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Open AccessJournal Article

Atherosclerosis is an Inflammatory Disease

光宏 横山, +1 more
- 28 Feb 1998 - 
- Vol. 62, pp 8
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TLDR
Despite changes in lifestyle and the use of new pharmacologic approaches to lower plasma cholesterol concentrations, cardiovascular disease continues to be the principal cause of death in the United States, Europe, and much of Asia.
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This article is published in Japanese Circulation Journal-english Edition.The article was published on 1998-02-28 and is currently open access. It has received 9749 citations till now. The article focuses on the topics: Disease.

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Casein hydrolysate containing the antihypertensive tripeptides Val-Pro-Pro and Ile-Pro-Pro improves vascular endothelial function independent of blood pressure-lowering effects: contribution of the inhibitory action of angiotensin-converting enzyme.

TL;DR: It is concluded that casein hydrolysate containing VPP and IPP improves the vascular endothelial dysfunction in subjects with mild hypertension and could help to prevent cardiovascular diseases in hypertensive subjects.
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Reduced expression of endothelial cell markers after 1 year treatment with simvastatin and atorvastatin in patients with coronary heart disease

TL;DR: The reduction in proinflammatory and to some extent haemostatic markers of endothelial function after 1 year treatment with either simVastatin or atorvastatin may be indicative of a less activated state of the endothelium which possibly may contribute to modulation of the progression of atherosclerosis.
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Endothelial nitric oxide synthase transgenic models of endothelial dysfunction.

TL;DR: Together, eNOS knockout mice and ENOS S1177 mutant mice are useful tools to study the effects of total genetic deficiency of eN OS as well as varying degrees of endothelial dysfunction caused by eNos S 1177 phosphorylation.
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Three-dimensional numerical simulation of receptor-mediated leukocyte adhesion to surfaces: Effects of cell deformability and viscoelasticity

TL;DR: Numerical simulations demonstrate the formation and breakup of membrane tethers observed in vitro and suggest that the elasticity of the cytoplasm is responsible for a teardrop shape of rolling leukocytes in vivo.
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Aged garlic extract improves endothelial function in men with coronary artery disease

TL;DR: It is suggested that short‐term treatment with AGE may improve impaired endothelial function in men with CAD treated with aspirin and a statin and whether improvement in endothelium function decreases the risk of future cardiovascular events remains to be determined.
References
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The pathogenesis of atherosclerosis: a perspective for the 1990s

TL;DR: The ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation.
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Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group

TL;DR: Treatment with pravastatin significantly reduced the incidence of myocardial infarction and death from cardiovascular causes without adversely affecting the risk of death from noncardiovascular causes in men with moderate hypercholesterolemia and no history of my Cardiac Infarction.
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Inflammation, Aspirin, and the Risk of Cardiovascular Disease in Apparently Healthy Men

TL;DR: The reduction associated with the use of aspirin in the risk of a first myocardial infarction appears to be directly related to the level of C-reactive protein, raising the possibility that antiinflammatory agents may have clinical benefits in preventing cardiovascular disease.
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The Pathogenesis of Atherosclerosis — An Update

TL;DR: A response-to-injury hypothesis of atherogenesis proposes that "injury" to the endothelium is the initiating event in atherosclerosis, and intimal smooth-muscle proliferation as the key event in the development of the advanced lesions of Atherosclerosis.
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Compensatory Enlargement of Human Atherosclerotic Coronary Arteries

TL;DR: It is concluded that human coronary arteries enlarge in relation to plaque area and that functionally important lumen stenosis may be delayed until the lesion occupies 40 percent of the internal elastic lamina area.