ABSTRACT
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 670 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 670
Near-infrared (NIR) spectrometry can be a useful tool in the study of cardiovascular diseases (CVDs) including atherosclerosis and aneurysm. Atherosclerosis in the vessel wall has been linked to aneurysm, although it is not clear that this is a causal relationship. Studies have been undertaken in both animal models of CVD and in human patients. There is widespread agreement that new diagnostic techniques are required to identify coronary plaques that are prone to disruption. The type of plaque considered most vulnerable to disruption is a thin-capped fibroatheroma with increased inflammatory cell content. Multiple techniques are being tested to identify such plaques before they disrupt and cause thrombosis. Identification of these potentially lethal plaques before they disrupt will facilitate the development of therapeutic strategies to prevent acute coronary events. In animal research, several genetic “knockout” mouse models have been developed recently to mimic human atherosclerosis [1] and abdominal aortic aneurysm (AAA) [2]. Techniques for monitoring the onset, progression, and regression of these processes in mouse models could provide valuable pathophysiological insights into the disease processes. Nondestructive in vivo techniques will be needed for proteomics studies in these models. Finally, these analytical methods may be useful in assessing the effectiveness of possible treatments. Atherosclerosis is a chronic inflammatory process [3-5] with complications that are the leading cause of death in Western societies. Extensive research has been done to determine the complex pathophysiology of atherosclerosis, although mechanisms for various aspects are still being elucidated. Among the earliest changes in the vessel wall is an increase in retained lipoproteins [6-8] and subsequent oxidation [7,9,10] in the subendothelial matrix. Development of lipid-laden macrophages (foam cells) is another hallmark of the early atherosclerotic process [11,12]. Proliferation and phenotypic changes in smooth muscle cells are seen as well [13,14]. The advanced atherosclerotic lesion may be characterized by accumulation of extracellular lipid, development of a lipid-rich necrotic core, formation of a fibrous cap, and calcification [15].
