Background: Central arterial stiffness is an emerging risk factor of age-related cognitive impairment and Alzheimer’s disease (AD). However, the underlying pathophysiological mechanisms remain unclear. Objective: We tested the hypothesis that carotid arterial stiffness is associated with reduced cerebral blood flow (CBF) and increased cerebrovascular resistance (CVR) in patients with amnestic mild cognitive impairment (MCI), a prodromal stage of AD. Methods: Fifty-four patients with amnestic MCI and 24 cognitively normal subjects (CN) of similar age and sex to MCI patients underwent measurements of CBF and carotid β-stiffness index using ultrasonography and applanation tonometry. Total CBF was measured as the sum of CBF from both the internal carotid and vertebral arteries, and divided by total brain tissue mass (assessed with MRI) to obtain normalized CBF (nCBF). Results: Relative to CN subjects, MCI patients showed lower nCBF (53.3 ± 3.2 vs 50.4±3.4 mL/100 g/min, P < 0.001) and higher CVR (0.143 ± 0.019 vs 0.156 ± 0.023 mmHg/mL/min, P < 0.015). Multiple linear regression analysis showed that nCBF was negatively associated with carotid β-stiffness index (B = -0.822, P < 0.001); CVR was positively associated with carotid systolic pressure (B = 0.001, P < 0.001) after adjustment for age, sex, body mass index, and MCI status. Conclusion: These findings suggest that carotid artery stiffening may contribute at least in part to the reduced nCBF and increased CVR in patients with MCI associated with augmented carotid arterial pulsatility.
Aerobic exercise training (AET) may improve cerebralperfusion and reduce the risk of dementia. Changes in central arterialstiffness and pulsatile cerebral blood flow (CBF) associated with exercise training may be one of the underlying pathophysiological mechanism. The purpose of this study was to investigate: (1) The effects of AET on central arterialstiffness and CBF, and (2) whether pulsatile CBF mediates the association between changes in arterial stiffness and cerebral perfusion in amnestic mildcognitive impairment (aMCI), a prodromal stage of Alzheimer disease. Seventy aMCI patients were randomized to 12 months of moderate‐intensity AET (n=31) or stretching program (n=39). CBF and carotid β‐stiffness index were assessed by ultrasonography and applanation tonometry. Cerebral perfusion was calculated by normalizing total CBF to brain tissue mass measured by magnetic resonance imaging. Pulsatile CBF was measured from the middle cerebralartery using transcranial Doppler. Cardiorespiratory fitness was assessed by peak oxygen uptake (VO2peak). VO2peak and cerebralperfusion increased and carotid β‐stiffness index decreased in the AET group, while remained unchanged in the stretching group. The change in VO2peak was significantly associated with the change in cerebral perfusion, carotidβ‐stiffness index, and pulsatile CBF (Fig. 1). The decrease in carotidβ‐stiffness was associated with increased in cerebral perfusion (Fig. 2). Mediation analysis showed that changes in pulsatile CBF mediates the association between carotidβ‐stiffness index and cerebral perfusion (Fig. 2). These results suggest that AET decreases arterial stiffness and increases cerebral perfusion, which is mediated by pulsatile CBF in aMCI patients. Support or Funding Information This work was funded by the National Institutes of Health ((R01AG033106, R01HL102457, P30AG012300) Associations between the change (Δ) in relative peak oxygen uptake (VO2) and the change in cerebral perfusion, carotid β‐stiffness index and pulsatile cerebral blood flow (CBF). Mediation analysis diagram of the effect of the change (Δ) in carotid β‐stiffness index on the change in cerebral perfusion through the change in pulsatile cerebral blood flow (CBF).
Introduction White matter hyperintensities (WMH) is a risk factor of cognitive impairment and Alzheimer’s disease (AD). Arterial stiffening is associated with increased arterial pressure and cerebral blood flow (CBF) pulsatility which may lead to WMH pathogenesis. However, the relations among WMH, arterial stiffness, and pulsatile change in arterial pressure and CBF remain unclear. Therefore, this study investigated the associations among WMH volume, carotid arterial stiffness, carotid arterial pressure, and CBF pulsatility in patients with amnestic mild cognitive impairment (MCI), a prodromal stage of AD. Methods Fifty‐four amnestic MCI patients and twenty‐four cognitively normal subjects (CN) underwent measurements of WMH volume using T2‐weighted‐fluid‐attenuated inversion recovery imaging. Carotid β‐stiffness index and arterial pressure at the common carotid artery (CCA) were measured using ultrasound and applanation tonometry. CBF pulsatility index (PI) was measured from the middle cerebral artery using transcranial Doppler. Results WMH volume, PI, carotid β‐stiffness index, carotid systolic blood pressure (cSBP) and pulse pressure (cPP) did not differ between groups. Greater WMH volume was correlated with higher CBF PI in both groups (MCI: r=0.373, NC: r=0.463, p<0.05), whereas it was correlated positively with carotid β‐stiffness index, cSBP, and cPP only in the MCI group (MCI: r=0.499, r=0.432, r=0.468, all p<0.01). In multiple linear regression analysis, cSBP was an independent determinant of WMH (β=0.293, p=0.005) with adjustment for age, sex, body mass index, and MCI status. Conclusion These findings collectively suggest that carotid arterial stiffness, carotid SBP, and pulse pressure may play an important role in WMH pathogenesis in MCI. Support or Funding Information This work was funded by the National Institutes of Health ((R01AG033106, R01HL102457, P30AG012300)
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