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“Arterial wall injury and temperature.”
AULUS CORNELIUS CELSUS,
25 B.C.-50 A.D.
For centuries, inflammation-derived heat
is known to exist in macroscopic tissues.
However,
Inflammation-derived heat is only recently
considered to exist at the arterial wall.
Active macrophages
UPC’s
[1(thermogenine), 2 and 3]
Short-circuit
in proton-pump of ATP
Local heat production
Arterial wall temperature elevation
(one possible scenario)
Potential
In vivo thermographic methods
Non-Ivasive Invasive
Non-contact ContactMagnetic Resonance
Thermometry (MRT)
Infrared Thermometry (IRT)
Intravascular MRT
Single
sensor
Multi
sensor
Catheters with
flexible arms
Thermographic
baskets
Wall injury and Inflammation
Coronary wall injury and temperature
Purpose of the study: To explore the temperature variations (if any)
of the arterial wall following coronary wall injury.
An animal study
Study population/protocol
Non-atherosclerotic pigs
Selection of a 60mm area in a normal cor.artery (AOI)
2 thermographic scans in AOI (autom.pullback 0.3mm/sec)
1.5:1 ratio balloon selection.
Fwd/Rev movements of the balloon in the AOI, maintaining
inflation pressure at 4 atm. (Injury), followed by
Stable inflation at 12atm for 30sec.
2 thermographic scans in AOI (autom.pullback 0.3mm/sec)
Injury
Histology
Macrophage concentration (IS: 0-4 )
0 = Rare appearance of histolymphocytes around the stent filament
1 = sparsely located histolymphocytes around the stent filament
2 = more densely located histolymphocytes covering the stent filament
3 = diffusely located histolymphocytes, giant cells, also invading the media
After 4 days
2 thermographic scans in AOI (autom.pullback 0.3mm/sec)
Sacrifice, and:
Methods
4F over-the-wire catheter
4 independent thermistor-sensors
Sensitivity 0.01o
C
Motorized pullback (0.1-0.5mm/sec)
Specifications
Integration of temperature with angiography
-0.1
0
0.1
0.2
0.3
0.4
0.5
0 10 20 30 40 50 60
Pullback distance (mm)
Temperaturedifference(oC)
Sensor 1
Sensor 2
Sensor 3
Sensor 4
Before injury
-0.1
0
0.1
0.2
0.3
0.4
0.5
0 10 20 30 40 50 60
Distance (mm)
Temperaturedifference(oC) Sensor 1
Sensor 2
Sensor 3
Sensor 4
Immediately after
-0.1
0
0.1
0.2
0.3
0.4
0.5
0 10 20 30 40 50 60
Distance (mm)
Temperaturediff.(oC)
Sensor 1
Sensor 2
Sensor 3
Sensor 4
4 days after injury
Macrophage concentration versus temperature
0.00
0.10
0.20
0.30
0.40
0.50
0.60
0 1 2 3 4
IS
oC
temp. increment
P<0.001
Conclusions
•PTCA balloon injury disrupts the temperature homogeneity inside
a normal coronary artery.
•This temperature disruption correlates with macrophage
concentration at the site of the injury.
•Since local inflammation could initiate hyperplasia and/or promote
thrombosis, efforts should be made to minimize wall trauma during
coronary interventions.

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127 arterial wall injury and temperature

  • 1. “Arterial wall injury and temperature.”
  • 2. AULUS CORNELIUS CELSUS, 25 B.C.-50 A.D. For centuries, inflammation-derived heat is known to exist in macroscopic tissues. However, Inflammation-derived heat is only recently considered to exist at the arterial wall.
  • 3.
  • 4. Active macrophages UPC’s [1(thermogenine), 2 and 3] Short-circuit in proton-pump of ATP Local heat production Arterial wall temperature elevation (one possible scenario)
  • 5. Potential In vivo thermographic methods Non-Ivasive Invasive Non-contact ContactMagnetic Resonance Thermometry (MRT) Infrared Thermometry (IRT) Intravascular MRT Single sensor Multi sensor Catheters with flexible arms Thermographic baskets
  • 6. Wall injury and Inflammation Coronary wall injury and temperature Purpose of the study: To explore the temperature variations (if any) of the arterial wall following coronary wall injury. An animal study
  • 7. Study population/protocol Non-atherosclerotic pigs Selection of a 60mm area in a normal cor.artery (AOI) 2 thermographic scans in AOI (autom.pullback 0.3mm/sec) 1.5:1 ratio balloon selection. Fwd/Rev movements of the balloon in the AOI, maintaining inflation pressure at 4 atm. (Injury), followed by Stable inflation at 12atm for 30sec. 2 thermographic scans in AOI (autom.pullback 0.3mm/sec) Injury Histology Macrophage concentration (IS: 0-4 ) 0 = Rare appearance of histolymphocytes around the stent filament 1 = sparsely located histolymphocytes around the stent filament 2 = more densely located histolymphocytes covering the stent filament 3 = diffusely located histolymphocytes, giant cells, also invading the media After 4 days 2 thermographic scans in AOI (autom.pullback 0.3mm/sec) Sacrifice, and:
  • 8. Methods 4F over-the-wire catheter 4 independent thermistor-sensors Sensitivity 0.01o C Motorized pullback (0.1-0.5mm/sec) Specifications
  • 9. Integration of temperature with angiography
  • 10. -0.1 0 0.1 0.2 0.3 0.4 0.5 0 10 20 30 40 50 60 Pullback distance (mm) Temperaturedifference(oC) Sensor 1 Sensor 2 Sensor 3 Sensor 4 Before injury
  • 11. -0.1 0 0.1 0.2 0.3 0.4 0.5 0 10 20 30 40 50 60 Distance (mm) Temperaturedifference(oC) Sensor 1 Sensor 2 Sensor 3 Sensor 4 Immediately after
  • 12. -0.1 0 0.1 0.2 0.3 0.4 0.5 0 10 20 30 40 50 60 Distance (mm) Temperaturediff.(oC) Sensor 1 Sensor 2 Sensor 3 Sensor 4 4 days after injury
  • 13. Macrophage concentration versus temperature 0.00 0.10 0.20 0.30 0.40 0.50 0.60 0 1 2 3 4 IS oC temp. increment P<0.001
  • 14. Conclusions •PTCA balloon injury disrupts the temperature homogeneity inside a normal coronary artery. •This temperature disruption correlates with macrophage concentration at the site of the injury. •Since local inflammation could initiate hyperplasia and/or promote thrombosis, efforts should be made to minimize wall trauma during coronary interventions.