Myeloperoxidase – a link between inflammation and cardiovascular disease
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Abstract
The majority of acute myocardial infarctions occur because of the sudden development of a thrombus in a coronary artery. The thrombus is frequently associated with a ruptured plaque releasing tissue factor into the circulation which is highly thrombotic. Plaques that are prone to rupture tend to have large lipid pools, a large number of inflammatory cells, and a thin fibrous cap. The inflammatory cells are thought to contribute to the vulnerability of the plaque by inhibiting cells that synthesis collagen and by releasing proteinases that degrade collagen in the fibrous cap. The measurement of inflammatory makers such as C-reactive protein has been proposed as a potential way to identify patients that have inflamed and vulnerable plaques. Therapies, such as high doses of statins, can be initiated to reduce cardiovascular events in part by reducing inflammation and stabilizing vulnerable plaques.
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