W hite matter hyperintensities (WMH) are indicators of cerebral small vessel disease 1 and are implicated in the pathogenesis of cognitive impairment, stroke, and dementia. 2 WMH are associated with hypertension and increased risk of stroke, [3][4][5] but the mechanism through which elevated blood pressure (BP) affects the brain is unclear. Advancing age is associated with loss of elasticity in the large arteries and muscular arterioles and increased arterial stiffness. Several risk factors, particularly hypertension, contribute to the stiffness. 3,[6][7][8] Arterial stiffening impairs the damping of the arterial waveform in large arteries and could lead to excessive transmission of BP pulsation to the brain. 9,10 Increasing stiffness of the large central arteries is associated with WMH. [8][9][10][11][12] One explanation for the association between arterial stiffness and WMH is that arterial stiffening exposes small vessels in the brain to high pulsatility, damaging the small vessel wall. [7][8][9] Because this cyclic variation in BP is transmitted to the brain through the internal carotid arteries (ICA), an association among BP, ICA flow parameters, and WMH might be expected. 5 Few studies have compared BP, ICA or middle cerebral artery (MCA) blood flow velocity, and WMH. 9,13 Previous studies 9,10 that investigated BP and ICA or MCA velocity parameters and WMH have focused on the pulse pressure component of BP and the pulsatility index component of the Doppler MCA or ICA waveform. However, pulse pressure is determined by diastolic BP (DBP) and systolic BP (SBP), and the relative contribution of these is a function of age: in young adults, both DBP and SBP increase, whereas in the elderly SBP increases whereas DBP reduces with age.14 Here, we investigated the association between BP measured longitudinally, ICA blood flow velocity parameters, and Abstract-White matter hyperintensities (WMH) are associated with hypertension. We examined interactions among blood pressure (BP), internal carotid artery (ICA) flow velocity parameters, and WMH. We obtained BP measurements from 694 community-dwelling subjects at mean ages 69.6 (±0.8) years and again at 72.6 (±0.7) years, plus brain MRI and ICA ultrasound at age 73±1 years. Diastolic and mean BP decreased and pulse pressure increased, but systolic BP did not change between 70 and 73 years. Multiple linear regression, corrected for vascular disease and risk factors, showed that WMH at the age of 73 years were associated with history of hypertension (β=0.13; P<0.001) and with BP at the age of 70 years (systolic β=0.08, mean β=0.09, diastolic β=0.08; all P<0.05); similar but attenuated associations were seen for BP at the age of 73 years. Lower diastolic BP and higher pulse pressure were associated with higher ICA pulsatility index at the age 73 years (diastolic BP age 70 years: standardized β=−0. 15 Three years later (wave 2), repeat medical and cognitive assessments were conducted (n=866); in addition, at wave 2 they underwent carotid Doppler ultrasound imaging and bra...

Cognitive decline and carotid artery atheroma are common at older ages. In community-dwelling subjects, we assessed cognition at ages 70, 73 and 76 and carotid Doppler ultrasound at age 73, to determine whether carotid stenosis was related to cognitive decline. We used latent growth curve models to examine associations between four carotid measures (internal carotid artery stenosis, velocity, pulsatility and resistivity indices) and four cognitive ability domains (memory, visuospatial function, crystallised intelligence, processing speed) adjusted for cognitive ability at age 11, current age, gender and vascular risk factors. Amongst 866 participants, carotid stenosis (median 12.96%) was not associated with cognitive abilities at age 70 or cognitive decline from age 70 to 76. Increased ICA pulsatility and resistivity indices were associated with slower processing speed (both P < 0.001) and worse visuospatial function (P = 0.036, 0.031, respectively) at age 70, and declining crystallised intelligence from ages 70 to 76 (P = 0.008, 0.006, respectively). The findings suggest that vascular stiffening, rather than carotid luminal narrowing, adversely influences cognitive ageing and provides a potential target for ameliorating age-related cognitive decline.

No abstract

No abstract