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Open AccessJournal ArticleDOI

Mechanisms of plaque vulnerability and rupture.

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TLDR
Reducing the lipid component and inflammation in atherosclerotic plaques may help reduce the risk of plaque rupture, and may account for the clinical benefit of risk-factor reduction gained from changes in lifestyle and from drug therapy.
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This article is published in Journal of the American College of Cardiology.The article was published on 2003-02-19 and is currently open access. It has received 522 citations till now. The article focuses on the topics: Fibrous cap.

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Lack of Toll-like receptor 4 or myeloid differentiation factor 88 reduces atherosclerosis and alters plaque phenotype in mice deficient in apolipoprotein E

TL;DR: An important role for TLR4 and MyD88 signaling in atherosclerosis in a hypercholesterolemic mouse model is suggested, providing a pathophysiologic link between innate immunity, inflammation, and atherogenesis.
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Multimodality Imaging Probes: Design and Challenges

TL;DR: This review provides an overview of the many strategies that have been applied to achieve multimodal functionality in a single probe unit and the caveat is that because the sensitivities of different imaging modalities can vary by 3 orders of magnitude, it may not be practical to simply add all functionalities to one molecule.
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Inflammation in Atherosclerosis

TL;DR: Accumulating experimental evidence supports a key role for inflammation as a link between risk factors for atherosclerosis and the biology that underlies the complications of this disease.
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Leukocyte count and coronary heart disease: Implications for risk assessment

TL;DR: Leukocytosis has been consistently shown to be an independent risk factor and prognostic indicator of future cardiovascular outcomes, regardless of disease status, and the leukocyte count is inexpensive, reliable, easy to interpret, and ordered routinely in inpatient and outpatient settings.
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Rho Kinases in Cardiovascular Physiology and Pathophysiology

TL;DR: This review, based on recent molecular, cellular, and animal studies, focuses on the current understanding of ROCK signaling and its roles in cardiovascular physiology and pathophysiology.
References
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Coronary Plaque Disruption

TL;DR: This review will explore potential mechanisms responsible for the sudden conversion of a stable atherosclerotic plaque to an unstable and life-threatening atherothrombotic lesion—an event known as plaque fissuring, rupture, or disruption.
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Prevalence of Total Coronary Occlusion during the Early Hours of Transmural Myocardial Infarction

TL;DR: Total coronary occlusion is frequent during the early hours of transmural infarction and decreases in frequency during the initial 24 hours, suggesting that coronary spasm or thrombus formation with subsequent recanalization or both may be important in the evolution ofinfarction.
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Sudden Cardiac Death

TL;DR: Total mortality, rather than classifications of cardiac and arrhythmic mortality, should be used as primary objectives for many outcome studies.
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Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques.

TL;DR: A method is devised which allows the detection and microscopic localization of MMP enzymatic activity directly in tissue sections and may promote destabilization and complication of atherosclerotic plaques and provide novel targets for therapeutic intervention.
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Regression of Coronary Artery Disease as a Result of Intensive Lipid-Lowering Therapy in Men with High Levels of Apolipoprotein B

TL;DR: In men with coronary artery disease who were at high risk for cardiovascular events, intensive lipid-lowering therapy reduced the frequency of progression of coronary lesions, increased the frequencyof regression, and reduced the incidence of cardiovascular events.
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