Hugo J Aparicio1, Rodica E Petrea2, Joseph M Massaro3, Warren J Manning4, Noriko Oyama-Manabe5, Alexa S Beiser6, Carlos S Kase7, Ralph B D'Agostino3, Philip A Wolf8, Ramachandran S Vasan9, Charles DeCarli10, Christopher J O'Donnell11, Sudha Seshadri8. 1. Department of Neurology, Boston University School of Medicine, 72 East Concord Street, C-3, Boston, MA 02118, USA; National Heart, Lung, and Blood Institute's Framingham Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702, USA. Electronic address: hugoa@bu.edu. 2. Department of Neurology, Boston University School of Medicine, 72 East Concord Street, C-3, Boston, MA 02118, USA; National Heart, Lung, and Blood Institute's Framingham Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702, USA; Department of Neurology, Creighton University School of Medicine, 601 North 30th Street, Suite 5300, Omaha, NE 68131, USA. 3. National Heart, Lung, and Blood Institute's Framingham Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702, USA; Department of Biostatistics, Boston University School of Public Health, Crosstown Building, 801Massachusetts Avenue, 3rd Floor, Boston, MA 02118, USA. 4. National Heart, Lung, and Blood Institute's Framingham Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702, USA; Departments of Medicine and Radiology, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA 02215, USA. 5. Departments of Medicine and Radiology, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA 02215, USA. 6. Department of Neurology, Boston University School of Medicine, 72 East Concord Street, C-3, Boston, MA 02118, USA; National Heart, Lung, and Blood Institute's Framingham Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702, USA; Department of Biostatistics, Boston University School of Public Health, Crosstown Building, 801Massachusetts Avenue, 3rd Floor, Boston, MA 02118, USA. 7. Department of Neurology, Boston University School of Medicine, 72 East Concord Street, C-3, Boston, MA 02118, USA; National Heart, Lung, and Blood Institute's Framingham Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702, USA; Department of Neurology, Emory University School of Medicine, 201 Dowman Drive, Atlanta, GA 30322, USA. 8. Department of Neurology, Boston University School of Medicine, 72 East Concord Street, C-3, Boston, MA 02118, USA; National Heart, Lung, and Blood Institute's Framingham Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702, USA. 9. National Heart, Lung, and Blood Institute's Framingham Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702, USA; Sections of Preventive Medicine and Cardiology, Boston University School of Medicine, Crosstown Building, 801 Massachusetts Avenue, 4th Floor, Boston, MA, USA. 10. Department of Neurology, School of Medicine, and Imaging of Dementia and Aging Laboratory, Center for Neuroscience, University of California-Davis, 1544 Newton Court, Davis, CA 95616, USA. 11. National Heart, Lung, and Blood Institute's Framingham Study, 73 Mt. Wayte Avenue, Suite 2, Framingham, MA 01702, USA; Department of Medicine, Massachusetts General Hospital, 55 Fruit St, Boston, MA 02215, USA; Cardiology Section, Boston Veterans Administration Healthcare, 150 S Huntington Ave, Boston, MA 02130, USA.
Abstract
BACKGROUND AND AIMS: Aortic atherosclerosis is an aggregate marker of vascular risk factor exposure and has been associated with intracranial atherosclerosis and stroke. We hypothesized that atherosclerosis of the descending aorta (DAo) could be a risk marker for brain aging and injury. METHODS: We evaluated 1527 participants (mean age 59.9 years, 53.5% women) in the Framingham Offspring cohort who underwent both aortic and brain MRI. Participants were free of clinical stroke, dementia, or other neurological illness at the time of axial MRI of the thoracic and abdominal DAo and subsequent brain MRI. We related the prevalence and burden of aortic plaque to total cerebral brain volume (TCBV) and white matter hyperintensity volume (WMHV). An additional analysis compared incidence of stroke or TIA in participants with and without DAo plaques. RESULTS: Presence of thoracic DAo plaque (8%) was associated with decreased TCBV in sex-pooled analysis (-0.77, SE 0.25, p = 0.002, equivalent to 4.5 years of aging) and with increased WMHV only in men (0.26, SE 0.12, p = 0.032, equivalent to 6.5 years aging). We observed similar associations of DAo plaque burden with TCBV and WMHV. There were 43 strokes and 11 TIAs in prospective follow-up (median 7 years). Presence of DAo plaque was not associated with subsequent stroke or TIA. CONCLUSIONS: In this cross-sectional community-based study, we found DAo plaque is associated with accelerated brain aging. These data underscore the potential implications of incidentally identified subclinical aortic atherosclerosis and question whether targeted intervention in these high risk individuals can modulate cognitive decline.
BACKGROUND AND AIMS: Aortic atherosclerosis is an aggregate marker of vascular risk factor exposure and has been associated with intracranial atherosclerosis and stroke. We hypothesized that atherosclerosis of the descending aorta (DAo) could be a risk marker for brain aging and injury. METHODS: We evaluated 1527 participants (mean age 59.9 years, 53.5% women) in the Framingham Offspring cohort who underwent both aortic and brain MRI. Participants were free of clinical stroke, dementia, or other neurological illness at the time of axial MRI of the thoracic and abdominal DAo and subsequent brain MRI. We related the prevalence and burden of aortic plaque to total cerebral brain volume (TCBV) and white matter hyperintensity volume (WMHV). An additional analysis compared incidence of stroke or TIA in participants with and without DAo plaques. RESULTS: Presence of thoracic DAo plaque (8%) was associated with decreased TCBV in sex-pooled analysis (-0.77, SE 0.25, p = 0.002, equivalent to 4.5 years of aging) and with increased WMHV only in men (0.26, SE 0.12, p = 0.032, equivalent to 6.5 years aging). We observed similar associations of DAo plaque burden with TCBV and WMHV. There were 43 strokes and 11 TIAs in prospective follow-up (median 7 years). Presence of DAo plaque was not associated with subsequent stroke or TIA. CONCLUSIONS: In this cross-sectional community-based study, we found DAo plaque is associated with accelerated brain aging. These data underscore the potential implications of incidentally identified subclinical aortic atherosclerosis and question whether targeted intervention in these high risk individuals can modulate cognitive decline.
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