Collagenases and cracks in the plaque
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The core of an atheromatous plaque contains lipids, macrophages, and cellular debris, typically covered by a fibrous cap that separates the thrombogenic core from the blood, which causes most fatal myocardial infarctions.Abstract:
The core of an atheromatous plaque contains lipids, macrophages, and cellular debris, typically covered by a fibrous cap that separates the thrombogenic core from the blood. Rupture of the fibrous cap causes most fatal myocardial infarctions. Interstitial collagen confers tensile strength on the cap, as it does in skin and tendons. In 1994, Peter Libby and colleagues demonstrated overexpression of collagenolytic enzymes in atheromatous plaques and implicated MMPs in the destabilization of these lesions.read more
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References
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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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Pathophysiology of Coronary Artery Disease
Peter Libby,Pierre Theroux +1 more
TL;DR: Treatment of coronary atherosclerosis should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid “stabilization” of other plaques that may produce recurrent events.
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Population Trends in the Incidence and Outcomes of Acute Myocardial Infarction
TL;DR: Reductions in short-term case fatality rates for myocardial infarction appear to be driven, in part, by a decrease in the incidence of ST-segment elevation myocardia infarctions and a lower rate of death after non-ST-se segment elevation my Cardiac Infarction.
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Pravastatin Treatment Increases Collagen Content and Decreases Lipid Content, Inflammation, Metalloproteinases, and Cell Death in Human Carotid Plaques Implications for Plaque Stabilization
Milita Crisby,Gunilla Nordin-Fredriksson,Prediman K. Shah,Juliana Yano,Jenny Zhu,Jan Nilsson +5 more
TL;DR: Pravastatin decreased lipids, lipid oxidation, inflammation, MMP-2, and cell death and increased TIMP-1 and collagen content in human carotid plaques, confirming its plaque-stabilizing effect in humans.
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Mechanisms of Acute Coronary Syndromes and Their Implications for Therapy
TL;DR: The notion that heart attacks develop from coronary-artery stenosis is an oversimplification of a process involving lipid metabolism, inflammation, macrophage activation, collagen breakdown, and plaque rupture.