Atherosclerotic plaque atheromas

Atherosclerotic plaques (atheroma) may promote occlusive clot formation and/or so reduce the size of the blood vessel lumen that areas of heart muscle become deprived of oxygen. This deprivation may be particularly acute during exercise and lead to the pain characteristic of angina pectoris. 

Chronic diseases such as atherosclerosis are also propagated by oxidative stress (73). The sequence of events leading to arterial occlusion is complex and not fully understood. However, both platelet adhesion and macrophage activation participate in the formation of atherosclerotic plaques in the environment of elevated serum cholesterol (74). Oxidative chemistry can profoundly affect several steps in the formation of atheroma (75), including recruitment of immune cells such as macrophages, and as during ischemia-reperfusion, the antioxidant nature of NO can inhibit this process (76). 

Leon MB, Lu DY, Prevosti LG, et al. Human arterial surface fluorescence atherosclerotic plaque identification and effects of laser atheroma ablation. J Am Coll Cardiol 1988 12(I ) 94-102. 

Figure 13.2 Examples of infrared reflectivity from aortic atheromas. Typical intensity profiles of (a) the incoming synchrotron IR beam, (b) reflected signals from atheromas, and (c) from non-atherosclerotic sites, (d) The corresponding reflection-absorption spectra of (b) shared spectral characteristics that were consistent with known excitation effects by IR photons on atoms of molecules that are known to characterize atherosclerotic plaques. Each plot shows the averaged spectrum (black trace) 1.0 standard deviation (gray trace) n = 26.

Atherosclerotic plaque is a complex lesion which is a result of an inflammatory and reparative process. The atheroma plaque contains extracellular deposits of calcium salts, blood components, cholesterol crystals, and acid mucopolysaccharides. The initial changes, however, seem to occur at the cellular level, often accompanied by an abnormal intracellular storage of lipids, particularly cholesterol esters, fatty acids, and lipoprotein complexes. The rupture of the plaque can generate thrombosis, reductions in the vessel lumen and consequently in the cardiac perfusion, and acute or chronic consequences. 

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