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Why study inflammation in heart disease? Two general hypotheses emerging from the basic science community have driven this research. The first is the concept that inflammation itself may determine plaque stability. Unstable plaques have increased leukocytic infiltrates in them, and T-cells and macrophages predominate at the rupture sites in these plaques. Also, cytokines and metalloproteinases may influence plaque stability and the degradation of the fibrous cap. But in addition to the idea that atherosclerosis is fundamentally an inflammatory disorder is the recognition in the basic science literature that lipid lowering in general may reduce plaque inflammation. That is to say, experimental studies have now demonstrated reduced macrophage number within atherosclerotic plaques treated with lipid-lowering statin therapy as well as decreased expression of collagenolytic enzymes and the attenuation of other markers of the inflammatory process.

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