Estimated Pulse-Wave Velocity and Magnetic Resonance Imaging Markers of Cerebral Small-Vessel Disease in the NOMAS.

BACKGROUND: Pulse-wave velocity is a measure of arterial stiffness and a risk factor for cardiovascular disease. Recently, an estimated pulse-wave velocity (ePWV) was introduced that was predictive of increased risk of cardiovascular disease. Our objective was to determine whether ePWV was associated with cerebral small-vessel disease on magnetic resonance imaging. METHODS AND RESULTS: We included 1257 participants from the NOMAS (Northern Manhattan Study). The ePWV values were calculated using a nonlinear function of age and mean arterial blood pressure. The association between ePWV and white matter hyperintensity volume was assessed. Modification by race and ethnicity was evaluated. Associations between ePWV and other cerebral small-vessel disease markers, covert brain infarcts, cerebral microbleeds, and enlarged perivascular spaces, were explored as secondary outcomes. Mean±SD age of the cohort was 64±8 years; 61% were women; 18% self-identified as non-Hispanic Black, 67% as Hispanic, and 15% as non-Hispanic White individuals. Mean±SD ePWV was 11±2 m/s in the total NOMAS population and was similar across race and ethnic groups. The ePWV was significantly associated with white matter hyperintensity volume (ß=0.23 [95% CI, 0.20-0.26]) after adjustment. Race and ethnicity modified the association between ePWV and white matter hyperintensity volume, with stronger associations in Hispanic and non-Hispanic Black individuals. Significant associations were found between ePWV and covert brain infarcts, cerebral microbleeds, and perivascular spaces after adjustment. CONCLUSIONS: The ePWV function may provide a vascular mechanism for deleterious cerebrovascular outcomes in individuals with cerebral small-vessel disease and is particularly apparent in the racial and ethnic minorities represented in the NOMAS cohort.

The neuropathological landscape of small vessel disease and Lewy pathology in a cohort of Hispanic and non-Hispanic White decedents with Alzheimer disease.

Cerebrovascular and α-synuclein pathologies are frequently observed alongside Alzheimer disease (AD). The heterogeneity of AD necessitates comprehensive approaches to postmortem studies, including the representation of historically underrepresented ethnic groups. In this cohort study, we evaluated small vessel disease pathologies and α-synuclein deposits among Hispanic decedents (HD, n = 92) and non-Hispanic White decedents (NHWD, n = 184) from three Alzheimer's Disease Research Centers: Columbia University, University of California San Diego, and University of California Davis. The study included cases with a pathological diagnosis of Intermediate/High AD based on the National Institute on Aging- Alzheimer's Association (NIA-AA) and/or NIA-Reagan criteria. A 2:1 random comparison sample of NHWD was frequency-balanced and matched with HD by age and sex. An expert blinded to demographics and center origin evaluated arteriolosclerosis, cerebral amyloid angiopathy (CAA), and Lewy bodies/Lewy neurites (LBs/LNs) with a semi-quantitative approach using established criteria. There were many similarities and a few differences among groups. HD showed more severe Vonsattel grading of CAA in the cerebellum (p = 0.04), higher CAA density in the posterior hippocampus and cerebellum (ps = 0.01), and increased LBs/LNs density in the frontal (p = 0.01) and temporal cortices (p = 0.03), as determined by Wilcoxon's test. Ordinal logistic regression adjusting for age, sex, and center confirmed these findings except for LBs/LNs in the temporal cortex. Results indicate HD with AD exhibit greater CAA and α-synuclein burdens in select neuroanatomic regions when compared to age- and sex-matched NHWD with AD. These findings aid in the generalizability of concurrent arteriolosclerosis, CAA, and LBs/LNs topography and severity within the setting of pathologically confirmed AD, particularly in persons of Hispanic descent, showing many similarities and a few differences to those of NHW descent and providing insights into precision medicine approaches.

Contribution of Racial and Ethnic Differences in Cerebral Small Vessel Disease Subtype and Burden to Risk of Cerebral Hemorrhage Recurrence.

OBJECTIVE: Black and Hispanic survivors of intracerebral hemorrhage (ICH) are at higher risk of recurrent intracranial bleeding. MRI-based markers of chronic cerebral small vessel disease (CSVD) are consistently associated with recurrent ICH. We therefore sought to investigate whether racial/ethnic differences in MRI-defined CSVD subtype and severity contribute to disparities in ICH recurrence risk. METHODS: We analyzed data from the Massachusetts General Hospital ICH study (n = 593) and the Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) study (n = 329). Using CSVD markers derived from MRIs obtained within 90 days of index ICH, we classified ICH cases as cerebral amyloid angiopathy (CAA)-related, hypertensive arteriopathy (HTNA)-related, and mixed etiology. We quantified CSVD burden using validated global, CAA-specific, and HTNA-specific scores. We compared CSVD subtype and severity among White, Black, and Hispanic ICH survivors and investigated its association with ICH recurrence risk. RESULTS: We analyzed data for 922 ICH survivors (655 White, 130 Black, 137 Hispanic). Minority ICH survivors had greater global CSVD (p = 0.011) and HTNA burden (p = 0.021) on MRI. Furthermore, minority survivors of HTNA-related and mixed-etiology ICH demonstrated higher HTNA burden, resulting in increased ICH recurrence risk (all p < 0.05). CONCLUSIONS: We uncovered significant differences in CSVD subtypes and severity among White and minority survivors of primary ICH, with direct implication for known disparities in ICH recurrence risk. Future studies of racial/ethnic disparities in ICH outcomes will benefit from including detailed MRI-based assessment of CSVD subtypes and severity and investigating social determinants of health.

Association Between the Angiotensin-Converting Enzyme I/D Polymorphism and Risk of Cerebral Small Vessel Disease: A Meta-Analysis Based on 7186 Subjects.

INTRODUCTION: Cerebral small vessel disease (CSVD) causes a quarter of all strokes and is the most common pathology underlying vascular dementia. However, the mechanism of CSVD remains unclear. Numerous studies have investigated whether the angiotensin-converting enzyme (ACE) intersection/deletion (I/D) polymorphism influences the risk of CSVD, but the results are controversial. METHODS: We searched English and Chinese databases and calculated the odds ratio (OR) and 95% confidence interval (CI) to examine the existence of genetic associations between the ACE I/D polymorphism and the risk of CSVD. All relevant studies were screened and meta-analyzed using Review Manager 5.4. RESULTS: A total of 27 studies involving 7,186 subjects were identified for the meta-analysis. The results of five genetic models showed a significantly increased risk of CSVD (allelic, OR=1.30; recessive, OR=1.41; dominant, OR=1.34; homozygous, OR=1.55 and heterozygous OR=1.22) in the overall analysis. Furthermore, in subgroup analysis, increased CSVD risks were also observed in Asian and Caucasian populations. We also found no relationship between ACE I/D and leukoaraiosis (LA) in patients with lacunar infarction (LI). CONCLUSION: The ACE I/D polymorphism was positively associated with CSVD in both populations. However, this polymorphism did not increase the risk of LA in LI patients.

Chronic Kidney Disease as Risk Factor for Enlarged Perivascular Spaces in Patients With Stroke and Relation to Racial Group.

BACKGROUND AND PURPOSE: Enlarged perivascular spaces (EPVS) are considered subclinical markers of small vessel disease, associated with increased risk of stroke and dementia. Increasing evidence links chronic kidney disease (CKD) to small vessel disease. We explored the relationship between CKD and EPVS burden and the influence of racial group in this relation. METHODS: Consecutive patients with stroke who underwent brain magnetic resonance imaging were included (n=894). Racial group was categorized as White, Black, or other (other racial groups). CKD was defined by glomerular filtration rate <60 mL/minute per 1.73 m2 for >3 months. EPVS were rated following a standardized method, dichotomized for analyses (mild [<20] versus severe [≥20]), and stratified by brain region (basal ganglia and centrum semiovale). RESULTS: In multivariable-adjusted analysis, the association of CKD with severe EPVS varied across racial groups. Comparing patients with and without CKD within racial groups, we found that Whites with CKD had higher odds of severe centrum semiovale EPVS (odds ratio [OR], 2.41 [95% CI, 0.98-5.88]). Among patients with CKD, Black patients had higher odds of severe EPVS in the basal ganglia and centrum semiovale compared with Whites (OR, 1.93 [95% CI, 1.18-3.16] and OR, 1.90 [95% CI, 1.16-3.11], respectively) and other racial groups (OR, 2.03 [95% CI, 1.23-3.36] and OR, 2.02 [95% CI, 1.22-3.34], respectively). CONCLUSIONS: CKD was more prevalent in our sample of patients with stroke with severe EPVS in the centrum semiovale. The relation differed when stratified by racial group and brain topography. Further studies are needed to confirm that CKD may relate differently to subclinical measures of small vessel disease according to race.

Vascular Cellular Adhesion Molecule-1 (VCAM-1) and Memory Impairment in African-Americans after Small Vessel-Type Stroke.

BACKGROUND: African-Americans (AA) are 3 times more likely to have small-vessel-type ischemic strokes (SVS) than Whites. Small vessel strokes are associated with cognitive impairment, a relationship incompletely explained by white matter hyperintensity (WMH) burden. We examined whether inflammatory/endothelial dysfunction biomarkers are associated with cognition after SVS in AAs. METHODS: Biomarkers were obtained in 24 subjects (median age 56.5 years, 54% women, median 12 years education). Cognition was assessed more than 6 weeks poststroke using the memory composite score (MCS), which was generated using recall from the Hopkins Verbal Learning Test-II and Brief Visuospatial Memory Test-Revised. A semi-automated, volumetric protocol was used to quantify WMH volume (WMHv) on clinical MRI scans. Potential biomarkers including vascular cell adhesion molecule-1 (VCAM-1), interleukin-1 receptor antagonist, interleukin-6, interleukin-8, interleukin-10, interferon gamma, and thrombin-antithrombin (TAT) were log-transformed and correlated with MCS with adjustment for potential confounders. RESULTS: Among serum biomarkers, only VCAM-1-correlated with poorer memory based on the MCS (r = -.659; P = .0006). VCAM-1 (r = .554; P = .005) and age (r = .479; P = .018) correlated with WMHv; VCAM-1 was independently associated with MCS after adjustment for WMHv, age, and education (P = .023). CONCLUSIONS: The findings of this exploratory analysis suggest that endothelial dysfunction and inflammation as reflected by VCAM-1 levels may play a role in poststroke cognitive impairment. Additional studies are needed to validate this observation and to evaluate this relationship in non-AAs and with other stroke types and compare this finding to cognitive impairment in nonstroke populations.

Age-Specific Associations of Renal Impairment and Cerebral Small Vessel Disease Burden in Chinese with Ischaemic Stroke.

BACKGROUND: Recent studies in Caucasians with transient ischaemic attack or ischaemic stroke have demonstrated significant age-specific associations between cerebral small vessel disease (SVD) burden on magnetic resonance imaging and renal impairment. We aimed to validate these findings in a large cohort of Chinese with ischaemic stroke. METHODS: In 959 Chinese with ischaemic stroke who received a brain magnetic resonance imaging at the University of Hong Kong, we determined the age-specific associations of renal impairment (glomerular filtration rate < 60 mL/min/1.73 m2) with neuroimaging markers of SVD as well as with the SVD score. RESULTS: Although renal impairment was associated with the SVD score in univariate analysis in all patients (odds ratio 1.61, 95% confidence interval 1.24-2.09, P < .0001), these associations were attenuated after adjusting for age and sex (P = .38). Similar findings were noted in patients with ischaemic stroke due to SVD and non-SVD subtypes. However, in 222 of 959 patients aged <60, renal impairment was independently associated with an increasing microbleed (adjusted odds ratio 6.82, 2.26-20.59), subcortical (4.97, 1.62-15.24) periventricular white matter hyperintensity (3.96, 1.08-14.51) and global SVD burden (3.41, 1.16-10.04; all P < .05) even after adjusting for age, sex, and vascular risk factors. Nevertheless, there were no associations between renal impairment and individual neuroimaging markers of SVD nor with the SVD score in patients aged ≥60 after adjusting for age and sex (all P > .05). CONCLUSIONS: In Chinese with ischaemic stroke, renal impairment was independently associated with microbleed, white matter hyperintensity and global SVD burden in individuals aged <60, but not in those aged ≥60, suggesting that there may be shared susceptibilities to premature systemic disease.

Distribution and Temporal Trends From 1993 to 2015 of Ischemic Stroke Subtypes: A Systematic Review and Meta-Analysis.

BACKGROUND AND PURPOSE: Preventive strategies, together with demographic and socioeconomic changes, might have modified the worldwide distribution of ischemic stroke (IS) subtypes. We investigated those changes by means of a systematic review and meta-analysis. METHODS: We evaluated all population- and hospital-based studies reporting the distribution of IS etiologic subtypes according to the TOAST criteria (Trial of ORG 10172 in Acute Stroke Treatment). Studies were identified by searching articles indexed on PubMed and Scopus from January 1, 1993, to June 30, 2017. Two independent investigators extracted data and checked them for accuracy. Proportions of each etiologic subtype were pooled according to a random effect meta-analytic model weighted by study size; temporal trends were assessed using a mixed-effect meta-regression model. RESULTS: Sixty-five studies including patients from 1993 to 2015 were finally included. Overall, ISs were attributed to cardioembolism (22%; 95% confidence interval [CI], 20-23); large artery atherosclerosis (23%; 95% CI, 21-25); small artery occlusion (22%; 95% CI, 21-24); other determined cause (3%; 95% CI, 3-3); and undetermined cause (26%; 95% CI, 24-28). Cardioembolism was the leading IS etiologic subtype in whites (28%; 95% CI, 26-29) and large artery atherosclerosis in Asians (33%; 95% CI, 31-36). Meta-regression showed an increasing temporal trend for cardioembolism in whites (2.4% annually, P=0.008) and large artery atherosclerosis in Asians (5.7% annually, P<0.001), and a decrease for small artery occlusion in whites (-4.7% annually, P=0.001); there was considerable heterogeneity across all the analyses. CONCLUSIONS: According to our systematic review and meta-analysis, cardioembolism in whites and large artery atherosclerosis in Asians are the leading causes of IS. The heterogeneous distribution of etiologic subtypes of IS may depend on the demographic and socioeconomic characteristics of the different populations. More extensive protocols should be adopted to reduce the persistently relevant proportion of undetermined cause IS.

Correlation of Plasma Vascular Endothelial Growth Factor and Endostatin Levels with Symptomatic Intra- and Extracranial Atherosclerotic Stenosis in a Chinese Han Population.

BACKGROUND: Symptomatic intracranial atherosclerotic stenosis (ICAS) and extracranial atherosclerotic stenosis (ECAS) are different in many aspects. Here, we explored the association between the location or severity of atherosclerotic stenosis and pro- or antiangiogenic factors, specifically vascular endothelial growth factor (VEGF) and endostatin (ES). METHODS: We evaluated 198 consecutive patients with acute ischemia stroke: 132 with large-artery atherosclerosis (LAA) and 66 with small-artery occlusion (small-vessel occlusion). The LAA group was subclassified into 102 patients with ICAS and 30 with ECAS. Independent associations of VEGF, ES levels, and VEGF/ES ratio with the location of cerebral stenosis and the severity or short-term prognosis (14th day modified Rankin Scale) of ICAS were evaluated. RESULTS: Plasma concentrations of VEGF and ES were lower (P < .05) in ICAS (38.07, 32.76-46.28 pg/mL and 58.95, 55.04-59.77 ng/mL) than those in ECAS (45.00, 34.30-83.34 pg/mL and 140.74, 85.63-231.21 ng/mL). Logistic regression analysis showed that VEGF concentrations and dyslipidemia were independently associated with ICAS, with odds ratios of .987 [95% CI = (.976, .998)] and .265 [95% CI = (.103, .792)], respectively. Moreover, plasmatic VEGF levels increased gradually along with the severity of ICAS (P = .003), and lower levels of ES (P = .040) or a higher VEGF/ES ratio (P = .048) were related to unfavorable short-term prognosis of ICAS. CONCLUSION: Lower VEGF levels are associated with the presence of symptomatic ICAS, but not with ECAS. Furthermore, the severity of ICAS is positively correlated with the levels of VEGF, and lower ES levels or a predominance of VEGF over ES are predictors of poor short-term prognosis of ICAS.

Serum Lipid Fractions and Cerebral Microbleeds in a Healthy Japanese Population.

BACKGROUND: Cerebral microbleeds (CMBs) are associated with focal hemosiderin deposits and represent a form of cerebral small vessel disease. To date, indefinite and inconsistent reports are available regarding the association between serum lipid fractions and CMBs. In addition, these previous studies did not include Asian populations, who may have a higher risk of cerebral hemorrhage. The purpose of this study was to examine the associations between serum lipid fractions and CMBs in healthy Japanese subjects. METHODS: We performed a cross-sectional study involving 4,024 neurologically normal Japanese subjects (mean age 61.6 years). All the participants underwent 1.5-Tesla magnetic resonance imaging scan, and CMBs were classified into 3 groups based on their locations. The concentrations of lipid fractions were categorized into quartiles and the association between the lipid fractions and CMBs were investigated using logistic regression analysis. RESULTS: CMBs were observed in 164 (4.1%) of participants. Of these participants with CMBs, 33 (20.1%) had lobar CMBs and 91 (55.5%) had deep CMBs. Subjects with deep CMBs had lower total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) levels. After adjusting for confounding factors, lower TC and HDL-C levels were still associated with the presence of deep CMBs (OR for the highest vs. the lowest quartiles of TC and HDL-C was 2.28 [95% CI 1.05-4.94], and 1.93 [95% CI 1.02-3.65], respectively). The presence of subcortical infarcts and periventricular hyperintensities was more frequently observed in deep CMBs, whereas white matter hyperintensities were more frequently observed in lobar CMBs. CONCLUSIONS: Our results suggest that low serum TC and HDL-C levels are closely associated with deep CMBs.

Hypertensive retinopathy and cerebral small vessel disease in Amerindians living in rural Ecuador: The Atahualpa Project.

BACKGROUND: Diagnosis of cerebral small vessel disease (SVD) is a challenge in remote areas where MRI is not available. Hypertensive retinopathy (HTRP) has shown to correlate with SVD in different ethnic groups, but there is no information from indigenous Latin American people. We assessed the usefulness of retinal photographs to detect cases with SVD among Amerindians living in rural Ecuador. METHODS: Atahualpa residents aged ≥60years with arterial hypertension or prehypertension were identified during a door-to-door survey. A confocal line scanning laser ophthalmoscope was used to identify and grade HTRP (according to the Keith-Wagener-Barker classification). MRIs were read with attention to the presence of white matter hyperintensities (WMH) of presumed vascular origin and lacunar infarcts. Using logistic regression models, we evaluated whether HTRP was independently associated with neuroimaging signatures of SVD. RESULTS: Of 323 eligible candidates, 241 (75%) were enrolled. MRI readings revealed moderate-to-severe WMH in 49 (20%) cases and lacunar infarcts in 29 (12%). HTRP Grade 1 was noticed in 90 (37%) individuals and Grade 2-3 in 42 (17%). After adjusting for demographics and cardiovascular risk factors, multivariate analyses showed a significant association between Grades 2-3 HTRP and moderate-to-severe WMH (OR: 3.87, 95% C.I.: 1.64-9.13) but not with lacunar infarcts (OR: 2.22, 95% C.I.: 0.83-5.92). CONCLUSION: Amerindians with HTRP Grades 2-3 are almost four times more likely to have SVD-related subcortical damage than those with no- or only Grade 1-HTRP. Retinal photographs might allow recognition of people who need further investigation and therapy.

Update on cerebral small vessel disease: a dynamic whole-brain disease.

Cerebral small vessel disease (CSVD) is a very common neurological disease in older people. It causes stroke and dementia, mood disturbance and gait problems. Since it is difficult to visualise CSVD pathologies in vivo, the diagnosis of CSVD has relied on imaging findings including white matter hyperintensities, lacunar ischaemic stroke, lacunes, microbleeds, visible perivascular spaces and many haemorrhagic strokes. However, variations in the use of definition and terms of these features have probably caused confusion and difficulties in interpreting results of previous studies. A standardised use of terms should be encouraged in CSVD research. These CSVD features have long been regarded as different lesions, but emerging evidence has indicated that they might share some common intrinsic microvascular pathologies and therefore, owing to its diffuse nature, CSVD should be regarded as a 'whole-brain disease'. Single antiplatelet (for acute lacunar ischaemic stroke) and management of traditional risk factors still remain the most important therapeutic and preventive approach, due to limited understanding of pathophysiology in CSVD. Increasing evidence suggests that new studies should consider drugs that target endothelium and blood-brain barrier to prevent and treat CSVD. Epidemiology of CSVD might differ in Asian compared with Western populations (where most results and guidelines about CSVD and stroke originate), but more community-based data and clear stratification of stroke types are required to address this.

Population-Based Study of Cerebral Microbleeds in Stroke-Free Older Adults Living in Rural Ecuador: The Atahualpa Project.

BACKGROUND AND PURPOSE: Prevalence of cerebral microbleeds (CMB) in white and Asian populations range from 4% to 15%. However, there is no information from indigenous Latin American people. We aimed to assess prevalence and cerebrovascular correlates of CMB in stroke-free older adults living in rural Ecuador. METHODS: Of 311 Atahualpa residents aged ≥60 years identified during a door-to-door survey, 258 (83%) underwent brain magnetic resonance imaging. Twenty-one were further excluded for a diagnosis of overt stroke. Using multivariate logistic regression models, adjusted for demographics and cardiovascular risk factors, we evaluated whether CMB were independently associated with silent strokes, white matter hyperintensities, and global cortical atrophy. RESULTS: Twenty-six (11%) of 237 participants had CMB, which were single in 54% of cases. CMB were deep in 11 patients, cortical in 9, and located both deep and cortical in 6. In univariate analyses, CMB were associated with age, systolic blood pressure, moderate-to-severe white matter hyperintensities, silent lacunar infarcts, and cortical atrophy. Mean (±SD) values for systolic blood pressure were 155±27 mm Hg in patients who had CMB versus 142±26 mm Hg in those who did not (P=0.017). In the adjusted models, moderate-to-severe white matter hyperintensities (P=0.009), silent lacunar infarcts (P=0.003), and global cortical atrophy (P=0.04) were independently associated with CMB. CONCLUSIONS: Prevalence of CMB in stroke-free older adults living in Atahualpa is comparable with those reported from other ethnic groups. There is a strong relationship between CMB and increased age, high systolic blood pressure, silent markers of cerebral small vessel disease, and cortical atrophy.

Poor sleep quality and silent markers of cerebral small vessel disease: a population-based study in community-dwelling older adults (The Atahualpa Project).

BACKGROUND/OBJECTIVES: Evidence of a relationship between non-breathing-related sleep symptoms and silent markers of cerebral small vessel disease (SVD) is scarce. The present study aimed to evaluate this association in older people living in rural Ecuador, where the burden of stroke is on the rise. METHODS: A group of Atahualpa residents, aged ≥60 years, were interviewed with a validated Spanish version of the Pittsburgh Sleep Quality Index, and underwent magnetic resonance imaging (MRI) for identification of silent markers of SVD. Using multinomial logistic regression analysis, after adjusting for demographics and cardiovascular health status, it was evaluated whether sleep quality is associated with the severity of white matter hyperintensity (WMH), lacunar infarcts, and deep microbleeds. RESULTS: Out of 311 people aged ≥60 years, 237 (76%) were enrolled into the study. Mean age was 70 ± 8 years, 59% were women, 83% had primary school education only, and 73% had a poor cardiovascular health status. Seventy-eight (33%) had poor sleep quality. The MRI showed: WMH in 154 (65%) participants (moderate-to-severe in 52); silent lacunar infarcts in 28 (12%); and deep microbleeds in 17 (7%). Poor sleep quality was associated with WMH presence (OR 2.44, 95% CI 1.26 to 4.71, p = 0.008) and severity (ß coefficient 0.77, SE 0.37, p = 0.037), but not with silent lacunar infarcts or deep microbleeds. CONCLUSIONS: The present study showed an association between poor sleep quality and WMH severity. Further longitudinal studies would help to elucidate the cause and effect of this relationship.

Race-ethnicity and cerebral small vessel disease--comparison between Chinese and White populations.

BACKGROUND AND AIM: Studies in stroke patients suggest that lacunar stroke and intracerebral hemorrhage might be more common in Chinese than Whites. We hypothesized that other manifestations of subclinical cerebral small vessel disease, namely white matter hyperintensities (WMH), lacunes, and microbleeds, are also more common in Chinese than Whites. We compared the community prevalence of these lesions between Han Chinese and White Australians. METHODS: Magnetic resonance imaging (1·5-Tesla) was performed on participants of the Shanghai Aging Study (n = 321, mean age 69 ± 6 years) and Tasmanian Study of Cognition and Gait (n = 397, mean age 72 ± 7 years). A single-rater recorded measures of WMH, lacunes, and microbleeds. We compared lesion prevalence between age- and gender-matched subgroups from the two cohorts. Among all subjects (n = 718), we performed multivariable logistic regression to examine if race-ethnicity was independently associated with these lesions. RESULTS: Among age- and gender-matched subjects, confluent WMH were significantly more prevalent in Chinese (38·5%) than Whites (28·4%; P = 0·01). There was no difference in the prevalence of lacunes (Chinese 29·1% vs. Whites 29·5%, P = 0·93) and microbleeds (Chinese 10·1% vs. 9·0%, P = 0·67) between Chinese and Whites. In multivariable logistic regression, Chinese ethnicity was associated with confluent WMH (odds ratio 1·7, 95% confidence interval 1·1-2·6, P = 0·01), but no differences were seen for lacunes and microbleeds. The association between Chinese ethnicity with confluent WMH became insignificant when subjects with history of stroke were excluded. CONCLUSIONS: In this population-based cross-national comparison, Han Chinese had a higher prevalence of confluent WMH than White Australians, but had a similar prevalence of lacunes and microbleeds.