Abstract MP90: Carotid Arterial Stiffness is Associated with An Increased Risk of Incident Cerebral Microbleeds in Older People: the Age, Gene/Environment Susceptibility-Reykjavik Study
Introduction: Cerebral microbleeds (CMBs) resulting from cerebral amyloid angiopathy are predominantly located in lobar regions, whereas those from hypertension are in deep and infratentorial regions. Although age and high blood pressure are major risk factors for CMBs, the underlying mechanisms remain unclear; arterial stiffness may be important.
Hypothesis: We hypothesized that carotid arterial stiffness, would be associated with incident CMBs. Given the spatial distributions of the underlying arteriopathies in which hypertensive arteriopathy typically affects the small perforating end-arteries of the deep structures, we further hypothesized that the associations would be more robust for deep CMBs attributed to hypertensive arteriopathy.
Methods: In the prospective, population-based Age, Gene/Environment Susceptibility-Reykjavik Study, 2,512 participants aged 66-97 years underwent a baseline brain MRI examination and carotid ultrasound in 2002-2006, and returned for a repeat brain MRI in 2007-2011. Common carotid arterial stiffness was assessed using a standardized protocol and expressed as carotid arterial strain (CAS), distensibility coefficient (DC) and Young’s elastic modulus (YEM). Log-binomial regression was applied to relate carotid arterial stiffness parameters to CMBs incidence.
Results: During a mean follow-up of 5.2 years, 463 people (18.4%) developed new CMBs, of whom 292 had CMBs restricted to lobar regions and 171 had CMBs in a deep or infratentorial region. After adjusting for age, sex and brain MRI interval, all arterial stiffness parameters were each significantly associated with incident CMBs (Risk ratio [RR] per SD decrease in CAS, 1.11 [95%CI, 1.02-1.21]; RR per SD decrease in natural log-transformed DC, 1.14[1.05-1.23]; RR per SD decrease in natural log-transformed YEM, 1.13[1.04-1.22]) and deep CMBs (RR, 1.17[1.00-1.36]; 1.24[1.07-1.43]; 1.22[1.06-1.41] respectively) but not with lobar CMBs. When further adjusted for baseline vascular risk factors including blood pressure and use of blood pressure lowering drugs, the presence of carotid plaque, prevalent CMBs, subcortical infarcts and white matter hyperintensities, the associations persisted.
Conclusion: Our findings support the hypothesis that localized increases in carotid arterial stiffness may contribute to the development of CMBs, especially those occuring in a deep location.
Author Disclosures: J. Ding: None. M.L. Bots: None. S. Sigurdsson: None. M. Garcia: None. T.B. Harris: None. G. Eiriksdottir: None. M.A. van Buchem: None. V. Gudnason: None. L.J. Launer: None.
- © 2015 by American Heart Association, Inc.