Optical detection of triggered atherosclerotic plaque disruption by fluorescence emission analysis

Alexander Christov, Erbin Dai, Maria Drangova, Liying Liu, George S. Abela, Piers Nash, Douglas McFadden, Alexandra Lucas

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Fluorescence emission analysis (FEA) has proven to be very sensitive for the detection of elastin, collagen and lipids, which are recognized as the major sources of autofluorescence in vascular tissues. FEA has also been reported to detect venous thromboemboli. In this paper we have tested the hypothesis that FEA can reproducibly detect in viva and in vitro triggered plaque disruption and thrombosis in a rabbit model. Fluorescence emission (FE) spectra, recorded in vivo, detected Russell's viper venom (RVV)-induced transformation of atherosclerotic plaque. FE intensity at 410-490 nm 4 weeks after angioplasty was significantly lower (P < 0.0033 by analysis of variance) in RVV-treated rabbits when compared to control animals with stable plaque. FE spectral profile analyses also demonstrated a significant change in curve shape as demonstrated by polynomial regression analysis (R2 from 0.980 to 0.997). We have also demonstrated an excellent correlation between changes in FE intensity and the structural characteristics detected at different stages of "unstable atherosclerotic plaque" development using multiple regression analysis (R2 = 0.989). Thus, FEA applied in viva is a sensitive and highly informative diagnostic technique for detection of triggered atherosclerotic plaque disruption and related structural changes, associated with plaque transformation, in a rabbit model.

Original languageEnglish (US)
Pages (from-to)242-252
Number of pages11
JournalPhotochemistry and Photobiology
Volume72
Issue number2
DOIs
StatePublished - Aug 1 2000
Externally publishedYes

Fingerprint

Atherosclerotic Plaques
Fluorescence
fluorescence
rabbits
Russell's Viper
Viper Venoms
Rabbits
Regression analysis
regression analysis
Regression Analysis
elastin
thrombosis
analysis of variance
spectral emission
Elastin
collagens
Analysis of variance (ANOVA)
Angioplasty
Blood Vessels
animals

ASJC Scopus subject areas

  • Biochemistry
  • Physical and Theoretical Chemistry

Cite this

Optical detection of triggered atherosclerotic plaque disruption by fluorescence emission analysis. / Christov, Alexander; Dai, Erbin; Drangova, Maria; Liu, Liying; Abela, George S.; Nash, Piers; McFadden, Douglas; Lucas, Alexandra.

In: Photochemistry and Photobiology, Vol. 72, No. 2, 01.08.2000, p. 242-252.

Research output: Contribution to journalArticle

Christov, Alexander ; Dai, Erbin ; Drangova, Maria ; Liu, Liying ; Abela, George S. ; Nash, Piers ; McFadden, Douglas ; Lucas, Alexandra. / Optical detection of triggered atherosclerotic plaque disruption by fluorescence emission analysis. In: Photochemistry and Photobiology. 2000 ; Vol. 72, No. 2. pp. 242-252.
@article{cd3f336f61294b1ab1378eb5755ab46a,
title = "Optical detection of triggered atherosclerotic plaque disruption by fluorescence emission analysis",
abstract = "Fluorescence emission analysis (FEA) has proven to be very sensitive for the detection of elastin, collagen and lipids, which are recognized as the major sources of autofluorescence in vascular tissues. FEA has also been reported to detect venous thromboemboli. In this paper we have tested the hypothesis that FEA can reproducibly detect in viva and in vitro triggered plaque disruption and thrombosis in a rabbit model. Fluorescence emission (FE) spectra, recorded in vivo, detected Russell's viper venom (RVV)-induced transformation of atherosclerotic plaque. FE intensity at 410-490 nm 4 weeks after angioplasty was significantly lower (P < 0.0033 by analysis of variance) in RVV-treated rabbits when compared to control animals with stable plaque. FE spectral profile analyses also demonstrated a significant change in curve shape as demonstrated by polynomial regression analysis (R2 from 0.980 to 0.997). We have also demonstrated an excellent correlation between changes in FE intensity and the structural characteristics detected at different stages of {"}unstable atherosclerotic plaque{"} development using multiple regression analysis (R2 = 0.989). Thus, FEA applied in viva is a sensitive and highly informative diagnostic technique for detection of triggered atherosclerotic plaque disruption and related structural changes, associated with plaque transformation, in a rabbit model.",
author = "Alexander Christov and Erbin Dai and Maria Drangova and Liying Liu and Abela, {George S.} and Piers Nash and Douglas McFadden and Alexandra Lucas",
year = "2000",
month = "8",
day = "1",
doi = "10.1562/0031-8655(2000)072<0242:ODOTAP>2.0.CO;2",
language = "English (US)",
volume = "72",
pages = "242--252",
journal = "Photochemistry and Photobiology",
issn = "0031-8655",
publisher = "Wiley-Blackwell",
number = "2",

}

TY - JOUR

T1 - Optical detection of triggered atherosclerotic plaque disruption by fluorescence emission analysis

AU - Christov, Alexander

AU - Dai, Erbin

AU - Drangova, Maria

AU - Liu, Liying

AU - Abela, George S.

AU - Nash, Piers

AU - McFadden, Douglas

AU - Lucas, Alexandra

PY - 2000/8/1

Y1 - 2000/8/1

N2 - Fluorescence emission analysis (FEA) has proven to be very sensitive for the detection of elastin, collagen and lipids, which are recognized as the major sources of autofluorescence in vascular tissues. FEA has also been reported to detect venous thromboemboli. In this paper we have tested the hypothesis that FEA can reproducibly detect in viva and in vitro triggered plaque disruption and thrombosis in a rabbit model. Fluorescence emission (FE) spectra, recorded in vivo, detected Russell's viper venom (RVV)-induced transformation of atherosclerotic plaque. FE intensity at 410-490 nm 4 weeks after angioplasty was significantly lower (P < 0.0033 by analysis of variance) in RVV-treated rabbits when compared to control animals with stable plaque. FE spectral profile analyses also demonstrated a significant change in curve shape as demonstrated by polynomial regression analysis (R2 from 0.980 to 0.997). We have also demonstrated an excellent correlation between changes in FE intensity and the structural characteristics detected at different stages of "unstable atherosclerotic plaque" development using multiple regression analysis (R2 = 0.989). Thus, FEA applied in viva is a sensitive and highly informative diagnostic technique for detection of triggered atherosclerotic plaque disruption and related structural changes, associated with plaque transformation, in a rabbit model.

AB - Fluorescence emission analysis (FEA) has proven to be very sensitive for the detection of elastin, collagen and lipids, which are recognized as the major sources of autofluorescence in vascular tissues. FEA has also been reported to detect venous thromboemboli. In this paper we have tested the hypothesis that FEA can reproducibly detect in viva and in vitro triggered plaque disruption and thrombosis in a rabbit model. Fluorescence emission (FE) spectra, recorded in vivo, detected Russell's viper venom (RVV)-induced transformation of atherosclerotic plaque. FE intensity at 410-490 nm 4 weeks after angioplasty was significantly lower (P < 0.0033 by analysis of variance) in RVV-treated rabbits when compared to control animals with stable plaque. FE spectral profile analyses also demonstrated a significant change in curve shape as demonstrated by polynomial regression analysis (R2 from 0.980 to 0.997). We have also demonstrated an excellent correlation between changes in FE intensity and the structural characteristics detected at different stages of "unstable atherosclerotic plaque" development using multiple regression analysis (R2 = 0.989). Thus, FEA applied in viva is a sensitive and highly informative diagnostic technique for detection of triggered atherosclerotic plaque disruption and related structural changes, associated with plaque transformation, in a rabbit model.

UR - http://www.scopus.com/inward/record.url?scp=0034256867&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034256867&partnerID=8YFLogxK

U2 - 10.1562/0031-8655(2000)072<0242:ODOTAP>2.0.CO;2

DO - 10.1562/0031-8655(2000)072<0242:ODOTAP>2.0.CO;2

M3 - Article

VL - 72

SP - 242

EP - 252

JO - Photochemistry and Photobiology

JF - Photochemistry and Photobiology

SN - 0031-8655

IS - 2

ER -