The photosensitizer, mono-L-aspartyl chlorin e6 (NPe6), specifically accumulates in the atheromatous plaque. We detected the fluorescence spectra of NPe6 emitted from atheromatous plaques on the descending thoracic aorta by an angioscopic approach using the animal model of atherosclerosis. We also showed that a fluorescence spectrum peak at 675 nm was obtained laparoscopically only in parts of the abdominal aorta with an atheromatous plaque. By a fluorescence endoscope, atheromatous plaques on the carotid artery were recognized as reddish spots from outside the artery. In addition, we visualized specifically at the beating heart surface small coronary atherosclerosis using an epifluorescence stereoscope system.

We examined the effects of photodynamic treatment with NPe6 on the atheromatous plaque. The change in the elastic framework in the atheromatous plaque after photodynamic treatment was evaluated using scanning electron microscopy. The destruction of the architecture of the elastic fiber network in the atheromatous plaque was revealed. We also studied the change in the lipid components of the atheromatous plaque using Fourier transform infrared (FTIR) microspectroscopy. FTIR microspectroscopic analysis showed a dissociation of ester bonds of cholesterol esters in the atheromatous plaque after photodynamic treatment. The framework of the atheromatous plaque and the lipids accumulated in the plaque could be destroyed following such treatment.