SummaryLysophosphatidylcholine (LPC) is a proinflammatory and proatherogenic substance, and it plays an important role in the initiation, progression, and destabilization of atherosclerotic plaques. If LPC in the vascular wall is visualized in vivo, the mechanisms of atherosclerosis and the effects of medical and interventional therapies on atherosclerosis can be objectively evaluated. Therefore, this study was carried out to visualize LPC in human coronary plaques using a color fluorescence angioscopy (CFA) system.(1) The fluorescence characteristics of LPC were investigated by color fluorescence microscopy (CFM) using Trypan blue dye (TB) as an indicator. For fluorescence imaging, a combination of a band-pass filter (345 nm) and a band-absorption filter of 420 nm (A imaging), or a combination of a band-pass filter (470 nm) and a band-absorption filter of 520 nm (B imaging) was employed. (2) The fluorescence of LPC in the excised human coronary plaques was investigated by CFA and CFM scanning using the same filters as those in CFM.In the presence of TB, LPC exhibited a red fluorescence in both A and B imaging. This red fluorescence color in both A and B imaging was not observed for the other known major substances that constitute the atherosclerotic plaques. This red fluorescence color in both A and B imaging was detected by CFA in both white and yellow plaques that were classified by conventional angioscopy. This fluorescence color was found to be distributed in a web-like or diffuse configuration by CFM scanning.LPC in the human coronary plaques was successfully visualized by CFA using TB as an indicator. ( and frequently induces fatal diseases such as acute coronary syndromes and cerebral events. Lysophosphatidylcholine (LPC) is a proinflammatory substance, and it is the major bioactive phospholipid component of oxidized low-density lipoprotein and plays a critical role in the atherogenic activity of oxidized low-density lipoprotein.2) This substance is generated by lipoprotein-associated phospholipase A2;3) induces vascular endothelial cell dysfunction; 4) causes endothelial cell apoptosis by DNA fragmentation; 5) stimulates adhesion and activation of lymphocytes and initiates chemotaxis of macrophages; 6) causes transformation of vascular smooth muscle cells that is characteristic of atherosclerosis;2) impairs endothelin-induced vascular relaxation; 7) and induces release of IL-6, IL-8, and arachidonic acid from vascular smooth muscle cells.2) It is well known that this detrimental substance is abundantly contained in human atherosclerotic lesions, 8) and it is released from human coronary vessels in vivo.
9)Therefore, if LPC is visualized in vivo, its role in the initiation and progression of atherosclerosis, and the effects of medical and interventional therapies on atherosclerotic plaques can be more objectively evaluated. However, there are no clinically available modalities for visualization of LPC in vivo.To date, coronary plaques have been investigated by many imaging modalities such as angiography,...