TY - JOUR
T1 - Detection of rupture-prone atherosclerotic plaques by time-resolved laser-induced fluorescence spectroscopy
AU - Marcu, Laura
AU - Jo, Javier A.
AU - Fang, Qiyin
AU - Papaioannou, Thanassis
AU - Reil, Todd
AU - Qiao, Jian Hua
AU - Baker, J. Dennis
AU - Freischlag, Julie A.
AU - Fishbein, Michael C.
N1 - Funding Information:
This study was supported by the National Institute of Health Grant R01 HL 67377. We thank the vascular surgeons and nurses at the UCLA Vascular Center for their support with data collection from patients; and Dr. Pramod Butte for his contribution to data acquisition.
PY - 2009/5
Y1 - 2009/5
N2 - Objective: Plaque with dense inflammatory cells, including macrophages, thin fibrous cap and superficial necrotic/lipid core is thought to be prone-to-rupture. We report a time-resolved laser-induced fluorescence spectroscopy (TR-LIFS) technique for detection of such markers of plaque vulnerability in human plaques. Methods: The autofluorescence of carotid plaques (65 endarterectomy patients) induced by a pulsed laser (337 nm, 0.7 ns) was measured from 831 distinct areas. The emission was resolved spectrally (360-550 nm range) and temporally (0.3 ns resolution) using a prototype fiber-optic TR-LIFS apparatus. Lesions were evaluated microscopically and quantified as to the % of different components (fibrous cap, necrotic core, inflammatory cells, foam cells, mature and degraded collagen, elastic fibers, calcification, and smooth muscle cell of the vessel wall). Results: We determined that the spectral intensities and time-dependent parameters at discrete emission wavelengths (1) allow for discrimination (sensitivity >81%, specificity >94%) of various compositional and pathological features associated with plaque vulnerability including infiltration of macrophages into intima and necrotic/lipid core under a thin fibrous cap, and (2) show a linear correlation with plaque biochemical content: elastin (P < 0.008), collagen (P < 0.02), inflammatory cells (P < 0.003), necrosis (P < 0.004). Conclusion: Our results demonstrate the feasibility of TR-LIFS as a method for the identification of markers of plaque vulnerability. Current findings enable future development of TR-LIFS-based clinical devices for rapid investigation of atherosclerotic plaques and detection of those at high-risk.
AB - Objective: Plaque with dense inflammatory cells, including macrophages, thin fibrous cap and superficial necrotic/lipid core is thought to be prone-to-rupture. We report a time-resolved laser-induced fluorescence spectroscopy (TR-LIFS) technique for detection of such markers of plaque vulnerability in human plaques. Methods: The autofluorescence of carotid plaques (65 endarterectomy patients) induced by a pulsed laser (337 nm, 0.7 ns) was measured from 831 distinct areas. The emission was resolved spectrally (360-550 nm range) and temporally (0.3 ns resolution) using a prototype fiber-optic TR-LIFS apparatus. Lesions were evaluated microscopically and quantified as to the % of different components (fibrous cap, necrotic core, inflammatory cells, foam cells, mature and degraded collagen, elastic fibers, calcification, and smooth muscle cell of the vessel wall). Results: We determined that the spectral intensities and time-dependent parameters at discrete emission wavelengths (1) allow for discrimination (sensitivity >81%, specificity >94%) of various compositional and pathological features associated with plaque vulnerability including infiltration of macrophages into intima and necrotic/lipid core under a thin fibrous cap, and (2) show a linear correlation with plaque biochemical content: elastin (P < 0.008), collagen (P < 0.02), inflammatory cells (P < 0.003), necrosis (P < 0.004). Conclusion: Our results demonstrate the feasibility of TR-LIFS as a method for the identification of markers of plaque vulnerability. Current findings enable future development of TR-LIFS-based clinical devices for rapid investigation of atherosclerotic plaques and detection of those at high-risk.
KW - Atherosclerosis
KW - Diagnosis
KW - Fluorescence spectroscopy
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U2 - 10.1016/j.atherosclerosis.2008.08.035
DO - 10.1016/j.atherosclerosis.2008.08.035
M3 - Article
C2 - 18926540
AN - SCOPUS:67349286996
SN - 0021-9150
VL - 204
SP - 156
EP - 164
JO - Atherosclerosis
JF - Atherosclerosis
IS - 1
ER -