Background And Purpose: Placenta growth factor (PlGF) mediates angiogenesis and inflammation, but its role in human atherosclerosis is unknown. This study was designed to test the hypothesis that PlGF-expression in human atherosclerotic carotid plaques is related to inflammation, vascularization and clinical plaque instability.
Methods: The expression of PlGF, C-reactive protein (CRP) and CD40L was analyzed with Western blots in carotid plaques of 60 patients. Cellular infiltration (CD68, CD3) and vascularization (von-Willebrand-factor) was assessed by immunohistochemistry.
Results: Symptomatic patients showed higher levels of PlGF than asymptomatic patients (115.4+/-8.2 versus 83.6+/-10.5 densitometric units (DU), p<0.05) and higher grading for inflammatory cells and microvessels (CD3: 2.3+/-0.1 versus 0.6+/-0.1, p<0.001, CD68: 2.4+/-0.1 versus 0.8+/-0.1, p<0.001, microvessels: 2.3+/-0.1 versus 1.5+/-0.1, p<0.01). PlGF-expression showed a positive correlation to the expression of CRP (r=0.5, p<0.001) and CD40L (r=0.4, p<0.01).
Conclusions: PlGF-expression within human atherosclerotic lesions is associated with plaque inflammation and microvascular density, suggesting a role for PlGF in plaque destabilization and, thus, in clinical manifestation of the disease.
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http://dx.doi.org/10.1016/j.atherosclerosis.2006.10.038 | DOI Listing |
Circulation
January 2025
Divisions of Cardiac Surgery (H.T., A.Q., R.E., R.V., M.M., J.H.C., S.V.), Li Ka Shing Knowledge Institute, St. Michael's Hospital of Unity Health Toronto, Ontario, Canada.
J Am Heart Assoc
January 2025
Research Institute of Internal Medicine, Oslo University Hospital Oslo Norway.
Background: Complement activation may promote atherosclerosis. Yet, data on the to which extent complement, and more specifically the alternative complement pathway, is activated in patients with carotid atherosclerosis and related to adverse outcome in these patients, are scarce.
Methods And Results: We measured, by ELISA, plasma levels of factor D, properdin, C3bBbP (C3 convertase), and factor H in patients with advanced carotid atherosclerosis in a (n=324) and in a (n=206) cohort in relation to adverse outcome (mean follow-up 7.
Circulation
January 2025
Johns Hopkins Ciccarone Center for Prevention of Cardiovascular Disease, Baltimore, MD (Z.Y., E.T., Z.A.D., K.K.J., N.O., T.R., E.B., M.J.B.).
Background: Understanding the association of tobacco product use with subclinical markers is essential in evaluating health effects to inform regulatory policy. This is particularly relevant for noncigarette products (eg, cigars, pipes, and smokeless tobacco), which have been understudied because of their low prevalence in individual cohort studies.
Methods: This cross-sectional study included 98 450 participants from the Cross-Cohort Collaboration-Tobacco data set.
Ann Indian Acad Neurol
January 2025
Departments of Clinical Neurosciences and Community Health Sciences, The Hotchkiss Brain Institute, The Mathison Centre for Mental Health Research and Education, and The O'Brien Institute for Public Health, University of Calgary Cumming School of Medicine, Calgary, Alberta, Canada.
Symptomatic carotid disease, characterized by atherosclerotic or non-atherosclerotic internal carotid artery disease with ipsilateral stroke symptoms, represents a critical condition in stroke neurology. This "hot carotid" state carries a high risk of stroke recurrence, with almost one-fourth of the patients experiencing recurrent ischemic events within 2 weeks of initial presentation. The global prevalence of significant carotid stenosis (conventionally defined as ≥50% narrowing) is estimated at around 1.
View Article and Find Full Text PDFJ Atheroscler Thromb
January 2025
Department of Neurology, National Cerebral and Cardiovascular Center.
Aim: Branch atheromatous disease (BAD), characterized by the occlusion of perforating branches near the orifice of a parent artery, often develops early neurological deterioration because the mechanisms underlying BAD remain unclear. Abnormal wall shear stress (WSS) is strongly associated with endothelial dysfunction and plaque growth or rupture. Therefore, we hypothesized that computational fluid dynamics (CFD) modeling could detect differences in WSS between BAD and small-vessel occlusion (SVO), both of which result from perforating artery occlusion/stenosis.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!