Introduction: The early identification of the unstable carotid plaque together with the best medical treatment, are two missing parts of the stroke-prevention puzzle. This review summarizes the available evidence on the effects of statins on carotid plaque morphology.
Methods: A systematic review of the PubMed, Scopus and Cochrane Library databases was performed. Studies evaluating the effect of statins on plaque imaging features other than intima media thickness as well as on the serum inflammatory profile were eligible for inclusion.
Results: Seventeen studies were eligible for inclusion. The majority of the studies used MRI and ultrasound imaging. Plaque composition (fibrous cap and lipid core size), and size (plaque area and volume) were mainly used to evaluate the changes in plaque morphology. All studies showed slower progression, remodelling or even regression of the plaque even after only 1 month of statin administration, although the type, dosage and duration of treatment varied significantly between them. Intensive statin treatment was suggested to have a more pronounced effect on plaque morphology, however, that was mainly associated with maintaining LDL-levels <100 mg/mL and not with the intensity of the dosage. Seven studies measured CRP, four of which found significantly decreased levels with statin use.
Conclusion: This review suggests that statins may have a beneficial effect on plaque morphology and the inflammatory response. Further validation of whether this is an LDL-associated effect or a separate pleiotropic phenomenon of statins is needed. There are significant inherent limitations to the safe extraction of solid conclusions from the studies due to data heterogeneity and publication bias.
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http://dx.doi.org/10.1016/j.atherosclerosis.2010.04.032 | DOI Listing |
Matrix Biol
January 2025
Department of Surgery, Emory University, Atlanta, GA, USA; Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA; Research Services, Atlanta VA Medical Center, Decatur, GA, USA. Electronic address:
Arterial endothelial cells (ECs) reside in a complex biomechanical environment. ECs sense and respond to wall shear stress. Low and oscillatory wall shear stress is characteristic of disturbed flow and commonly found at arterial bifurcations and around atherosclerotic plaques.
View Article and Find Full Text PDFAnn Ital Chir
January 2025
Institute of Central Nervous System Vascular Injury and Repair, Jining Medical Science Research Institute, The First People's Hospital of Jining, 272000 Jining, Shandong, China.
Aim: This study aims to report a rare case of an embolization protection device (EPD) entrapment during Carotid Artery Stent (CAS) and to discuss the management strategy, including open surgery and concurrent carotid endarterectomy (CEA).
Case Presentation: A 71-year-old female presented with left limb weakness and unclear speech following CAS. Imaging revealed a new cerebral infarction and right internal carotid artery stenosis.
Sci Rep
January 2025
Department of Cardiology, Second Norman Bethune Hospital of Jilin University, No. 218 Ziqiang Street, Changchun, China.
Atherosclerosis (AS) is the principal pathological cause of atherosclerotic cardiovascular diseases. Chronic endoplasmic reticulum stress (ERS) has been implicated in AS aetiopathogenesis, but the underlying molecular interactions remain unclear. This study aims to identify the molecular mechanisms of ERS in AS pathogenesis to inform innovative diagnostic approaches and therapeutic targets for managing AS.
View Article and Find Full Text PDFJ Cardiovasc Transl Res
January 2025
Department of Vascular and Endovascular Surgery, Changzheng Hospital, Affiliated to the Naval Medical University, Shanghai, 200003, China.
CHI3L1 is strongly associated with atherosclerosis, but its role in macrophages remains unknown. In this study, we observed a significant up-regulation of CHI3L1 in both carotid plaques and serum of symptomatic patients, and demonstrated that CHI3L1 impairs the efferocytosis of macrophages by down-regulating crucial efferocytic mediator MFGE8 through inhibiting ATF2, which binds directly to the enhancer of MFGE8. In human plaques, we observed a negative correlation between CHI3L1 expression and both ATF2 and MFGE8 levels, further proved their involvement in plaque destabilization.
View Article and Find Full Text PDFVasc Biol
January 2025
M Daemen, Pathology, Amsterdam UMC Location AMC, Amsterdam, Netherlands.
Background: Although mice are used extensively to study atherosclerosis of different vascular beds, limited data is published on the occurrence of intracranial atherosclerosis. Since intracranial atherosclerosis is a common cause of stroke and is associated with dementia, a relevant animal model is needed to study these diseases.
Methods And Results: We examined the presence of intracranial atherosclerosis in different atherogenic mouse strains and studied differences in vessel wall characteristics in mouse and human tissue in search for possible explanations for the different atherosclerotic susceptibility between extracranial and intracranial vessels.
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