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MRI Cerebral White Matter Lesions and Paraoxonase PON1 Polymorphisms : Three-Year Follow-Up of the Austrian Stroke Prevention Study
- Reinhold Schmidt,
- Helena Schmidt,
- Franz Fazekas,
- Peter Kapeller,
- Gudrun Roob,
- Anita Lechner,
- Gert M. Kostner and
- Hans-Peter Hartung
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 20, Issue 71 July 2000

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Abstract—White matter lesions (WMLs) on magnetic resonance imaging (MRI) scans of older persons are thought to be caused by cerebral small-vessel disease. As they progress, these brain abnormalities frequently result in cognitive decline and gait disturbances, and their predictors are incompletely understood. Genetic risk factors have been implicated but remain undetermined so far. We examined whether 2 common polymorphisms of the paraoxonase (PON1) gene leading to a methionine (M allele)–leucine (L allele) interchange at position 54 and an arginine (B allele)–glutamine (A allele) interchange at position 191 are associated with the presence and progression of WMLs. We studied 264 community-dwelling subjects without neuropsychiatric disease (ages 44 to 75 years). All underwent vascular risk factor assessment, brain MRI, and PON1 genotyping. MRI scanning was repeated after 3 years. The extent and number of WMLs were recorded by 3 independent readers. Progression of WMLs was assessed by direct scan comparison. The final rating relied on the majority judgment of the 3 readers. The LL, LM, and MM genotypes were noted in 111 (42.0%), 118 (44.7%), and 35 (13.3%) subjects, respectively; the AA,AB, and BB genotypes occurred in 146 (55.3%), 98 (37.1%), and 20 (7.8%) individuals, respectively. Carriers of the LL genotype showed a nonsignificant trend toward more extensive WMLs and more frequently demonstrated lesion progression over the 3-year observation period (P=0.03). The polymorphism at position 191 had no effect. Logistic regression analysis yielded age (odds ratio, 1.08/y), diastolic blood pressure (odds ratio, 1.05/mm Hg), and LL paraoxonase genotype (odds ratio, 2.65) to be significant predictors of WML progression. These data suggest that the LLPON1 genotype at position 54 influences the extent and progression of WMLs in elderly subjects.
C-Reactive Protein, Carotid Atherosclerosis, and Cerebral Small-Vessel Disease: Results of the Austrian Stroke Prevention Study
- Reinhold Schmidt,
- Helena Schmidt,
- Martin Pichler,
- Christian Enzinger,
- Katja Petrovic,
- Kurt Niederkorn,
- Susanna Horner,
- Stefan Ropele,
- Norbert Watzinger,
- Martin Schumacher,
- Andrea Berghold,
- Gerhard M. Kostner and
- Franz Fazekas
Stroke Volume 37, Issue 121 December 2006

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Background and Purpose— C-reactive protein (CRP) is an inflammatory marker known to be a risk factor for stroke. We examined the associations between CRP, carotid atherosclerosis, white matter lesions, and lacunes as manifestations of cerebral large- and small-vessel disease.Methods— In the community-based Austrian Stroke Prevention Study, CRP concentrations were measured by a highly sensitive assay in 700 participants at baseline. All underwent carotid duplex scanning, and a subset of 505 subjects underwent brain magnetic resonance imaging. Imaging was repeated after 3 and 6 years. We graded carotid atherosclerosis in both common and internal carotid arteries on a 5-point scale and calculated the sum of scores as an index of the severity of carotid atherosclerosis. The volume of white matter lesions and the number of lacunes were considered small vessel disease–related brain abnormalities.Results— After adjustment for vascular risk factors, the severity and progression of extracranial carotid atherosclerosis increased with increasing quintiles of CRP. Only study participants in the fourth and fifth quintile (>2.50 mg/L) had significantly more baseline atherosclerosis and greater progression when we used the first quintile (<0.80 mg/L) as a reference. No interactions were seen between CRP quintiles and vascular risk factors for carotid atherosclerosis. The associations between severity and progression of small vessel disease–related brain abnormalities and CRP were nonsignificant.Conclusions— We found evidence for differential effects of CRP in different beds of the arterial brain supply. CRP was a marker for active carotid atherosclerosis but not for small vessel disease–related brain lesions.
Renin-Angiotensin System Genetic Polymorphisms and Cerebral White Matter Lesions in Essential Hypertension
- Cristina Sierra,
- Antonio Coca,
- Elisenda Gómez-Angelats,
- Esteban Poch,
- Javier Sobrino and
- Alejandro de la Sierra
Hypertension Volume 39, Issue 21 February 2002

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It has been reported that both the DD genotype of the angiotensin converting enzyme (ACE) gene and the presence of cerebral white matter lesions (WML) may represent risk factors for the development of stroke. The present study investigates a possible association between 3 different genetic polymorphisms of the renin-angiotensin system and the presence of WML in 60 never-treated essential hypertensive patients (36 men, 24 women), aged 50 to 60 years, without clinical evidence of target organ damage. All patients underwent brain magnetic resonance imaging to establish the presence or absence of WML. The insertion/deletion (I/D) ACE gene, the M235T angiotensinogen (AGT) gene, and the A1166C angiotensin II type 1 receptor gene polymorphisms were determined by standard polymerase chain reaction. Twenty-five hypertensive patients (41.6%) were found to have WML on brain magnetic resonance imaging. No significant association between the M235T angiotensinogen or A1166C angiotensin II type 1 receptor genotypes and the presence of WML was found. However, the frequency of the DD genotype in patients with WML (64%) was significantly higher than that observed in patients without WML (28.6%; P=0.022). The DD genotype odds ratio for the presence of WML was 4.44 (95% confidence interval: 1.48 to 13.3). Likewise, the proportion of the D allele in patients with WML (74%) was significantly higher (P=0.014) than that observed in patients without WML (51.4%). We conclude that the presence of the DD genotype and/or the D allele of the ACE gene may be a predisposing factor for developing WML in essential hypertensive patients. However, because of the small sample size, these results require confirmation in a larger study.
Blood Pressure Components and Changes in Relation to White Matter Lesions: A 32-Year Prospective Population Study
- Xinxin Guo,
- Leonardo Pantoni,
- Michela Simoni,
- Calle Bengtsson,
- Cecilia Björkelund,
- Lauren Lissner,
- Deborah Gustafson and
- Ingmar Skoog
Hypertension Volume 54, Issue 11 July 2009

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This study aimed to examine the long-term effect of high blood pressure (systolic blood pressure, diastolic blood pressure, pulse pressure, and mean arterial pressure) on white matter lesions and to study changes in different blood pressure components in relation to white matter lesions. A representative population of women was examined in 1968 and re-examined in 1974, 1980, 1992, and 2000. The presence and severity of white matter lesions on computed tomography were rated by a visual rating scale in 1992 and 2000 in 539 women. Systolic and diastolic blood pressures were measured at all of the examinations. We found that presence and severity of white matter lesions in 1992/2000 were associated with higher diastolic blood pressure and mean arterial pressure at each examination but not with systolic blood pressure and pulse pressure. Odds ratios (95% CIs) for the presence of white matter lesions per 10-mm Hg increase in diastolic pressure were 1.4 (1.0 to 1.9) in 1968, 1.3 (1.0 to 1.8) in 1974, 1.4 (1.1 to 1.9) in 1980, and 1.3 (1.0 to 1.6) in 1992 after adjustment for confounders. The presence of white matter lesions was also associated with a 24-year increase in diastolic pressure (>10 mm Hg), systolic pressure (>40 mm Hg), pulse pressure (>24 mm Hg), and mean arterial pressure (>6 mm Hg; odds ratios [95% CIs]: 2.6 [1.3 to 5.1] for diastolic pressure; 2.0 [1.2 to 3.4] for systolic pressure; 1.8 [1.1 to 2.7] for pulse pressure; and 2.2 [1.4 to 3.4] for mean arterial pressure). Our findings suggest that lowering high diastolic blood pressure and preventing large increases in systolic and diastolic blood pressures may have a protective effect on white matter lesions.
Unrecognized Myocardial Infarction in Relation to Risk of Dementia and Cerebral Small Vessel Disease
- M. Arfan Ikram,
- Marieke van Oijen,
- Frank Jan de Jong,
- Jan A. Kors,
- Peter J. Koudstaal,
- Albert Hofman,
- Jacqueline C.M. Witteman and
- Monique M.B. Breteler
Stroke Volume 39, Issue 51 May 2008

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Background and Purpose— Men, but not women, with unrecognized myocardial infarction (MI) have an increased risk of cardiac events and stroke compared with those without MI or with recognized MI. We investigated whether unrecognized MI is also a risk factor for dementia and cerebral small vessel disease (white matter lesions and brain infarction) in 2 population-based cohort studies.Methods— In the Rotterdam Study, 6347 participants were classified at baseline (1990 to 1993) into those with recognized MI (subdivided into Q-wave and non-Q-wave MI), with unrecognized MI, and without MI based on electrocardiography and interview and were followed for incident dementia (n=613) until January 1, 2005. In the Rotterdam Scan Study, 436 nondemented persons were similarly classified based on electrocardiography and interview and underwent brain MRI for the assessment of white matter lesions and brain infarction.Results— In men, unrecognized MI was associated with an increased risk of dementia (compared with men without MI hazard ratio, 2.14; 95% CI, 1.37 to 3.35) and with more white matter lesions and more often brain infarction on MRI. In women, no associations were found with unrecognized MI. Recognized MI was not associated with the risk of dementia in either sex. Men, but not women, with recognized MI had more often any brain infarction or asymptomatic brain infarction, especially if they had Q-wave MI. No consistent associations were found between recognized Q-wave or non-Q-wave MI and severity of white matter lesions. Additional adjustment for cardiovascular risk factors did not change the results.Conclusions— Men with unrecognized MI have an increased risk of dementia and more cerebral small vessel disease.
Regional White Matter Pathology in Mild Cognitive Impairment: Differential Influence of Lesion Type on Neuropsychological Functioning
- Lisa Delano-Wood,
- Norm Abeles,
- Joshua M. Sacco,
- Christina E. Wierenga,
- Nikki R. Horne and
- Andrea Bozoki
Stroke Volume 39, Issue 31 March 2008

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Background and Purpose— Associations between regional white matter lesion pathology and neuropsychological performance across the aging spectrum are not well understood and, to date, research has been largely contradictory and inconclusive. The current study set out to clarify some of the inconsistencies in the literature by relating volumetric analyses of white matter lesions (deep white matter lesions and periventricular lesions) to neuropsychological performance in a large clinical sample of older adults diagnosed with mild cognitive impairment.Methods— Seventy older adults with mild cognitive impairment were administered a comprehensive neuropsychological battery. White matter lesions identified on T2-weighted FLAIR images were quantified using a semi-automated volumetric approach (pixel thresholding).Results— Results showed that, in contrast to performance on memory and naming tasks, total white matter lesions strongly predicted executive impairments, slowed processing speed, and visuospatial/construction difficulties. In addition, separate regression analyses demonstrated that results were primarily accounted for by deep white matter lesions (but not periventricular lesions), most likely due to frontal-subcortical circuitry disruption. Moreover, deep white matter lesions, but not periventricular lesions, significantly predicted overall poorer neuropsychological functioning after controlling for age, education, and level of depression.Conclusions— Taken together, findings demonstrate a differential influence of lesion type on cognitive impairment in mild cognitive impairment and implicate deep white matter lesions as being most detrimental in terms of neuropsychological functioning. Clinical, theoretical, and methodological implications of these results are discussed.
Progression of Cerebral Small Vessel Disease in Relation to Risk Factors and Cognitive Consequences: Rotterdam Scan Study
- Ewoud J. van Dijk,
- Niels D. Prins,
- Henri A. Vrooman,
- Albert Hofman,
- Peter J. Koudstaal and
- Monique M.B. Breteler
Stroke Volume 39, Issue 101 October 2008

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Background and Purpose— Cerebral white matter lesions and lacunar infarcts are small vessel disease-related lesions, which are associated with cognitive decline and dementia. We aimed to assess the relationship between risk factors, effect modifiers, and progression of these lesions. Furthermore, we studied the cognitive consequences of lesion progression.Methods— Six hundred sixty-eight people, aged 60 to 90 years, underwent repeated MRI scanning and neuropsychological testing within 3-year follow-up. We rated incident lacunar infarcts and change in periventricular and subcortical white matter lesion severity with a semiquantitative scale. We assessed the relationships between age, sex, baseline lesion load, risk factors, lesion progression, and change in cognitive function by multivariate regression analyses and additional stratified analyses.Results— Baseline lesion load, higher age, high blood pressure, and current smoking were independently associated with progression of white matter lesions. Women had more marked progression of subcortical white matter lesions and incident lacunar infarcts compared with men. Carotid atherosclerosis was associated with incident lacunar infarcts. Higher blood pressure did not contribute to lesion progression in people with already severe lesions at baseline nor in the very old. Lesion progression was associated with a paralleled decline in general cognitive function and in particular with a decreased information processing speed.Conclusions— Higher age, female sex, cigarette smoking, elevated blood pressure, and baseline lesion load were associated with small vessel disease progression. Age and baseline lesion load influenced the risk relations with blood pressure. Progression of small vessel disease was related to a paralleled decline in cognitive function.
Periventricular White Matter Lucencies Relate to Low Vitamin B12 Levels in Patients With Small Vessel Stroke
- Barbe Pieters,
- Julie Staals,
- Iris Knottnerus,
- Rob Rouhl,
- Paul Menheere,
- AlFons Kessels and
- Jan Lodder
Stroke Volume 40, Issue 51 May 2009

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Background and Purpose— Blood–brain barrier dysfunction may be an early phenomenon in the development of the small vessel disease, which underlies white matter lesions. Because vitamin B12 plays a role in maintaining the integrity of the blood–brain barrier, we studied serum vitamin B12 level in relation to such lesions.Methods— In 124 patients with first lacunar stroke, we measured serum vitamin B12 level and rated the degree of white matter lesions on MRI.Results— Mean vitamin B12 level was 202 pmol/L (SD, 68.9). Thirty-nine patients (31.5%) had a vitamin B12 level less than the lower reference value of 150 pmol/L. Lower vitamin B12 level was (statistically significant) associated with more severe periventricular white matter lesions (odds ratio/100 pmol/L decrease, 1.773; 95% CI, 1.001–3.003), but not with deep white matter lesions (odds ratio/100 pmol/L decrease, 1.441; 95% CI, 0.881–2.358; ordered multivariate regression analysis).Conclusions— More severe periventricular white matter lesions in lacunar stroke patients relate to lower vitamin B12 levels. A possible causal relationship should now be studied prospectively.
Cerebral White Matter Lesions, Gait, and the Risk of Incident Falls: A Prospective Population-Based Study
- Velandai Srikanth,
- Richard Beare,
- Leigh Blizzard,
- Thanh Phan,
- Jennifer Stapleton,
- Jian Chen,
- Michele Callisaya,
- Kara Martin and
- David Reutens
Stroke Volume 40, Issue 11 January 2009

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Background and Purpose— The association between cerebral white matter lesions (WMLs) and the risk of falls in older people is uncertain, with no supporting prospective evidence. We aimed to determine the risk of incident falls associated with WML volume, and the interactions between WML volume, gait, and other sensorimotor factors leading to falls.Methods— We conducted a prospective, population-based study (n=294, mean age 72.3 years, independently mobile). Volumetric MRI, computerized gait measures, and sensorimotor measures of falls risk were obtained at baseline. Incident falls were recorded prospectively over a 12-month period. Using regression modeling, we estimated the risk of incident falls associated with baseline WML volume.Results— Increasing baseline WML volume was independently associated with any incident fall (P=0.01) and multiple incident falls (P=0.02). The risk of incident falls was doubled in people with lesion volumes in the highest quintile of its distribution compared with the lowest (adjusted relative risk, 2.32; 95% CI, 1.28–4.14). Greater lesion volume was also associated with poorer gait and greater gait variability (both P<0.001). The effect of WML volume on the risk of falls was magnified in people with poorer quadriceps muscle strength (P=0.03) and greater gait variability (P=0.001).Conclusions— These data provide the first prospective evidence to our knowledge demonstrating that WMLs are strong risk factors for falls in the general older population. WMLs present potential therapeutic targets for interventional trials in falls prevention.
Vascular Care in Patients With Alzheimer Disease With Cerebrovascular Lesions Slows Progression of White Matter Lesions on MRI: The Evaluation of Vascular Care in Alzheimer’s Disease (EVA) Study
- Edo Richard,
- Alida A. Gouw,
- Philip Scheltens and
- Willem A. van Gool
Stroke Volume 41, Issue 31 March 2010

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Background and Purpose— White matter lesions (WMLs) and cerebral infarcts are common findings in Alzheimer disease and may contribute to dementia severity. WMLs and lacunar infarcts may provide a potential target for intervention strategies. This study assessed whether multicomponent vascular care in patients with Alzheimer disease with cerebrovascular lesions slows progression of WMLs and prevents occurrence of new infarcts.Methods— A randomized controlled clinical trial, including 123 subjects, compared vascular care with standard care in patients with Alzheimer disease with cerebrovascular lesions on MRI. Progression of WMLs, lacunes, medial temporal lobe atrophy, and global cortical atrophy were semiquantitatively scored after 2-year follow-up.Results— Sixty-five subjects (36 vascular care, 29 standard care) had a baseline and a follow-up MRI and in 58 subjects, a follow-up scan could not be obtained due to advanced dementia or death. Subjects in the vascular care group had less progression of WMLs as measured with the WML change score (1.4 versus 2.3, P=0.03). There was no difference in the number of new lacunes or change in global cortical atrophy or medial temporal lobe atrophy between the 2 groups.Conclusions— Vascular care in patients with Alzheimer disease with cerebrovascular lesions slows progression of WMLs. Treatment aimed at vascular risk factors in patients with early Alzheimer disease may be beneficial, possibly in an even earlier stage of the disease.
Belgian Fabry Study: Prevalence of Fabry Disease in a Cohort of 1000 Young Patients With Cerebrovascular Disease
Stroke Volume 41, Issue 51 May 2010

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Background and Purpose— Data on the prevalence of Fabry disease in patients with central nervous system pathology are limited and controversial. In this study, we assessed the prevalence of Fabry disease in young patients presenting with cerebrovascular disease in Belgium.Methods— In this national, prospective, multicenter study, we screened for Fabry disease in 1000 patients presenting with ischemic stroke, transient ischemic attack, or intracranial hemorrhage; unexplained white matter lesions; or vertebrobasilar dolichoectasia. In male patients, we measured α-galactosidase A (α-GAL A) activity in dried blood spots. Female patients were screened for mutations by exonic DNA sequencing of the α-GAL A gene.Results— α-GAL A activity was deficient in 19 men (3.5%), although all had normal α-GAL A gene sequences. Enzymatic deficiency was confirmed on repeat assessment in 2 male patients (0.4%). We identified missense mutations in 8 unrelated female patients (1.8%): Asp313Tyr (n=5), Ala143Thr (n=2), and Ser126Gly (n=1). The pathogenicity of the 2 former missense mutations is controversial. Ser126Gly is a novel mutation that can be linked to late-onset Fabry disease.Conclusion— α-GAL A deficiency may play a role in up to 1% of young patients presenting with cerebrovascular disease. These findings suggest that atypical variants of Fabry disease with late-onset cerebrovascular disease exist, although the clinical relevance is unclear in all cases.
Gait in Elderly With Cerebral Small Vessel Disease
Stroke Volume 41, Issue 81 August 2010

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Background and Purpose— Gait disorders are common in the elderly and are related to loss of functional independence and death. White matter lesions (WMLs) may be related, but only a minority of individuals with WMLs has gait disorders. Probably other factors are involved, including location and the independent effect of frequently coinciding lacunar infarcts, the other aspect of cerebral small vessel disease. The aim of our study was to investigate the effect of both the severity and location of both WMLs and lacunar infarcts on gait.Methods— Four hundred thirty-one independently living, nondemented elderly aged between 50 and 85 years with cerebral small vessel disease were included in this analysis and underwent MRI scanning. The number and location of lacunar infarcts were rated and WML volume was assessed by manual segmentation with automated delineating of different regions. Gait was assessed quantitatively with an electronic walkway as well as the semiquantitatively Tinetti and Timed-Up-and-Go test.Results— WMLs and lacunar infarcts were both independently associated with most gait parameters with stride length as the most sensitive parameter related to WMLs. WMLs in the sublobar (basal ganglia/internal capsule) and limbic areas and lacunar infarcts in the frontal lobe and thalamus were related to a lower velocity.Conclusions— Cerebral small vessel disease is related to gait disturbances. Because small vessel disease may, in part, be preventable, it should be regarded as a potentially important target for postponing gait impairment.
Carotid Intima-Media Thickness and Cerebrovascular Disease in Community-Dwelling Older People Without Stroke
- Susan D. Shenkin,
- Mark E. Bastin,
- Tom J. MacGillivray,
- Elizabeth Eadie,
- Ian J. Deary,
- John M. Starr and
- Joanna M. Wardlaw
Stroke Volume 41, Issue 91 September 2010

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Background and Purpose—Carotid intima-media thickness (CIMT) is a noninvasive measure of atherosclerosis, but it is unclear whether it is a stronger risk factor for large vessel disease or small vessel disease.Methods—One hundred seven volunteers, aged 75 to 81 years, underwent measurements of CIMT and vascular risk factors and brain MRI (structural and diffusion tensor); those with history of stroke were excluded.Results—In 96 subjects without stroke, there were significant associations between CIMT and markers of large vessel disease (carotid stenosis: ρ=0.28; P=0.01) and intermediary risk factors (systolic blood pressure: ρ=0.34; P=0.001). However, there were no significant associations between CIMT and markers of small vessel disease (white matter lesion load and water diffusion parameters).Conclusions—CIMT was not associated with neuroimaging biomarkers of small vessel disease in older volunteers without stroke. Any association between CIMT and white matter lesion in previous studies is likely to be mediated via common intermediary risk factors like hypertension.
Autoantibodies Against Oxidized Low-Density Lipoprotein in Cerebral Small Vessel Disease
Stroke Volume 41, Issue 111 November 2010

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Background and Purpose—Oxidized low-density lipoprotein (oxLDL) induces endothelial dysfunction and antibody formation. Because endothelial dysfunction is involved in cerebral small vessel disease (CSVD) (dilated Virchow Robin spaces, lacunar infarcts, and white matter lesions), oxLDL antibodies could play a role in CSVD pathogenesis. Therefore, we studied oxLDL antibodies in patients with high prevalence of CSVD: lacunar stroke patients and essential hypertensive patients.Methods—A total of 158 lacunar stroke patients, 158 hypertensive patients, and 43 healthy controls were included. We determined levels of IgG and IgM against hypochlorite (HOCl) and malondialdehyde (MDA) oxLDL using ELISA (values in optical density).Results—Patients with CSVD had higher levels of IgG-HOCl-oxLDL (0.77 versus 0.70; P<0.01), as well as lower levels of IgM-MDA-oxLDL (0.55 versus 0.65; P<0.05) than patients without such lesions. Higher IgG-HOCl-oxLDL levels were only independently associated with higher numbers of Virchow Robin spaces at the level of the basal ganglia (β=0.218; P<0.001).Conclusions—An autoinflammatory process with lower levels of IgM antibodies and higher levels of IgG antibodies against oxLDL may be involved in CSVD.
Impact of White Matter Lesions on Physical Functioning and Fall Risk in Older People: A Systematic Review
Stroke Volume 42, Issue 71 July 2011

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Background and Purpose—White matter lesions (WMLs) are common findings on neuroimaging in older people. This review systematically evaluates the published literature on the associations between WMLs and balance, gait, mobility, and falls in older people.Methods—Studies were identified with searches of the MEDLINE databases. Articles reporting associations between WMLs and balance, gait, mobility, and falls in older people in cross-sectional and longitudinal studies were included.Results—Thirty-one articles reporting data from 19 studies met the inclusion criteria. There were consistent findings from both cross-sectional and longitudinal studies indicating greater WML volumes are associated with impaired balance, slower gait, and reduced mobility. Most studies addressing regional WML distributions have reported that WMHs in the frontal lobe and periventricular regions show the strongest relationships with balance, gait, and mobility impairments. In relation to falls, a threshold effect was apparent in that only those with severe WML volumes were found to be at increased risk of falling.Conclusions—The findings of this systematic review indicate that WMLs are common and are significantly associated with impaired balance, gait, mobility, and falls in older people. In many studies, however, impaired mobility and increased fall risk are only evident in people who have the most severe degree of WMLs.
The Origin of White Matter Lesions: A Further Piece to the Puzzle
- Franz Fazekas and
- Joanna M. Wardlaw
Stroke Volume 44, Issue 41 April 2013

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Diastolic Carotid Artery Wall Shear Stress Is Associated With Cerebral Infarcts and Periventricular White Matter Lesions
Stroke Volume 42, Issue 121 December 2011

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Background and Purpose—Low wall shear stress (WSS) is an early marker in the development of vascular lesions. The present study aims to assess the relationship between diastolic and systolic WSS in the internal carotid artery and periventricular (PWML), deep white matter lesions, and cerebral infarcts (CI).Methods—Early, mid, and late diastolic and peak systolic WSS were derived from shear rate obtained by gradient echo phase contrast magnetic resonance sequences multiplied by individually modeled viscosity.PWML, deep white matter lesions, and CI were derived from proton density (PD), T2, and fluid attenuated inversion recovery (FLAIR) MRI in 329 participants (70–82 years; PROSPER baseline). Analyses were adjusted, if appropriate, for age, gender, intracranial volume, and multiple cardiovascular risk factors.Results—Mid-diastolic WSS was significantly correlated with the presence of PWML (B=−10.15; P=0.006) and CI (B=−2.06; P=0.044), but not with deep white matter lesions (B=−1.30; P=0.050; adjusted for age, gender, WML, and intracranial volume). After adjustment for cardiovascular risk factors, these correlations weakened but remained significant. Systolic WSS was not correlated with any of the cerebrovascular parameters.Conclusions—This study is the first to our knowledge to present a cross-sectional correlation between carotid artery WSS and cerebrovascular pathology such as PWML and CI in a large population. Furthermore, it shows that diastolic hemodynamics may be more important than systolic or mean hemodynamics. Future studies exploring vascular hemodynamic damage should focus on diastolic WSS.
Angiogenic T-Cells and Putative Endothelial Progenitor Cells in Hypertension-Related Cerebral Small Vessel Disease
Stroke Volume 43, Issue 11 January 2012

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Background and Purpose—Cerebral small vessel disease (CSVD) may be caused by endothelial dysfunction, whereas endothelial progenitor cells (EPC) may attenuate endothelial dysfunction. Their vitality is lower in CSVD. A subset of lymphocytes, angiogenic T-cells, is capable to stimulate EPC function. The purpose of our study was to explore the relation between CSVD manifestations, angiogenic T-cells, and EPC in hypertensive patients with CSVD.Methods—We compared 32 essential hypertensive patients with CSVD (white matter lesions, asymptomatic lacunar infarcts, or microbleeds on 1.5-Tesla MRI) to 29 age-matched and sex-matched hypertensive controls. We counted angiogenic T-cells (CD3⁺/CD31⁺/CD184⁺) and putative EPC (CD31⁺/CD34⁺/CD45^-/KDR⁺) by flow cytometry and determined EPC vitality by in vitro cluster formation.Results—Putative EPC numbers were lower in hypertensive individuals with CSVD than in those without (10±7^.10³/mL versus 13±6^.10³/mL [median±interquartile range]; P=0.011). Angiogenic T-cell numbers were also lower in hypertensive individuals with CSVD than in those without (0.56±0.25^.10⁹/mL versus 0.78±0.50^.10⁹/mL; P=0.008). Higher angiogenic T-cell numbers independently related to absence of CSVD (odds ratio, 0.088; 95% confidence interval, 0.012–0.627).Conclusions—Our data suggest that angiogenic T-cells and putative EPC independently relate to radiological CSVD manifestations in hypertensive patients.
Silent Infarcts and Cerebral Microbleeds Modify the Associations of White Matter Lesions With Gait and Postural Stability: Population-Based Study
- Philip Choi,
- Mandy Ren,
- Thanh G. Phan,
- Michele Callisaya,
- John V. Ly,
- Richard Beare,
- Winston Chong and
- Velandai Srikanth
Stroke Volume 43, Issue 61 June 2012

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Background and Purpose—Although cerebral white matter lesions (WMLs), silent infarcts (SIs), and microbleeds (MBs) are individually associated with poorer gait and balance, it is unknown if they interact. We studied the interactions of WML volume with SI and MB on gait and postural stability.Methods—Participants in a population-based study aged 60 to 86 years underwent brain MRI, computerized gait measurement, and a physiological profile assessment of postural stability. Segmentation procedures and standard rating methods were used to measure WML, SI, and MB. Linear regression was used to test interactions between lesions on gait and postural stability, adjusting for age, sex, and total intracranial volume.Results—There were 395 participants (mean age, 72 years; SD, 7.0). SIs were predominantly located in subcortical frontal white matter and in deep gray structures, and MBs were largely lobar. Participants with SI or MB had higher WML volumes than those without (P<0.001 and P=0.05, respectively). The presence of SI (P for interaction=0.01) or MB (P for interaction <0.01) magnified the adverse association of WML volume with gait. SI (P for interaction=0.02), but not MB, magnified the adverse association of WML volume with postural stability.Conclusions—Subclinical cerebrovascular lesions are adversely associated with gait and postural stability in older people in a cumulative fashion.
Different Impacts of Blood Pressure Variability on the Progression of Cerebral Microbleeds and White Matter Lesions
- Wenhong Liu,
- Ran Liu,
- Wei Sun,
- Qing Peng,
- Weiwei Zhang,
- En Xu,
- Yan Cheng,
- Meiping Ding,
- Yansheng Li,
- Zhen Hong,
- Jiang Wu,
- Jinsheng Zeng,
- Chen Yao,
- Yining Huang and
Stroke Volume 43, Issue 111 November 2012

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Background and Purpose—Cerebral microbleeds (CMB) and white matter lesions (WML) are cerebral small vessel diseases. Hypertension is considered the most important risk factor. Its mechanism is not yet clarified. Our study assessed the association of blood pressure variability (BPV) with CMB and WML progression.Methods—Patients with a history of ischemic stroke within 1 to 6 months were consecutively recruited and followed-up for 12 to 18 months. Blood pressure was measured monthly and controlled to a target level. BPV was quantified by the maximum, standard deviation, coefficient of variation, successive variation, standard deviation independent of mean, and successive variation independent of mean. Magnetic resonance imaging was performed at baseline and the end of the study. CMB and WML were rated using Microbleed Anatomic Rating Scale and Age-Related White Matter Changes scales, respectively. Multiple logistic analyses assessed BPV associations with CMB and WML development.Results—Of 720 patients recruited, 500 and 584 had follow-up results for CMB and WML, respectively; 13.2% and 48.1% showed CMB and WML progression, respectively, over a median of 14 months. Patients with CMB had a higher mean, maximum, standard deviation, coefficient of variation, successive variation, standard deviation independent of the mean, and successive variation independent of the mean in either systolic blood pressure or diastolic blood pressure (P<0.05). Systolic blood pressure variability was an independent risk factor for deep and infratentorial CMB progression, whereas diastolic blood pressure variability was independently associated with CMB development in deep regions. WML progression was not significantly associated with BPV between visits.Conclusion—BPV independently predicts CMB progression in deep and infratentorial regions.Clinical Trial Registration Information—URL: http://www.clinicaltrials.gov. Unique identi-fier: NCT00202020.

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