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Near-infrared spectroscopic characterization of human advanced atherosclerotic plaques

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
卷 39, 期 8, 页码 1305-1313

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ELSEVIER SCIENCE INC
DOI: 10.1016/S0735-1097(02)01767-9

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OBJECTIVES Living human carotid atherosclerotic plaques were examined in vitro by near-infrared (NIR) spectroscopy to determine the spectral features of plaque vulnerability. BACKGROUND Plaque disruption, a major cause of heart attacks and strokes, cannot generally be predicted, but is thought to depend mainly on plaque composition. Near-infrared spectroscopy has been used to detect components in tissues noninvasively. METHODS Using an NIR spectrometer fitted with a fiberoptic probe, living human carotid atherosclerotic plaques (from 25 patients) were examined ex vivo for plaque vulnerability. The plaques were cut into smaller sections according to their gross pathologic features, and NIR measurements were done at 20degreesC, usually within 10 min, RESULTS According to the American Heart Association's recommended classification scheme, the lesions were classified into three groups: the first group comprised of vulnerable tvpe V/VI lesions; the second group, stable tvpe I/II lesions; and the third (intermediate) group, mainly type III/IV lesions. Cluster analysis of the specimens' NIR spectra identified three major p composition groups in each of the three NIR spectral regions: 2,200 to 2,330 nm, 1,620 to 1,820 nm and 1,130 to 1,260 nm. Calculation of the lipid/protein ratios in each group at two NIR regions (2,200 to 2,330 nm) revealed ratios of 1.49 +/- 1.20, 2.12 +/- 1.00 and 3.37 +/- 0.88 for type I/II, type III/IV and advanced type V/VI lesions, respectively (p < 0.03). At 1,620 to 1,820 nm, the respective ratios for these histologic groups were 0.57 +/- 0.21, 1.54 +/- 0.46 and 2.40 +/- 0.44 (p < 0.00003). CONCLUSIONS The good ex vivo discrimination of histologically vulnerable and stable plaques in this studs suggests that NIR spectroscopy has the potential to identify vulnerable atherosclerotic plaques in vivo. (C) 2002 by the American College of Cardiology Foundation.

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