17. CLINICAL:
RISK
FACTORS:
59Y Female with
Cardiomyopathy
and Angina
Smoker
Family
history of
CAD
LAD
Thermal Mapping in RCA Using Pressure Wire
39.65
39.66
39.67
39.68
39.69
39.7
39.71
39.72
39.73
1
26
51
76
101
126
151
176
201
226
251
276
301
326
351
376
401
426
451
476
501
526
# of Measurements
Temperature(C)
DISTAL END
STENOSES
90%
OSTIUM
18. stenosis
Distal end
CLINICAL:
39 y male with
MI
RISK
FACTORS:
Hypertension
DM
Family history
Thermal Mapping of LCX using Pressure Wire
38.765
38.775
38.785
38.795
38.805
38.815
38.825
38.835
38.845
1 126 251 376 501 626 751 876 1001 1126
# of Measurements
Temp(C)
STENOSI
S
22. of Atherosclerotic Plaques and its Correlation with
•Morteza Naghavi MD,
•Reji John MD, Said Siadaty MD,
•Sameh Naguib MD, Roxana Grasu MD,
•KC Kurian MD, Mohammad Madjid MD,
•James T. Willerson MD, Ward Casscells
MD,
The University of Texas-HoustonTexas Heart Institute
pH HeterogeneitypH Heterogeneity
Temperature HeterogeneityTemperature Heterogeneity
27. Correlation of pH and Temperature in Human Carotid Plaques Varied by the Areas
We see a marked inverse correlation between temperature and pH of
plaques that varies by macroscopic characteristics of plaques.
p < 0.01
28. Fluorescence Single-Emission Imaging Microscopy
of a Predominantly Lipid Rich Plaque Shows
Significant Microscopic pH Heterogeneity Mostly
Acidic
40. Conclusions
1.1. Temperature at the lumen of living carotid plaquesTemperature at the lumen of living carotid plaques
correlates with density of inflammatory cells, andcorrelates with density of inflammatory cells, and
inversely with cap thickness.inversely with cap thickness.
2.2. Differences of more than 0.3 C were seen in allDifferences of more than 0.3 C were seen in all
specimens but only a minority had differences of 2specimens but only a minority had differences of 2oo
C orC or
more.more.
3.3. Large differences in temperatures were more oftenLarge differences in temperatures were more often
found in patients who were younger, symptomatic,found in patients who were younger, symptomatic,
female, and not taking aspirin.female, and not taking aspirin.
41. Conclusions
continued
4.4. These temperature differences can be detectedThese temperature differences can be detected
by infrared cameras.by infrared cameras.
5.5. Compared to normal arteries, inflamed andCompared to normal arteries, inflamed and
lipid-rich plaques are acidic, while calcified andlipid-rich plaques are acidic, while calcified and
thrombosed plaques are alkaline.thrombosed plaques are alkaline.
6.6. Plaque pH correlates moderately and inverselyPlaque pH correlates moderately and inversely
with plaque temperature.with plaque temperature.
42. Conclusions
continued
7.7. Stefanadis and colleagues have reported that hotStefanadis and colleagues have reported that hot
plaques confer higher risk; it will be important toplaques confer higher risk; it will be important to
determine whether plaque prognosis is best determineddetermine whether plaque prognosis is best determined
by T,by T, ∆∆T, pH,T, pH, ∆∆pH or a combination.pH or a combination.
8.8. Heating to 41Heating to 41oo
C decreases expression of pro-C decreases expression of pro-
inflammatory genes.inflammatory genes.
9.9. Heating to 42-43Heating to 42-43oo
C causes apoptosis, mainly ofC causes apoptosis, mainly of
macrophages.macrophages.
43. 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 plaque Hinferences as to concentrations of plaque H++
,,
NO, glucose, ONO, glucose, O22 and oxidants.and oxidants.
11.11. IR and near IR may predict plaque behaviourIR and near IR may predict plaque behaviour
alone or in combination with ultrasound,alone or in combination with ultrasound,
angioscopy, magnetic resonance orangioscopy, magnetic resonance or
immunoscintigraphyimmunoscintigraphy
