Discrimination of human coronary artery atherosclerotic lipid-rich lesions by time-resolved laser-induced fluorescence spectroscopy

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Abstract

Lesion composition plays a significant role in atherosclerotic lesion instability and rupture. Current clinical techniques cannot fully characterize lesion composition or accurately identify unstable lesions. This study investigates the use of time-resolved fluorescence spectroscopy for unstable atherosclerotic lesion diagnosis. The fluorescence of human coronary artery samples was induced with nitrogen laser and detected in the 360- to 510-nm wavelength range. The samples were sorted into 7 groups according to the AHA classification: normal wall and types I, IIa (fatty streaks), III (preatheroma), IV (atheroma), Va (fibrous), and Vb (calcified) lesions. Spectral intensities and time-dependent parameters [average lifetime τf; decay constants: τ1 (fast-term), τ2 (slow-term), A1 (fast-term amplitude contribution)] derived from the time-resolved spectra of coronary samples were used for tissue characterization. We determined that a few intensity values at longer wavelengths (>430 nm) and time-dependent parameters at peak emission region (390 nm) discriminate between all types of arterial samples except between normal wall and type I lesions. The lipid-rich lesions (more unstable) can be discriminated from fibrous lesions (more stable) on the basis of time-dependent parameters (lifetime and fast-term decay). We inferred that features of lipid fluorescence are reflected on lipid-rich lesion emission. Our results demonstrate that analysis of the time-resolved spectra may be used to enhance the discrimination between different grades of atherosclerotic lesions and provide a means of discrimination between lipid-rich and fibrous lesions.

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Marcu, L., Fishbein, M. C., Maarek, J. M. I., & Grundfest, W. S. (2001). Discrimination of human coronary artery atherosclerotic lipid-rich lesions by time-resolved laser-induced fluorescence spectroscopy. Arteriosclerosis, Thrombosis, and Vascular Biology, 21(7), 1244–1250. https://doi.org/10.1161/hq0701.092091

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