Association between cerebral microbleeds and prior primary intracerebral hemorrhage in ischemic stroke patients

Chen, Ying‐Fa; Chang, Yung‐Yee; Liu, Jiashou; Lui, Chun‐Chung; Kao, Yi-Fen; Lan, Min‐Yu

doi:10.1016/j.clineuro.2008.06.003

Cited by 16 publications

(10 citation statements)

References 16 publications

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“…1–3 Although CMB in different locations have the same MRI appearance, CMB in lobar regions are generally attributed to cerebral amyloid angiopathy (CAA) and those in deep regions to hypertensive vasculopathy. 4, 5 Recent studies suggest an association of inflammation to both CAA and hypertension affecting the cerebral vessels.…”

Section: Introductionmentioning

confidence: 99%

Lipoprotein Phospholipase A2 and Cerebral Microbleeds in the Framingham Heart Study

Romero

Preis

Beiser

et al. 2012

Stroke

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Background and Purpose Cerebral microbleeds (CMBs) due to cerebral amyloid angiopathy generally occur in lobar regions, while those due to hypertensive vasculopathy are deep. Inflammation may be an underlying mechanism for CMB, with varying associations according to CMB location. Lipoprotein phospholipase-A2 (Lp-PLA2) is a circulating enzyme marker of vascular inflammation associated with risk of ischemic stroke and dementia. We hypothesized that higher Lp-PLA2 levels would be related to higher prevalence of CMBs, with possible regional specificity. Methods Framingham Offspring participants aged ≥65 years with available Lp-PLA2 measures and brain MRI were included. Logistic regression models were used to relate Lp-PLA2 activity and mass to presence of CMBs, adjusted for age, sex, medication use (aspirin, anticoagulants, and statins), systolic blood pressure, APOE, current smoking, and diabetes. Results 819 participants (mean age 73 years; 53% women) were included; 106 (13%) had CMBs; 82 (10%) lobar and 27 (3%) deep. We did not observe significant associations of CMB and LpPLA2 measures in multivariable adjusted analyses. However, there was a significant interaction between APOE genotype and Lp-PLA2 activity in their relation to presence of deep CMBs (p-interaction=0.01). Among persons with APOE ε3/ε3, the OR for deep CMB was 0.95 [0.59–1.53; p=0.83], while among those with at least one ε2 or ε4 allele, OR=3.46 [1.43–8.36; p=0.006]. Conclusions In our community-based sample of older adults, there was no significant association of Lp-PLA2 with total or lobar CMBs. The association of higher levels of Lp-PLA2 activity with deep CMBs among those with at least one APOE ε2 or ε4 allele merits replication.

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Section: Introductionmentioning

confidence: 99%

Lipoprotein Phospholipase A2 and Cerebral Microbleeds in the Framingham Heart Study

Romero

Preis

Beiser

et al. 2012

Stroke

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“…Much of the recent attention T2*-weighted MRI scans have garnered centers around their ability to detect small areas of heme deposition (so called “microbleeds”) as well as their use as a marker of secondary damage after stroke [7-9]. These sequences have not been studied as a tool to measure changes in the brain surrounding ICH, however.…”

Section: Resultsmentioning

confidence: 99%

T2* Magnetic Resonance Imaging Sequences Reflect Brain Tissue Iron Deposition Following Intracerebral Hemorrhage

Hua

et al. 2010

Transl. Stroke Res.

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Background and Purpose To examine the utility of magnetic resonance imaging (MRI) T2* sequences as a measure of iron overload in the brain following intracerebral hemorrhage (ICH). Methods We examined the time course of T2* changes in the brain around intracerebral hemorrhages in a series of patients. We also performed a series of experiments in an animal model of ICH, examining the time course of T2* changes along with correlation of these changes with histological markers of ferric iron deposition. Results We found that T2* changes in the brain occur with increasing intensity and spatial distribution over a three month period. Experimental ICH in the rat model induces similar changes, and these changes correlate tightly with histological markers of ferric iron deposition. Conclusions MRI T2* changes after ICH can be used to measure the degree of iron overload in the brain. The T2* sequence may be useful as a measure of interventions aimed at reducing ICH-related brain injury by reducing iron deposition.

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“…Cerebral microbleeds (CMBs) detected using brain MRI are emerging as a marker to allow identification of individuals at risk of dementia in the preclinical stages of disease. (Akoudad et al, 2016) CMB are associated with stroke,(Charidimou et al, 2013, Chen et al, 2008, Fan et al, 2003, Wardlaw et al, 2006) poor cognition(Charidimou and Werring, 2012, Cordonnier et al, 2006, Poels et al, 2012, Werring et al, 2004, Yakushiji et al, 2008) and mortality risk. (Akoudad et al, 2013, Benedictus et al, 2015) CMBs represent the most common forms of hemorrhage-prone cerebral small vessel disease in the elderly and in persons with dementia: hypertensive arteriopathy and/or cerebral amyloid angiopathy based on their brain location.…”

Section: Introductionmentioning

confidence: 99%

Cerebral microbleeds and risk of incident dementia: the Framingham Heart Study

Romero

Beiser

Himali

et al. 2017

Neurobiology of Aging

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Cerebral microbleeds (CMB) are MRI markers attributed to the most common cerebral angiopathies in the elderly and in patients with dementia: hypertensive and cerebral amyloid angiopathy (CAA). CMB detection in asymptomatic persons may help identify those at risk for dementia, and may influence preventive strategies and design of clinical trials testing treatments for dementia. We studied the association of CMB with risk of incident dementia in community dwelling individuals. 1296 dementia-free Framingham Heart Study participants (mean age 72years; 54% women) with available brain MRI and incident dementia data during a mean follow-up period of 6.7 years were included. Using Cox-proportional hazards models we related CMB presence to incident dementia. Multivariable models were adjusted for age, sex, APOE status, and education, with additional models adjusting for vascular risk factors and MRI markers of ischemic brain injury. CMB were observed in 10.8% and incident dementia in 85 participants (6.6% over study period). Participants with any CMB had 1.74 times higher risk of dementia (HR 1.74, 95% CI 1.00–3.01), while those with deep and mixed CMB had a three-fold increased risk (HR 2.99, 95% CI 1.52–5.90). The associations were independent of vascular risk factors, and for deep and mixed CMB also independent of MRI markers of ischemia (HR 2.44, 95% CI 1.22–4.88). Purely lobar CMB were not associated with incident dementia. Our findings support a role for hypertensive vasculopathy and the interplay of hypertensive and CAA in risk of dementia, and suggest that CMB presence can identify individuals at risk of dementia.

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Association between cerebral microbleeds and prior primary intracerebral hemorrhage in ischemic stroke patients

Cited by 16 publications

References 16 publications

Lipoprotein Phospholipase A2 and Cerebral Microbleeds in the Framingham Heart Study

Lipoprotein Phospholipase A2 and Cerebral Microbleeds in the Framingham Heart Study

T2* Magnetic Resonance Imaging Sequences Reflect Brain Tissue Iron Deposition Following Intracerebral Hemorrhage

Cerebral microbleeds and risk of incident dementia: the Framingham Heart Study

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