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Cerebrovascular Damage Mediates Relations Between Aortic Stiffness and Memory.

ABSTRACT: Aortic stiffness is associated with cognitive decline. Here, we examined the association between carotid-femoral pulse wave velocity and cognitive function and investigated whether cerebrovascular remodeling and parenchymal small vessel disease damage mediate the relation. Analyses were based on 1820 (60% women) participants in the Age, Gene/Environment Susceptibility-Reykjavik Study. Multivariable linear regression models adjusted for vascular and demographic confounders showed that higher carotid-femoral pulse wave velocity was related to lower memory score (standardized ?: -0.071±0.023; P=0.002). Cerebrovascular resistance and white matter hyperintensities were each associated with carotid-femoral pulse wave velocity and memory (P<0.05). Together, cerebrovascular resistance and white matter hyperintensities (total indirect effect: -0.029; 95% CI, -0.043 to -0.017) attenuated the direct relation between carotid-femoral pulse wave velocity and memory (direct effect: -0.042; 95% CI, -0.087 to 0.003; P=0.07) and explained ?41% of the observed effect. Our results suggest that in older adults, associations between aortic stiffness and memory are mediated by pathways that include cerebral microvascular remodeling and microvascular parenchymal damage.

SUBMITTER: Cooper LL

PROVIDER: S-EPMC4679440 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature

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Cerebrovascular Damage Mediates Relations Between Aortic Stiffness and Memory.

Cooper Leroy L LL Woodard Todd T Sigurdsson Sigurdur S van Buchem Mark A MA Torjesen Alyssa A AA Inker Lesley A LA Aspelund Thor T Eiriksdottir Gudny G Harris Tamara B TB Gudnason Vilmundur V Launer Lenore J LJ Mitchell Gary F GF

Hypertension (Dallas, Tex. : 1979) 20151116 1

Aortic stiffness is associated with cognitive decline. Here, we examined the association between carotid-femoral pulse wave velocity and cognitive function and investigated whether cerebrovascular remodeling and parenchymal small vessel disease damage mediate the relation. Analyses were based on 1820 (60% women) participants in the Age, Gene/Environment Susceptibility-Reykjavik Study. Multivariable linear regression models adjusted for vascular and demographic confounders showed that higher caro ...[more]

PMID: 26573713

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Project description:BACKGROUND:Mechanisms underlying the association between age-related arterial stiffening and poor brain health remain elusive. Cerebral blood flow (CBF) homeostasis may be implicated. This study evaluates how aortic stiffening relates to resting CBF and cerebrovascular reactivity (CVR) in older adults. METHODS:Vanderbilt Memory & Aging Project participants free of clinical dementia, stroke, and heart failure were studied, including older adults with normal cognition (n=155; age, 72±7 years; 59% male) or mild cognitive impairment (n=115; age, 73±7 years; 57% male). Aortic pulse wave velocity (PWV; meters per second) was quantified from cardiac magnetic resonance. Resting CBF (milliliters per 100 g per minute) and CVR (CBF response to hypercapnic normoxia stimulus) were quantified from pseudocontinuous arterial spin labeling magnetic resonance imaging. Linear regression models related aortic PWV to regional CBF, adjusting for age, race/ethnicity, education, Framingham Stroke Risk Profile (diabetes mellitus, smoking, left ventricular hypertrophy, prevalent cardiovascular disease, atrial fibrillation), hypertension, body mass index, apolipoprotein E4 ( APOE ?4) status, and regional tissue volume. Models were repeated testing PWV× APOE ?4 interactions. Sensitivity analyses excluded participants with prevalent cardiovascular disease and atrial fibrillation. RESULTS:Among participants with normal cognition, higher aortic PWV related to lower frontal lobe CBF (?=-0.43; P=0.04) and higher CVR in the whole brain (?=0.11; P=0.02), frontal lobes (?=0.12; P<0.05), temporal lobes (?=0.11; P=0.02), and occipital lobes (?=0.14; P=0.01). Among APOE ?4 carriers with normal cognition, findings were more pronounced with higher PWV relating to lower whole-brain CBF (?=-1.16; P=0.047), lower temporal lobe CBF (?=-1.81; P=0.004), and higher temporal lobe CVR (?=0.26; P=0.08), although the last result did not meet the a priori significance threshold. Results were similar in sensitivity models. Among participants with mild cognitive impairment, higher aortic PWV related to lower CBF in the occipital lobe (?=-0.70; P=0.02), but this finding was attenuated when participants with prevalent cardiovascular disease and atrial fibrillation were excluded. Among APOE ?4 carriers with mild cognitive impairment, findings were more pronounced with higher PWV relating to lower temporal lobe CBF (?=-1.20; P=0.02). CONCLUSIONS:Greater aortic stiffening relates to lower regional CBF and higher CVR in cognitively normal older adults, especially among individuals with increased genetic predisposition for Alzheimer's disease. Central arterial stiffening may contribute to reductions in regional CBF despite preserved cerebrovascular reserve capacity.

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Cerebrovascular Damage Mediates Relations Between Aortic Stiffness and Memory.

Publications

Cerebrovascular Damage Mediates Relations Between Aortic Stiffness and Memory.

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