Of late we have been concerned with the thrombogenic hypothesis in …
Encrustation or thrombogenic hypothesis: proposed that organization of repeated
Genetic, and Thrombogenic Markers of Atherosclerosis ..
Rupture of a plaque or denudation of the endothelium overlying a fibrous plaque may result in exposure of the highly thrombogenic subendothelium and lipid core. This exposure may result in thrombus formation, which may partially or completely occlude flow in the involved artery. Unstable angina pectoris, MI, transient ischemic attack, and stroke are examples of the clinical sequelae of partial or complete acute occlusion of an artery. Atheroembolism is a distinct clinical entity that may occur spontaneously or as a complication of aortic surgery, angiography, or thrombolytic therapy in patients with advanced and diffuse atherosclerosis.
In his response-to-injury hypothesis, Ross postulated that atherosclerosis begins with endothelial injury, making the endothelium susceptible to the accumulation of lipids and the deposition of thrombus. The mechanisms of atherogenesis remain uncertain, but the response-to-injury hypothesis is the most widely accepted proposal.
The thrombogenic hypothesis in coronary atherosclerosis
C-reactive protein (CRP) is a classic short pentraxin primarily synthesized in the liver during the course of inflammatory processes. Clinical studies suggest that this prototypic acute-phase reactant predicts cardiovascular risks better than conventional risks such as LDL-cholesterol levels. Accumulating evidence demonstrates in vitro that CRP elicits activation of cells associated with atherosclerosis and its acute thrombotic complications (e.g., endothelial cells, monocytes/macrophages, and smooth muscle cells). For example, CRP suppresses endothelial production of atheroprotective NO and induces pro-inflammatory VCAM-1 and IL-6. CRP augments activation of NF- k B, a transcription factor that contributes importantly to inflammation. CRP also increases macrophage production of tissue factor. Therefore, CRP may trigger a cascade of athero-thrombogenic events. Recent studies employing transgenic mice overexpressing human CRP in the liver demonstrated that CRP accelerates the formation of chronic atherosclerosis and acute thrombus formation in vivo. Notably, in these mice, total occlusion of mechanically-injured carotid arteries frequently occurred without significant neointima formation, suggesting more direct thrombogenic effects of CRP. From another exciting aspect of CRP biology, structural and functional analyses suggest that dissociation of CRP from its native pentameric to a monomeric form may play a key role in exerting its pro-inflammatory and thrombogenic effects. Further understanding of the mechanisms underlying this conformational rearrangement may lead to the development of more effective therapies for acute coronary events. The mechanism by which CRP binds to cells and activates signal transduction pathways also remains obscure. Furthermore, the fusion of data from cell biology and human genetics on CRP should help not only to identify genetic variation that predisposes to a particular set of clinical populations (e.g., elevated CRP associated with increased cardiovascular risk), but also to clarify the mechanism of CRP-induced cell activation and, in turn, the pathogenesis of acute thrombotic complications related to this pantraxin.
Much of this phenotypic variability is likely to be determined by the relative stability of the vascular plaque burden. Plaque rupture and exposure of the thrombogenic lipid core are critical events in the expression of this disease process and determine the prognosis. The ability to determine and quantify risk and prognosis in patients with atherosclerosis is limited by the inability to objectively measure plaque stability and other predictors of clinical events.
Atherosclerosis is a disease in which the inside of an artery ..
Darby formulated two hypotheses forbiological mechanisms that lead to increased morbidity andmortality from coronary artery disease following radiation exposure(). The first hypothesis statesthat radiation interacts with the pathogenesis of age-relatedatherosclerosis, as such accelerating the development ofatherosclerosis. The second hypothesis is that radiation increasesthe lethality of age-related myocardial infarction by decreasingthe heart tolerance to acute infarctions as a result ofmicrovascular damage in the myocardium. These hypotheses do notstand alone, and both macro- and microvascular effects most likelyact together to produce clinical heart disease ().
Although this so-called "thrombogenic" hypothesis of atherosclerosis was denied by Virchow, Duguid revived this hypothesis in 1946.
In 1976, Ross and Glomset emphasized the importance of intimal smooth-muscle proliferation as the key element in the development of the advanced lesions of atherosclerosis.
Hypercoagulability and Atherosclerosis - JST
Amide-adducts in atherosclerosis.
07/12/2016 · Amide-adducts in atherosclerosis
Westminster Hospital, London
Amide-Adducts in Atherosclerosis | SpringerLink
"I have always been impressed by the quick turnaround and your thoroughness. Easily the most professional essay writing service on the web."
"Your assistance and the first class service is much appreciated. My essay reads so well and without your help I'm sure I would have been marked down again on grammar and syntax."
"Thanks again for your excellent work with my assignments. No doubts you're true experts at what you do and very approachable."
"Very professional, cheap and friendly service. Thanks for writing two important essays for me, I wouldn't have written it myself because of the tight deadline."
"Thanks for your cautious eye, attention to detail and overall superb service. Thanks to you, now I am confident that I can submit my term paper on time."
"Thank you for the GREAT work you have done. Just wanted to tell that I'm very happy with my essay and will get back with more assignments soon."