This study explored temperature variations in the arterial wall following coronary wall injury using an animal model. Pigs underwent thermographic scans of a targeted coronary artery area before and after injury induced by a balloon. Temperature disruption was observed immediately after injury that correlated with macrophage concentration at the injury site. Four days later, temperature scans showed persistence of the disruption. The findings suggest wall injury promotes local inflammation that could initiate hyperplasia or thrombosis, so minimizing trauma during coronary interventions is important.

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.

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.