Aortic stiffness is associated with cognitive decline and cerebrovascular disease late in life, although these associations have not been examined in young adults. Understanding the effects of aortic stiffness on the brain at a young age is important both from a pathophysiological and public health perspective. The aim of this study was to examine the cross-sectional associations of aortic stiffness with cognitive function and brain aging in the Framingham Heart Study Third Generation cohort (47% men; mean age, 46 years). Participants completed the assessment of aortic stiffness (carotid-femoral pulse wave velocity), a neuropsychological test battery assessing multiple domains of cognitive performance and magnetic resonance imaging to examine subclinical markers of brain injury. In adjusted regression models, higher aortic stiffness was associated with poorer processing speed and executive function (Trail Making B-A; β±SE, -0.08±0.03; P<0.01), larger lateral ventricular volumes (β±SE, 0.09±0.03; P<0.01) and a greater burden of white-matter hyperintensities (β±SE, 0.09±0.03; P<0.001). When stratifying by age, aortic stiffness was associated with lateral ventricular volume in young adults (30-45 years), whereas aortic stiffness was associated with white-matter injury and cognition in midlife (45-65 years). In conclusion, aortic stiffness was associated with cognitive function and markers of subclinical brain injury in young to middle-aged adults. Prospective studies are needed to examine whether aortic stiffening in young adulthood is associated with vascular cognitive impairment later in life.
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http://dx.doi.org/10.1161/HYPERTENSIONAHA.115.06610 | DOI Listing |
J Hypertens
December 2024
Division of Internal Medicine, Candiolo Cancer Institutute FPO - IRCCS, Candiolo.
Background: Heart failure with preserved ejection fraction (HFpEF) is a high prevalence condition, with high rates of hospitalization and mortality. Arterial hypertension is the main risk factor for HFpEF. Among hypertensive patients, alterations in cardiac and vascular morphology identify hypertension-mediated organ damage (HMOD).
View Article and Find Full Text PDFJ Hypertens
December 2024
Department of Ultrasound Medicine, Tangdu Hospital, Air Force Medical University.
Background: The arterial stiffening is attributed to the intrinsic structural stiffening and/or load-dependent stiffening by increased blood pressure (BP). The respective lifetime alterations and major determinants of the two components with normal aging are not clear.
Methods: A total of 3053 healthy adults (1922 women) aged 18-79 years were enrolled.
Am J Hypertens
January 2025
HAND Research Group, School of Medicine and Health Sciences, Mulungushi University, Livingstone, Zambia.
Curr Probl Cardiol
January 2025
Department of Cardio-Thoracic Surgery, Chengdu Second People's Hospital, Chengdu, Sichuan 610017, China. Electronic address:
The importance of central hemodynamic metrics such as Central blood pressure (CBP), which directly measure the pressure exerted by the cardiac muscle on the major arteries, offering a more direct assessment of cardiovascular workload compared to brachial blood pressure (bBP), which measures pressure against the walls of peripheral arteries. This review consolidates findings that evaluate the correlation between CBP and key markers of aortovascular disease. The growth of thoracic aortic aneurysm (TAA) is a significant component of aortovascular assessment.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Vanderbilt Memory & Alzheimer's Center, Vanderbilt University Medical Center, Nashville, TN, USA.
Background: Cerebral arterial dilatation, signifying outward vascular remodeling, is linked to a higher risk of Alzheimer's disease and a higher burden of white matter hyperintensities (WMH). Arterial dilatation may disrupt cerebral hemodynamics and lead to delayed blood arrival to the brain, which is itself linked to an increased burden of WMH. We examined if arterial dilatation was associated with blood arrival timing and if blood arrival timing mediated the effect of arterial dilatation on WMH burden.
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