PMID- 22509411
OWN - NLM
STAT- MEDLINE
DCOM- 20120807
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 7
IP  - 4
DP  - 2012
TI  - Cellular imaging of human atherosclerotic lesions by intravascular electric 
      impedance spectroscopy.
PG  - e35405
LID - 10.1371/journal.pone.0035405 [doi]
LID - e35405
AB  - BACKGROUND: Newer techniques are required to identify atherosclerotic lesions 
      that are prone to rupture. Electric impedance spectroscopy (EIS) is able to 
      provide information about the cellular composition of biological tissue. The 
      present study was performed to determine the influence of inflammatory processes 
      in type Va (lipid core, thick fibrous cap) and Vc (abundant fibrous connective 
      tissue while lipid is minimal or even absent) human atherosclerotic lesions on 
      the electrical impedance of these lesions measured by EIS. METHODS AND RESULTS: 
      EIS was performed on 1 aortic and 3 femoral human arteries at 25 spots with 
      visually heavy plaque burden. Severely calcified lesions were excluded from 
      analysis. A highly flexible micro-electrode mounted onto a balloon catheter was 
      placed on marked regions to measure impedance values at 100 kHz. After paraffin 
      embedding, visible marked cross sections (n = 21) were processed. Assessment of 
      lesion types was performed by Movats staining. Immunostaining for CD31 (marker of 
      neovascularisation), CD36 (scavenger cells) and MMP-3 (matrix 
      metalloproteinase-3) was performed. The amount of positive cells was assessed 
      semi-quantitatively. 15 type Va lesions and 6 type Vc lesions were identified. 
      Lesions containing abundant CD36-, CD31- and MMP-3-positive staining revealed 
      significantly higher impedance values compared to lesions with marginal or 
      without positive staining (CD36 + 455 +/- 50 Omega vs. CD36- 346 +/- 53 Omega, p = 0.001; 
      CD31 + 436 +/- 43 Omega vs. CD31- 340 +/- 55 Omega, p = 0.001; MMP-3 + 400 +/- 68 Omega vs. MMP-3- 
      323 +/- 33 Omega, p = 0.03). CONCLUSIONS: Atherosclerotic lesions with abundant 
      neovascularisation (CD31), many scavenger receptor class B expressing cells 
      (CD36) or high amount of MMP-3 immunoreactivity reveal significantly higher 
      impedance values compared to lesions with marginal or no detection of 
      immunoreactivity. Findings suggest that inflammatory processes in vulnerable 
      plaques affect the impedance of atherosclerotic lesions and might therefore be 
      detected by EIS.
FAU - Streitner, Ines
AU  - Streitner I
AD  - 1st Department of Medicine-Cardiology, University Medical Centre Mannheim, 
      Mannheim, Germany. I.Streitner@t-online.de
FAU - Goldhofer, Markus
AU  - Goldhofer M
FAU - Cho, Sungbo
AU  - Cho S
FAU - Kinscherf, Ralf
AU  - Kinscherf R
FAU - Thielecke, Hagen
AU  - Thielecke H
FAU - Borggrefe, Martin
AU  - Borggrefe M
FAU - Suselbeck, Tim
AU  - Suselbeck T
FAU - Streitner, Florian
AU  - Streitner F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120411
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (CD36 Antigens)
RN  - 0 (Platelet Endothelial Cell Adhesion Molecule-1)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
SB  - IM
MH  - Angiography/*methods
MH  - Aorta/pathology
MH  - Atherosclerosis/*diagnosis/*pathology
MH  - CD36 Antigens/analysis
MH  - Connective Tissue/pathology
MH  - Dielectric Spectroscopy/*methods
MH  - Endovascular Procedures/*methods
MH  - Femoral Artery/pathology
MH  - Humans
MH  - Male
MH  - Matrix Metalloproteinase 3/analysis
MH  - Platelet Endothelial Cell Adhesion Molecule-1/analysis
PMC - PMC3324547
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2012/04/18 06:00
MHDA- 2012/08/08 06:00
PMCR- 2012/04/11
CRDT- 2012/04/18 06:00
PHST- 2011/11/30 00:00 [received]
PHST- 2012/03/15 00:00 [accepted]
PHST- 2012/04/18 06:00 [entrez]
PHST- 2012/04/18 06:00 [pubmed]
PHST- 2012/08/08 06:00 [medline]
PHST- 2012/04/11 00:00 [pmc-release]
AID - PONE-D-11-23883 [pii]
AID - 10.1371/journal.pone.0035405 [doi]
PST - ppublish
SO  - PLoS One. 2012;7(4):e35405. doi: 10.1371/journal.pone.0035405. Epub 2012 Apr 11.