Cardiosource: "Inflammation is now recognized as playing a fundamental role in atherosclerosis and its acute thrombotic complications.1 Although not necessarily the primary event, inflammation and cytokine activation during plaque formation and destabilization may represent a common final pathway to various stimuli. To the degree that inflammatory pathways play an important pathogenic mechanism in atherogenesis and plaque destabilization, a whole new approach to treating atherosclerosis is being proposed: immunomodulation.
Twenty years ago, the first reports were published showing the presence of activated immune cells in human atherosclerotic lesions.2 This was followed shortly thereafter by evidence that vascular cells can present antigen to T cells and that vascular cells can produce as well as respond to immune cytokines.3, 4 Several disease-associated antigens subsequently were identified, including oxidized low-density lipoprotein (oxLDL)5 and heat shock protein (HSP)-60.6 This led to various hypotheses regarding the role of immune/inflammatory mechanisms in atherosclerosis.
Today, it is clear that immune cells dominate early atherosclerotic lesions and their effector molecules accelerate lesion progression, ultimately leading to inflammation that can elicit acute coronary syndromes. Thus, inflammation and immunity play a key role in a number of specific cardiovascular diseases (Slide 1), presenting a long list of po"
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