Inflammation and atherosclerosis (original) (raw)
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Inflammatory Mediators and Cell Adhesion Molecules as Indicators of Severity of Atherosclerosis
2000
Inflammatory mediators and soluble cell adhesion molecules predict cardiovascular events. It is not clear whether they reflect the severity of underlying atherosclerotic disease. Within the Rotterdam Study, we investigated the associations of C-reactive protein (CRP), interleukin-6 (IL-6), soluble intercellular adhesion molecule-1, and soluble vascular cell adhesion molecule-1 with noninvasive measures of atherosclerosis. Levels of CRP were assessed in a random
Role of Inflammation in Atherosclerosis
Journal of Nuclear Medicine, 2007
Inflammation plays a major role in all phases of atherosclerosis. Stable plaques are characterized by a chronic inflammatory infiltrate, whereas vulnerable and ruptured plaques are characterized by an ''active'' inflammation involved in the thinning of the fibrous cap, predisposing the plaque to rupture. Although a single vulnerable atherosclerotic plaque rupture may cause the event, there are many other types of plaques, several of which are vulnerable. The existence of multiple types of vulnerable plaques suggests that atherosclerosis is a diffuse inflammatory process. A current challenge is to identify morphologic and molecular markers able to discriminate stable plaques from vulnerable ones, allowing the stratification of patients at high risk for acute cardiovascular and cerebrovascular events before clinical syndromes develop. With that aim in mind, this article summarizes the natural history of atherosclerotic plaques, focusing on molecular mechanisms affecting plaque progression and serum markers correlated with plaque inflammation.
Inflammatory markers and extent and progression of early atherosclerosis
2014
Background: Large-scale epidemiological evidence on the role of inflammation in early atherosclerosis, assessed by carotid ultrasound, is lacking. We aimed to quantify cross-sectional and longitudinal associations of inflammatory markers with common-carotid-artery intima-media thickness (CCA-IMT) in the general population. Methods: Information on high-sensitivity C-reactive protein, fibrinogen, leucocyte count and CCA-IMT was available in 20 prospective cohort studies of the PROG-IMT collaboration involving 49,097 participants free of pre-existing cardiovascular disease. Estimates of associations were calculated within each study and then combined using random-effects meta-analyses. Results: Mean baseline CCA-IMT amounted to 0.74 mm (SD ¼ 0.18) and mean CCA-IMT progression over a mean of 3.9 years to 0.011 mm/year (SD ¼ 0.039). Cross-sectional analyses showed positive linear associations between inflammatory markers and baseline CCA-IMT. After adjustment for traditional cardiovascular risk factors, mean differences in baseline CCA-IMT per one-SD higher inflammatory marker were: 0.0082 mm for high-sensitivity C-reactive protein (p < 0.001); 0.0072 mm for fibrinogen (p < 0.001); and 0.0025 mm for leucocyte count (p ¼ 0.033). 'Inflammatory load', defined as the number of elevated inflammatory markers (i.e. in upper two quintiles), showed a positive linear association with baseline CCA-IMT (p < 0.001). Longitudinal associations of baseline inflammatory markers and changes therein with CCA-IMT progression were null or at most weak. Participants with the highest 'inflammatory load' had a greater CCA-IMT progression (p ¼ 0.015). Conclusion: Inflammation was independently associated with CCA-IMT cross-sectionally. The lack of clear associations with CCA-IMT progression may be explained by imprecision in its assessment within a limited time period. Our findings for 'inflammatory load' suggest important combined effects of the three inflammatory markers on early atherosclerosis.
Inflammation in Atherosclerosis
Journal of the American College of Cardiology, 2009
Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet factors which would trigger the proliferation of smooth muscle cells in the arterial intima. These cells would then elaborate an extracellular matrix that would entrap lipoproteins, forming the nidus of the atherosclerotic plaque. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent investigations identified immune cells and mediators at work in atheromata, implicating inflammation in this disease. Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.
Journal of Hypertension, 2006
Background Among the markers of inflammation, a cytokine, interleukin (IL)-6, promotes the expression of intercellular adhesion molecule 1 (ICAM-1), C-reactive protein (CRP) synthesis, and leads to a series of procoagulant actions with potential major implications on the progression of atherosclerosis. Aim of the study To analyse in a population-based study, the relationship between IL-6 and atherosclerotic lesions and the role of serum ICAM-1 and CRP on this relationship. Population Among 1015 individuals randomly recruited between 1995 and 1997 in Haute-Garonne, a French region with a low cardiovascular risk, 953 subjects with complete data for all measurements were analysed. Common carotid intima-media thickness (IMT) and the presence of plaques in the carotid and femoral arteries were assessed by ultrasonography. Results Quartiles of IL-6, serum ICAM-1 and CRP were positively associated with plaques and IMT. After adjustment for traditional risk factors, IL-6 (P < 0.001) and serum ICAM-1 (P < 0.002) remained positively associated with plaques but not CRP (P U 0.20). Neither IL-6, nor serum ICAM-1, nor CRP were independently associated with IMT. When serum ICAM-1 was entered into the model in addition to traditional risk factors and IL-6, the percentage of variance in the number of plaques explained by the model did not increase significantly. Conclusion IL-6 levels are associated with subclinical atherosclerotic lesions independently of traditional risk factors; the influence of IL-6 on ICAM-1 secretion may play a role in this association. These results argue the interest of IL-6 in the stratification of cardiovascular risk.
Atherosclerosis as Inflammation
Annals of Vascular Surgery, 2005
Atherosclerosis has traditionally been attributed to disordered cholesterol metabolism with associated accumulation of lipid substrate in the arterial wall. It is now believed that systemic and local inflammatory events mediate all phases of plaque development, progression, and degeneration. No longer regarded as a bland, mechanical process, plaque evolution is now best understood as a pitched battle between proinflammatory and anti-inflammatory cellular and molecular elements. Not unlike models of chronic wound healing or ischemia-reperfusion, the biologic state of a plaque at any given time is transient and mutable, reflecting a dynamic balance of numerous local and circulating inflammatory forces. Dreaded complications of the disease such as myocardial infarction and stroke result from acute shifts in this balance in favor of plaque instability and vulnerability over stable states of chronic inflammation. The purpose of this article is (1) to review the inflammatory pathogenesis of atherosclerosis on a molecular basis, (2) describe several of the emerging inflammatory biomarkers currently being investigated with particular interest in their possible roles as direct mediators of vascular disease, and (3) identify several important implications for diagnosis and therapy.
The Role Of Inflammation In Atherosclerosis
2017
To the best people I have ever had in my life, my parents, Elmokhtar Saaoud and Salma Saaoud, for their endless love, support, and encouragements throughout my life pushing me always toward success. To my dear husband, Ismail Ben Issa, I give my deepest expression of love and appreciation for your support, encouragement, and the sacrifice you made during this graduate program. Thank you for your practical and emotional support. To my precious kids, Mohammed, Abdalmuizz, Danah, and Maryam who have been affected in every possible way by this quest. My love for you all can never be quantified. First and for most, I would like to thank my advisor, Dr. Daping Fan, for his admirable guidance, excellent advice, and patience over the past several years. I am very grateful to him for providing me such opportunity to work in his laboratory and great training that is valuable to my future development. I would like to thank all current and past members of Dr. Fan's lab, in particularly Xuemei Jia and Junfeng Wang for their invaluable training and assistance since the first day I joined the group. I would like to thank Yuzhen Wang for her help with the histological analysis.