Relationship of cerebral microbleeds to inflammatory marker levels

Abstract

Aim:The purpose of this study is to investigate the incidence, distribution and risk factors of cerebral microbleeds (CMBs) and the relation between CMBs and inflammation in ischemic cerebrovascular disease. Methods: Two hundred and one patients without acute infarction or transient ischemic attack were enrolled. The presence and number of CMB were assessed on susceptibility-weighted imaging. The traditional risk factors of CMB were recorded. Levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and matrix metalloproteinase-9 (MMP-9) were tested. Logistic regression analyses were used for multiple-factor analysis of risk factors of CMB. Results: Of the 201 patients, 49 (24.38%) had CMB. Multivariate logistic regression analyses showed that the age, the prevalence of hypertension, silent lacunar infarction, white matter lesion, Montreal Cognitive Assessment Score, the using rate of antithrombotic drugs and levels of hs-CRP, IL-6, MMP-9 were the risk factors for CMB. After adjustments for traditional risk factors, inflammatory marker levels remained to be associated with CMBs. The adjusted odd ratios of hs-CRP, IL-6 and MMP-9 were 1.745 (1.342-2.270), 1.223 (1.018-1.533) and 1.284 (1.082-1.423), respectively. Furthermore, inflammatory marker levels were the risk factor for deep or infratentorial CMBs and lobar CMBs. Conclusion: The age, prevalence of hypertension, silent lacunar infarction, white matter lesion, MoCA Score, the using rate of antithrombotic drugs and serum hs-CRP, IL-6, and MMP-9 levels were the independent risk factors for CMBs. Key words:Cerebral microbleed, traditional risk factor, inflammatory marker level, susceptibility-weighted imaging Topic: StrokeThis is an open access article distributed under the terms of the Creative Commons AttributionNonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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“…These associations may be explained by increased vascular permeability giving rise to enlarged PVS, and arteriolosclerosis is mainly involved in hypertensive vasculopathy resulting in deep CMBs, which are closely associated with elevated CRP levels 37 38. Our failure to confirm these associations, on the one hand, may be because our cohort included a relatively young population with a low prevalence of CMBs (10.31%), while studies describing associations have reported an estimated prevalence of approximately 20%–25%29 39; on the other hand, the hypothetical causes of CMBs also include both cerebral amyloid angiopathy and arteriolosclerosis, whereas lacunes mainly relate to arteriolosclerosis. The contribution of acute or chronic inflammation to these two pathological processes is still to be clarified 40.…”

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