Vascular Mechanisms in the Pathogenesis of Stroke

Sierra, Cristina; Coca, António; Schiffrin, Ernesto L.

doi:10.1007/s11906-011-0195-x

Cited by 133 publications

(125 citation statements)

References 51 publications

Supporting

Mentioning

110

Contrasting

Unclassified

Order By: Relevance

“…One possibility is that the CAVI reflects atherosclerosis in systemic large arteries, including the carotid, coronary and peripheral arteries. 8 Moreover, atherosclerosis in large extracranial 17 or intracranial arteries 18 also leads to arteriolosclerosis in small cerebral vessels and to the development of CMBs. Thus, systemic atherosclerosis may have a key role in the occurrence of cerebral arteriolosclerosis and CMBs.…”

Section: Discussionmentioning

confidence: 99%

Stroke patients with cerebral microbleeds on MRI scans have arteriolosclerosis as well as systemic atherosclerosis

et al. 2012

View full text Add to dashboard Cite

Cerebral microbleeds (CMBs) are recognized as a manifestation of arteriolosclerosis in cerebral small vessels. However, little is known regarding whether stroke patients with CMBs often have systemic atherosclerosis. The aim of the present study was to elucidate this issue using the cardio-ankle vascular index (CAVI), a new index of systemic atherosclerosis, in acute ischemic stroke patients. We prospectively studied 105 patients (71 males, median age ¼ 70.0 years) with acute ischemic stroke. All of the patients were examined using T2*-weighted gradient echo magnetic resonance imaging (MRI) to look for and assess the CMBs and using fluid-attenuated inversion recovery to evaluate white matter hyperintensity (WMH). We assigned the patients into CMB and non-CMB groups and compared the clinical characteristics of these groups. The factors associated with CMBs were investigated using multivariate logistic regression analysis. T2*-weighted gradient echo MRI revealed CMBs in 47 patients (44.8%) and no CMBs in 58 patients (55.2%). The CAVI was significantly higher in the CMBs group (10.5 vs. 8.6, Po0.001).In the multivariate logistic regression analysis, CAVI per one point increase (odds ratio (OR), 1.50; 95% confidence interval (CI), 1.12-2.00; P ¼ 0.006), advanced WMH (OR, 4.78; 95% CI, 1.55-14.74; P ¼ 0.006) and impaired kidney function (OR, 3.31; 95% CI, 1.16-9.81; P ¼ 0.031) were independent factors associated with the presence of CMBs. A high CAVI was independently associated with CMBs in patients with acute ischemic stroke. Our results indicated that ischemic stroke patients with CMBs may have cerebral arteriolosclerosis as well as systemic atherosclerosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Stroke patients with cerebral microbleeds on MRI scans have arteriolosclerosis as well as systemic atherosclerosis

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Oxidative stress, an imbalance between the production of the reactive oxygen species and the human body's antioxidant defense mechanism,4 has been proposed as an important underlying biological mechanism mediating this association 3, 5, 6, 7. Increased oxidative stress may induce endothelial dysfunction, which is characterized by increased endothelial permeability, altered vascular tone, platelet adhesion and aggregation, and enhanced thrombogenicity 8, 9…”

Section: Introductionmentioning

confidence: 99%

Short‐Term Exposure to Air Pollution and Biomarkers of Oxidative Stress: The Framingham Heart Study

Wilker

Dorans

et al. 2016

JAHA

122

View full text Add to dashboard Cite

BackgroundShort‐term exposure to elevated air pollution has been associated with higher risk of acute cardiovascular diseases, with systemic oxidative stress induced by air pollution hypothesized as an important underlying mechanism. However, few community‐based studies have assessed this association.Methods and ResultsTwo thousand thirty‐five Framingham Offspring Cohort participants living within 50 km of the Harvard Boston Supersite who were not current smokers were included. We assessed circulating biomarkers of oxidative stress including blood myeloperoxidase at the seventh examination (1998–2001) and urinary creatinine‐indexed 8‐epi‐prostaglandin F2α (8‐epi‐PGF 2α) at the seventh and eighth (2005–2008) examinations. We measured fine particulate matter (PM 2.5), black carbon, sulfate, nitrogen oxides, and ozone at the Supersite and calculated 1‐, 2‐, 3‐, 5‐, and 7‐day moving averages of each pollutant. Measured myeloperoxidase and 8‐epi‐PGF 2α were loge transformed. We used linear regression models and linear mixed‐effects models with random intercepts for myeloperoxidase and indexed 8‐epi‐PGF 2α, respectively. Models were adjusted for demographic variables, individual‐ and area‐level measures of socioeconomic position, clinical and lifestyle factors, weather, and temporal trend. We found positive associations of PM 2.5 and black carbon with myeloperoxidase across multiple moving averages. Additionally, 2‐ to 7‐day moving averages of PM 2.5 and sulfate were consistently positively associated with 8‐epi‐PGF 2α. Stronger positive associations of black carbon and sulfate with myeloperoxidase were observed among participants with diabetes than in those without.ConclusionsOur community‐based investigation supports an association of select markers of ambient air pollution with circulating biomarkers of oxidative stress.

show abstract

“…Agerelated increases in plaque formation, intima-media thickness, and arterial stiffness lead to decreased vascular compliance and variability in perfusion pressure (Ebrahimi 2009). These mechanical changes render a compromised vascular system vulnerable to the detrimental effects of oxidative stress, inflammation, and cerebral ischemia (Sierra et al 2011). Although numerous cellular and metabolic factors contribute to compromised vasculature, alterations in the brain reninangiotensin system (RAS) have been implicated in the pathogenesis of vascular aging (Diz et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Impact of the AGTR1 A1166C polymorphism on subcortical hyperintensities and cognition in healthy older adults

Salminen

Schofield

Pierce

et al. 2014

AGE

View full text Add to dashboard Cite

Vascular aging consists of complex and multifaceted processes that may be influenced by genetic polymorphisms of the renin-angiotensin system. A polymorphism in the angiotensin II type 1 receptor gene (AGTR1/rs5186) has been associated with an increased risk for arterial stiffness, hypertension, and ischemic stroke. Despite these identified relationships, the impact of AGTR1 A1166C on white matter integrity and cognition is less clear in a healthy aging population. The present study utilized indices of neuroimaging and neuropsychological assessment to examine the impact of the A1166C polymorphism on subcortical hyperintensities (SH) and cognition in 49 healthy adults between ages 51-85. Using a dominant statistical model (CC + CA (risk) vs. AA), results revealed significantly larger SH volume for individuals with the C1166 variant (p<0.05, partial eta 2 = 0.117) compared with those with the AA genotype. Post hoc analyses indicated that increased SH volume in C allele carriers could not be explained by vascular factors such as pulse pressure or body mass index. In addition, cognitive performance did not differ significantly between groups and was not significantly associated with SH in this cohort. Results suggest that presence of the C1166 variant may serve as a biomarker of risk for suboptimal brain integrity in otherwise healthy older adults prior to changes in cognition.

show abstract

Vascular Mechanisms in the Pathogenesis of Stroke

Cited by 133 publications

References 51 publications

Stroke patients with cerebral microbleeds on MRI scans have arteriolosclerosis as well as systemic atherosclerosis

Stroke patients with cerebral microbleeds on MRI scans have arteriolosclerosis as well as systemic atherosclerosis

Short‐Term Exposure to Air Pollution and Biomarkers of Oxidative Stress: The Framingham Heart Study

Impact of the AGTR1 A1166C polymorphism on subcortical hyperintensities and cognition in healthy older adults

Contact Info

Product

Resources

About