scholarly journals Do Lacunar Infarcts Have Different Aetiologies? Risk Factor Profiles of Lacunar Infarcts in Deep White Matter and Basal Ganglia: The Second Manifestations of ARTerial Disease-Magnetic Resonance Study

2017 ◽  
Vol 43 (3-4) ◽  
pp. 161-168 ◽  
Author(s):  
Raoul P. Kloppenborg ◽  
Paul J. Nederkoorn ◽  
Anne M. Grool ◽  
Laurens J.L. De Cocker ◽  
Willem P.T.M. Mali ◽  
...  

Background: Evidence suggests that lacunar infarcts have different etiologies, possibly related to their anatomical location and vascular territory. We investigated the risk factor profiles of patients with new lacunar infarcts in the basal ganglia and deep white matter. Methods: Within the Second Manifestations of ARTerial disease-Magnetic Resonance study, a prospective cohort on brain changes on MRI in patients with symptomatic atherosclerotic disease, 679 patients (57 ± 9 years) had vascular screening and MRI at baseline and after a mean follow-up of 3.9 years. We investigated the association between vascular risk factors at baseline and appearance of new lacunar infarcts in the basal ganglia and deep white matter at follow-up. Results: New lacunar infarcts appeared in 44 patients in the basal ganglia and in 37 patients in the deep white matter. In multivariable analysis, older age, history of cerebrovascular disease, and baseline white matter hyperintensity (WMH) volume were associated with increased risk of new lacunar infarcts in both locations. Hyperhomocysteinemia was associated with increased risk of lacunar infarcts in the basal ganglia (relative risk [RR] 2.0; 95% CI 1.0-4.2), whereas carotid stenosis >70% (RR 2.5; 95% CI 1.2-5.0), smoking (per 10 pack-year: RR 1.1; 95% CI 1.0-1.3), hypertension (RR 3.4; 95% CI 1.2-9.7), and progression of WMH volume (RR 2.4; 95% CI 1.1-5.2) were associated with increased risk of lacunar infarcts in the deep white matter. Conclusions: The different risk factor profiles for new lacunar infarcts in basal ganglia and deep white matter indicate different etiologies. The independent association between progression of WMH and new deep white matter lacunar infarcts suggest a common etiology for these radiological abnormalities.

2011 ◽  
Vol 42 (2) ◽  
pp. 359-370 ◽  
Author(s):  
A. M. Grool ◽  
Y. van der Graaf ◽  
W. P. Th. M. Mali ◽  
Th. D. Witkamp ◽  
K. L. Vincken ◽  
...  

BackgroundThe ‘vascular depression’ hypothesis states that brain changes located in frontal-subcortical pathways increase vulnerability for specific depressive symptom profiles, but studies examining locations of small-vessel and degenerative changes with individual symptoms are scarce. We examined whether location and progression of white-matter lesions (WMLs), lacunar infarcts and atrophy were associated with motivational and mood symptoms in patients with symptomatic atherosclerotic disease.MethodIn 578 patients [63 (s.d.=8) years] of the Second Manifestations of ARTerial disease (SMART)-Medea study, volumes of WMLs and atrophy and visually rated infarcts were obtained with 1.5 T magnetic resonance imaging at baseline and after 3.9 (s.d.=0.4) years' follow-up. Depressive symptoms were assessed with Patient Health Questionnaire-9 at follow-up and categorized into motivational and mood symptoms.ResultsRegression analyses adjusted for age, gender, education, Mini-Mental State Examination, physical functioning, antidepressant use and vascular risk factors showed that location in mainly deep white-matter tracts and progression of WMLs were associated with symptoms of anhedonia, concentration problems, psychomotor retardation and appetite disturbance. Lacunar infarcts in deep white matter were associated with greater motivational [Incidence rate ratio (IRR) 1.7, 95% confidence interval (CI) 1.2–2.4] and mood (IRR 1.7, 95% CI 1.1–2.6) sumscores, and with symptoms of psychomotor retardation, energy loss and depressed mood; lacunar infarcts in the thalamus were associated with psychomotor retardation only. Cortical atrophy was associated with symptoms of anhedonia and appetite disturbance. Excluding patients with major depression did not materially change the results.ConclusionsOur findings suggest that disruption of frontal-subcortical pathways by small-vessel lesions leads to a symptom profile that is mainly characteristic of motivational problems, also in the absence of major depression.


2021 ◽  
Vol 12 ◽  
Author(s):  
Eri Sano ◽  
Shigeki Arawaka

Objective: The occurrence of ischemic stroke in patients with systemic lupus erythematosus (SLE) can cause extended periods of reduced daily activities. However, the risk factors for ischemic stroke in SLE patients are not fully elucidated. Herein, we examined the effect of white matter hyperintensities (WMH) on the occurrence of ischemic stroke in SLE patients.Methods: We analyzed the relationship between WMH burden and ischemic stroke using follow-up brain magnetic resonance imaging (MRI) data of 79 patients with SLE. Of these patients, 16 developed stroke during the observation period. WMH on MRI were classified into periventricular hyperintensities and deep white matter hyperintensities (DWMH), while the lesion extent was graded using the Fazekas scale.Results: Kaplan–Meier curves showed that ischemic stroke events were significantly associated with age at initial brain MRI of ≥40 years (p = 0.015) and history of anti-phospholipid syndrome (p = 0.030). Additionally, ischemic stroke events were significantly associated with a one grade deterioration of periventricular hyperintensities (p = 0.003) and a one grade deterioration of DWMH (p = 0.002). Multivariate analysis using the logistic regression model showed that a one grade deterioration of DWMH was an independent risk factor for ischemic stroke (hazard ratio, 6.0; 95% confidence interval, 1.3–27.4).Conclusions: Although several factors affect the occurrence of ischemic stroke, SLE patients show increased risk of ischemic stroke via development of DWMH. An observation of DWMH deterioration on follow-up brain MRI may be useful for assessing the risk of ischemic stroke in SLE patients.


2013 ◽  
Vol 73 (2) ◽  
pp. 169-176 ◽  
Author(s):  
Anne M. Grool ◽  
Lotte Gerritsen ◽  
Nicolaas P.A. Zuithoff ◽  
Willem P.T.M. Mali ◽  
Yolanda van der Graaf ◽  
...  

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Magnus Johansson ◽  
Markus Jansson-Fröjmark ◽  
Annika Norell-Clarke ◽  
Steven J. Linton

Abstract Background The aim of this investigation was to examine the longitudinal association between change in insomnia status and the development of anxiety and depression in the general population. Methods A survey was mailed to 5000 randomly selected individuals (aged 18–70 years) in two Swedish counties. After 6 months, a follow-up survey was sent to those (n = 2333) who answered the first questionnaire. The follow-up survey was completed by 1887 individuals (80.9%). The survey consisted of questions indexing insomnia symptomatology, socio-demographic parameters, and the Hospital Anxiety and Depression Scale. Change in insomnia status was assessed by determining insomnia at the two time-points and then calculating a change index reflecting incidence (from non-insomnia to insomnia), remission (from insomnia to non-insomnia), or status quo (no change). Multivariate binary logistic regression analyses were used to examine the aim. Results Incident insomnia was significantly associated with an increased risk for the development of new cases of both anxiety (OR = 0.32, p < .05) and depression (OR = 0.43, p < .05) 6 months later. Incident insomnia emerged also as significantly associated with an elevated risk for the persistence of depression (OR = 0.30, p < .05), but not for anxiety. Conclusions This study extends previous research in that incidence in insomnia was shown to independently increase the risk for the development of anxiety and depression as well as for the maintenance of depression. The findings imply that insomnia may be viewed as a dynamic risk factor for anxiety and depression, which might have implications for preventative work.


2015 ◽  
Vol 36 (3) ◽  
pp. 1417-1423 ◽  
Author(s):  
Pieternella H. van der Veen ◽  
Majon Muller ◽  
Koen L. Vincken ◽  
Jan Westerink ◽  
Willem P.T.M. Mali ◽  
...  

Stroke ◽  
2005 ◽  
Vol 36 (6) ◽  
pp. 1184-1188 ◽  
Author(s):  
Gabriel Gold ◽  
Enikö Kövari ◽  
François R. Herrmann ◽  
Alessandra Canuto ◽  
Patrick R. Hof ◽  
...  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Rachel H Mackey ◽  
Greg G Grandits ◽  
Lewis H Kuller ◽  
Joel Estis ◽  
John A Todd ◽  
...  

Introduction: Higher levels of kidney-injury molecule-1 (KIM-1) measured in urine are associated with presence and progression of acute renal disease. A recent study reported similar results for KIM-1 measured in blood. Hypothesis: We hypothesized that KIM-1 measured in stored serum from middle-aged men who participated in the Multiple Risk Factor Intervention Trial (MRFIT) would differentiate very long-term risk of fatal CHD vs. survival to a mean age of 80 over approximately 30 year follow-up. Methods: We conducted a nested case-control study within MRFIT, which in 1973-76 randomized 12,866 high risk but CVD free men ages 35-57 to risk factor intervention vs. usual care. Serum samples were collected at baseline and stored for future use. The trial concluded in 1982 but long-term mortality follow-up was ascertained through 2005 using the National Death Index. From MRFIT participants with stored serum from baseline, we sampled 100 men who died of CHD (mean age 47.3 at baseline and 73.9 at death), and 100 men who survived to 2005 (mean age =48.4 at baseline and 80.1 in 2005.) KIM-1 was assayed from stored serum samples using high sensitivity single-molecule counting technology (Erenna ® Immunoassay System, Singulex), with limit of detection (LoD)=0.5 pg/ml, and lower limit of quantification (LLoQ)=2.0 pg/ml. Results were compared between cases and controls using Wilcoxon rank tests and logistic regression. Results: Inter-assay %CVs were 8%. Median KIM-1 was higher for smokers vs. non-smokers and for men with vs. without hypertension, but was not associated with high cholesterol. KIM-1 was significantly higher in cases (183 pg/ml (IQR: 137-239) versus controls, (161 pg/ml (IQR:109-212), p=0.03; OR (95%CI)for Q4 versus Q1 was 2.26 (1.02 - 5.02) Adjusted for age and smoking the OR(95%CI) of fatal CHD for Q4 vs. Q1 was 2.34 (1.02- 5.37), and further adjusted for diastolic BP and serum cholesterol at baseline, was 2.0 (95% CI: 0.8-4.7). Conclusions: Higher serum KIM-1 levels at midlife were associated with a ∼2-fold increased risk of fatal CHD vs. survival over ∼30 years of follow-up. This is the first report of a longitudinal association of circulating KIM-1 levels with fatal CHD in long-term follow-up.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Jennifer A Deal ◽  
Melinda C Power ◽  
Karen Bandeen-Roche ◽  
Michael Griswold ◽  
David Knopman ◽  
...  

Introduction: Cerebrovascular small vessel disease, seen on brain imaging as lacunes and white matter hyperintensities (WMH), is a substrate for dementia in older adults. Diffusion tensor imaging (DTI) is thought to provide early signs of loss of white matter (WM) integrity due to microvascular disease and predicts WM hyperintensity volume. Retinal fundus photography provides surrogate measures of cerebral microvasculature. No studies have quantified the long-term association between retinal signs and DTI measures. Hypothesis: Microvascular retinal signs measured in midlife are associated with small vessel disease measured on brain magnetic resonance imaging (MRI) 18 years later, including reduced WM microstructural integrity (lower fractional anisotrophy [FA] and greater mean diffusivity [MD] by DTI), greater WM hyperintensity volume and greater lacune prevalence. Methods: In a biracial prospective cohort study, retinal signs were measured using fundus photography (1993-1995) with 3-T magnetic resonance imaging conducted in 2011-13. Multivariable-adjusted linear regression was used to quantify the relationships of retinal signs with WM measures. Prevalence of lacunar infarcts by retinal sign status was estimated using log binomial regression. Analyses were adjusted for age [linear and quadratic terms], education, sex, race, intracranial volume, body mass index, smoking, diabetes, hypertension, and ≥1 APOE ε4 alleles. Results: In 1829 men and women (60% [N=1100] female, 27% [N=489] black race, aged 50-72 years when retinal signs were measured), a binary measure comprised of two retinal signs suggestive of arteriolar damage due to hypertension (focal arteriolar narrowing and/or arteriovenous nicking) was associated with worse (lower) FA (standardized β=-0.19, 95% confidence interval [CI]=-0.35, -0.02), worse (higher) MD (β=0.15, 95% CI=0.00, 0.30), greater WM hyperintensity volume (β=0.15, 95% CI=0.01, 0.30), and greater prevalence of lacunes (prevalence ratio=1.33, 95% CI: 0.99, 1.80). Generalized arteriolar narrowing, measured as the central retinal arteriolar equivalent (CRAE, narrowest quartile vs. widest three quartiles) was associated with worse FA (β=-0.13, 95% CI=-0.24, -0.01) and worse MD (β=0.12, 95% CI=0.01, 0.23). Results did not differ by sex, race, hypertension status or APOE ε4 genotype. No associations were found for retinopathy, but only 56 participants had retinopathy. Conclusions: Consistent with prior work, and as expected based on a common underlying pathology, retinal signs predicted WM disease and lacunar infarcts 18 years later. Novel to this study, we found that retinal signs related to arteriolar damage also predicted loss of white matter microvascular integrity measured using DTI.


2021 ◽  
Vol 15 (10) ◽  
pp. 3473-3475
Author(s):  
U. Sivakumar ◽  
Rinku Garg ◽  
Sunita Nighute

Introduction: PAD was asymptomatic in a large proportion of COPD patients and was associated with more severe lung disease than in COPD subjects without PAD. Materials and Methods: This was a Cross-sectional study conducted at Department of Physiology, Santosh Medical College diagnosed with COPD using Spirometry was recruited for the study with a Sample size of 130 patients. Results: The characteristics of the population for follow-up (n=130) are presented in table 1. The mean Mean±SD was 51.73±6.1 years. The prevalence of never smokers was 21.5%, former smokers were 51.5% and current smokers were 26.9%. In total, 41 out of 130 individuals (31.5%) had PAD based on an ABI of less than 0.6. A statistically significant association was found between COPD and newly diagnosed PAD during follow-up. The association between COPD and incident PAD was stronger (adjusted OR 1.91, 95% CI 1.14–3.21). Stratified analysis by smoking status revealed that the overall association between COPD and newly developed PAD was driven by the ever smoker group. Conclusion: Subjects with COPD have a higher risk of developing PAD. People with both COPD and PAD have a substantially increased risk of death. Consequently, early detection of PAD and preventive actions in people with COPD should receive more attention in clinical respiratory care. Keywords: Peripheral Arterial Disease, Chronic Obstructive Pulmonary Disease, Ankle-brachial index.


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