SHAPE Society

5. Hypothesis:
Monocyte-macrophages on or just
beneath the plaque surface are
detectable by the heat that they
produce.

10. Multiple
non-stenotic
coronary
plaques
In vivo live animal study
Marked temperature
heterogeneity observed with

11. Intravascular Thermosensor Basket Catheter
Volcano Therapeutics Inc
(prototype)

12. Stefanadis et al, 1999
First in vivo human intra-coronary
thermometry study

13. Stefanadis et al, 2000

14. Coronary Infrared Thermography Catheter
(prototype)

17. Apo-E aorta heated at 37C (staining for TUNEL and
DAPI)

18. Apo-E aorta heated at 42 C (TUNEL and DAPI staining)
TUNEL
DAPI

19. DNA isolation from atherosclerotic aorta of apo-E
mice by agarose gel electrophoresis
37C
37C
37C
42C
42C
42C

23. We hypothesized that plaque inflammation and
macrophage infiltration can be detected by:
1- Decreased plaque pH and
increased pH heterogeneity
and excessive lactate content
2- pH and temperature of
plaque are inversely correlated

24. pH Distribution in 48 Human Carotid Plaques
pH
9.00
8.88
8.75
8.63
8.50
8.38
8.25
8.13
8.00
7.88
7.75
7.63
7.50
7.38
7.25
7.13
7.00
6.88
6.75
6.63
Noofpointswiththesameph
140
120
100
80
60
40
20
0
There is a bimodal distribution of pH with a marked pH variation
ranging from 6.5 to 8.9 (in 858 points)

25. Correlation of pH and Temperature in
Human Carotid Plaques

27. Iron staining of mouse circulating
monocyte after 30 minutes

28. MR Image of Abdominal Aorta
After SPIO Injection in Mouse
Apo E
deficient
mouse
C57B1
(control)
mouse
Before injection After injection (5 Days )
Dark (negatively enhanced) aortic wall, full of iron particles
Bright aortic lumen and wall without negative enhancement
and no significant number of iron particles

29. The Online Cardiovascular Research Community
www.VulnerablePlaque.org

30. Conclusions
1. Temperature at the lumen of living carotid
plaques correlates with density of inflammatory
cells, and inversely with cap thickness.
2. Differences of more than 0.3 C were seen in all
specimens but only a minority had differences of
2o
C or more.
3. Large differences in temperatures were more
often found in patients who were younger,
symptomatic, female, and not taking aspirin.

31. Conclusions
continued
4. These temperature differences can be
detected by infrared cameras.
5. Compared to normal arteries, inflamed
and lipid-rich plaques are acidic, while
calcified and thrombosed plaques are
alkaline.
6. Plaque pH correlates moderately and
inversely) with plaque temperature.

32. Conclusions
continued
7. Stefanadis and colleagues have reported that hot
plaques confer higher risk; it will be important
to determine whether plaque prognosis is best
determined by T, ∆T, pH, ∆pH or a
combination.
8. Heating to 41o
C decreases expression of pro-
inflammatory genes.
9. Heating to 42-43o
C causes apoptosis, mainly of
macrophages.

33. Conclusions
continued
10.10. Near-IR Spectroscopy can estimate plaqueNear-IR Spectroscopy can estimate plaque
protein/lipid ratios and may also provideprotein/lipid ratios and may also provide
inferences as to concentrations of plaqueinferences as to concentrations of plaque
HH++
, NO, glucose, O, NO, glucose, O22 and oxidants.and oxidants.
11.11. IR and near IR may predict plaqueIR and near IR may predict plaque
behaviour alone or in combination withbehaviour alone or in combination with
ultrasound, angioscopy, magneticultrasound, angioscopy, magnetic
resonance or immunoscintigraphyresonance or immunoscintigraphy

34. www.HotPlaque.com