Abstract

Background and significance: Increased arterial stiffness causes vessel damage of the end-organs. Thus, in the brain, small vessels may be susceptible to increased arterial stiffness. Cerebral microbleeds (CMBs) are topographically categorized as non-lobar type, mostly due to hypertensive vasculopathy and lobar type, due to cerebral amyloid angiopathy. When considering CMBs in the nonlobar region are associated with small vessel pathology, arterial stiffness may be related with CMBs in the nonlobar region. We investigated relationship between CMBs by using brachial ankle pulse wave velocity (baPWV) representing arterial stiffness. Method: Between June 2006 and January 2012, we included 1290 consecutive patients with acute ischemic stroke admitted to hospital within 7 days after symptom onset and who underwent baPWV and brain gradient echo (GRE) and Fluid Attenuated Inversion Recovery (FLAIR) MRI. Patients with potential cardiac sources of embolism or peripheral arterial occlusive disease were not included. BaPWV was measured during ankle-brachial index examination using an automatic device. CMBs were classified as lobar and nonlobar type. Severity of leukoaraiosis was determined using the Fazekas’ scoring system. Binary and multinomial logistic regression analyses were performed to determine variables that were associated with presence and location of CMBs. Results: Mean age of the patients was 64±12 years and 61.9% (799/1290) were male. Of 1290 patients, CMBs were found in 28.6%. The patients with CMBs were older than those without CMBs (69±10 years versus 63±12 years, p=0.001). Mean baPWV was higher in patients with CMBs than those without (2240±512cm/s versus 1896±505cm/s, p=0.001). On multivariate binary logistic analysis, baPWV and high grade leukoaraiosis were independent predictors of the presence of CMBs. However, after adjustment of age, sex and variables with p value of less than 0.1on the univariate analysis, baPWV was independently associated with nonlobar CMBs. Conclusion: Arterial stiffness was independently associated with nonlobar CMBs but not with lobar CMBs. These findings suggest pathophysiologic association between arterial stiffness and CMBs in the nonlobar region.

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