive domains. Brain
magnetic resonance imaging
using 3‐Tesla scanners quantified lacunar infarcts; cerebral microbleeds; and volumes of white matter hyperintensities, total brain, and the Alzheimer disease signature region. We used logistic regression, adjusted for demographics,
apolipoprotein E
ɛ4, heart rate, mean arterial pressure, and select cardiovascular risk factors, to estimate the odds of lacunar infarcts or cerebral microbleeds. Linear regression, additionally adjusted for intracranial volume, estimated the difference in log‐transformed volumes of
white matter hyperintensities
, total brain, and the
Alzheimer disease
signature region. We estimated the mean difference in cognitive factor scores across quartiles of carotid‐femoral pulse wave velocity or
central pulse pressure
using linear regression. Compared with participants in the lowest carotid‐femoral pulse wave velocity quartile, participants in the highest quartile of carotid‐femoral pulse wave velocity had a greater burden of
white matter hyperintensities
(
P
=0.007 for trend), smaller total brain volumes (−18.30 cm
3
; 95%
CI
, −27.54 to −9.07 cm
3
), and smaller
Alzheimer disease
signature region volumes (−1.48 cm
3
; 95%
CI
, −2.27 to −0.68 cm
3
). These participants also had lower scores in executive function/processing speed (β=−0.04
z
score; 95%
CI
, −0.07 to −0.01
z
score) and general cognition (β=−0.09
z
score; 95%
CI
, −0.15 to −0.03
z
score). Similar results were observed for
central pulse pressure
.
Conclusions
Central arterial hemodynamics were associated with structural brain damage and poorer cognitive performance among older adults.
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