(Circulation. 1999;99:1965-1971.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Thermal Heterogeneity Within Human Atherosclerotic Coronary Arteries Detected In Vivo
A New Method of Detection by Application of a Special Thermography Catheter
From the Department of Cardiology, Hippokration Hospital, University of Athens, Athens, Greece.
Correspondence to Christodoulos Stefanadis, MD, FACC, FESC, 9 Tepeleniou Str, Paleo Psychico, Athens 15452, Greece. E-mail cstefan{at}atlas.uoa.gr
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Abstract |
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Background—Activated macrophages play an important role in the pathogenesis of acute ischemic syndromes. It has been postulated that detection of heat released by activated inflammatory cells of atherosclerotic plaques may predict plaque rupture and thrombosis. Previous ex vivo studies have shown that there is thermal heterogeneity in human carotid atherosclerotic plaques.
Methods and Results—To measure the temperature of human arteries in vivo, we developed a catheter-based technique. Ninety patients (45 with normal coronary arteries, 15 with stable angina [SA], 15 with unstable angina [UA], and 15 with acute myocardial infarction [AMI]) were studied. The thermistor of the thermography catheter has a temperature accuracy of 0.05°C, a time constant of 300 ms, and a spatial resolution of 0.5 mm. Temperature was constant within the arteries of the control subjects, whereas most atherosclerotic plaques showed higher temperature compared with healthy vessel wall. Temperature differences between atherosclerotic plaque and healthy vessel wall increased progressively from SA to AMI patients (difference of plaque temperature from background temperature, 0.106±0.110°C in SA, 0.683±0.347°C in UA, and 1.472±0.691°C in AMI). Heterogeneity within the plaque was shown in 20%, 40%, and 67% of the patients with SA, UA, and AMI, respectively, whereas no heterogeneity was shown in the control subjects.
Conclusions—Thermal heterogeneity within human atherosclerotic coronary arteries was shown in vivo by use of a special thermography catheter. This heterogeneity is larger in UA and AMI, suggesting that it may be related to the pathogenesis.
Key Words: ischemia • coronary disease • plaque • heat
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Activated macrophages play an important role in the pathogenesis of acute ischemic syndromes by promoting plaque rupture or thrombosis and vasoconstriction in nonruptured but inflamed plaques.1 2 3 4 In addition, recent evidence suggests a possible role for infection in the pathogenesis of atherosclerosis.5 Furthermore, relative blood viscosity rises and aggregation of red cells increases with temperature increases.6 Previous ex vivo studies have shown that there is thermal heterogeneity in human carotid atherosclerotic plaques.7 However, the temperature of coronary arteries has not been investigated in humans in vivo.
To measure the temperature of human coronary arteries in vivo, we developed a catheter-based technique that was applied in clinical practice.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Thermography Catheter
Design and Construction
A thermistor probe (Microchip NTC Thermistor, model 100K6 MCD368, BetaTHERM), 0.457 mm in diameter, was attached to the distal end of a long, 3F, nonthrombogenic polyurethane shaft. The gold-plated lead wires of the thermistor pass through the shaft and end in a connector at the distal part of the thermography catheter. At the distal 20 cm, the catheter has a second lumen for insertion of a guide wire; thus, the catheter can be inserted into the coronary artery over a standard guide wire (rapid exchange system; Figures 1
and 2).
Opposite the thermistor is a hydrofoil specially designed to ensure
contact of the thermistor on the vessel wall (thickness of the catheter
at this site, 4F).
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The technical characteristics of the polyamide thermistor include (1) temperature accuracy, 0.05°C; (2) time constant, 300 ms; (3) spatial resolution, 0.5 mm; and (4) linear correlation of resistance versus temperature over the range of 33°C to 43°C.
In Vitro Testing
Hydraulic in vitro testing with a special setup8
based on a glass coronary model and circulating heparinized
donor whole blood proved that the bloodstream drives the thermistor
against the wall (Figure 1
). A Doppler-tip guide wire
(FloWire Cardiometrics, Inc) and a catheter-tip
micromanometer (Millar Instruments) were used to
measure flow and pressure. Contact of the thermistor with the vessel
wall was also verified by experimental testing (see below) and
angiography in the first 10 patients of our series.
Experimental Testing
Twelve nonatherosclerotic pigs (either sex; weight, 15 to 25 kg)
were premedicated, anesthetized, and mechanically ventilated as
previously described.9 10 The investigation conforms with
institutional guidelines. The thermography catheter was inserted
through an 8F hockey-stick guiding catheter and positioned in the
coronary arteries (6 left anterior descending, 3 left
circumflex, and 3 right coronary arteries) under fluoroscopic
control. Luminal surface temperature was measured at 10 different
locations in each vessel. After measurements, 6 pigs were killed, and
samples of transverse blocks of coronary segments were obtained
and processed for light (hematoxylin and eosin and Masson's trichrome
stain) and scanning electron microscopy as previously
described.9 10 Contact of the device with the
arterial wall was tested in the remaining 6 pigs. After
temperature measurements in the left anterior descending artery, the
pigs were thoracotomized with a midline sternotomy, and the pericardium
was opened and suspended in a pericardial cradle. A 20-MHz ultrasound
probe (Visions Five-64 F/XTM, Endosonics Corp) was used to visualize
the coronary lumen from the epicardial surface. A loose
ligation was surgically passed around the origin of the left anterior
descending artery, and positioning of the thermography probe inside the
artery wall was tested during both unobstructed flow through the
coronary artery and tightening of the ligation at the origin of
the artery.
Data Acquisition and Processing
Thermistor leads were connected to a Wheatstone bridge (a type
of null comparator), which is used to correlate the change of
thermistor resistance (which varies with temperature) to voltage
changes. Subsequently, voltage changes were fed into a personal
computer (200-MHz Intel Pentium) with a multichannel 12-bit
analog-to-digital converter (Data Translation Inc) and displayed in
real-time mode. Voltage changes were correlated with temperature values
with commercially available software (Dataflow, Crystal Biotech).
Calibration was made against beakers of water at temperatures varying
from 33°C to 43°C (balancing the Wheatstone bridge to 0.00 V at
33°C).
Clinical Studies
Study Population
Ninety patients made up the study population. Forty-five
patients were catheterized for investigation of valvular heart
disease (30 patients) or chest pain (15 patients) and were found to
have normal coronary arteries (control subjects). Fifteen
patients suffered from stable angina (SA) and were catheterized for
elective coronary angioplasty. Fifteen patients suffered from
unstable angina (UA) and were selected for emergency angioplasty on the
basis of angiographic findings after a 2-day hospitalization during
which they were unresponsive to maximal medical treatment. The
remainder suffered from acute myocardial infarction (AMI) and were
catheterized for primary angioplasty within 6 hours after the onset of
pain. In the UA and AMI patients, only the culprit lesion was studied
by thermography.
No patient was under medication with corticosteroids or
nonsteroid anti-inflammatory drugs, except for aspirin (Table 1). No patient had intercurrent
inflammatory or neoplastic condition likely to be associated with an
acute-phase response. The patients with normal coronary
arteries and valvular heart disease were excluded from
C-reactive protein analysis.
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The study protocol was approved by the institutional ethical committee, and each patient provided written informed consent.
Lipid and Protein Measurements
Venous blood samples were obtained before
catheterization. Lipid levels were determined routinely
when the blood samples were obtained. For protein measurements, coded
plasma samples were stored at -70°C and analyzed in a single
batch at the end of the study. C-reactive protein was assayed by
immunonephelometry (Behring NA latex CRP mono, code No. OQIY210;
sensitivity, 0.0175 mg/dL; upper limit of the reference interval for
healthy nonpregnant adults, 0.5 mg/dL). Fibrinogen was determined by
immunonephelometry with a BNA 100 analyzer.
Procedure
After cannulation of the coronary ostium with an 8F
guiding catheter, mapping of the coronary vessel at the area of
interest was made with a 20-MHz intravascular ultrasound (IVUS)
catheter (Visions Five-64 F/XTM, Endosonics Corp). In the AMI patients,
IVUS imaging was performed after patency restoration of the
occluded artery.
Coronary Artery Disease Patients
The lesion of interest was outlined in 
2 well-opacified views
with biplane angiography. Quantitative angiographic measurements were
obtained with electronic digital calipers (DCI-S, Automated
Coronary Analysis, Philips). Thereafter, the
thermography catheter was advanced through the guiding catheter, and
blood temperature was measured when the thermistor had just emerged
from the tip of the guiding catheter so that it would not be in contact
with the vessel wall. Subsequently, temperature measurements at 5
locations over a length of 
1 cm of normal (verified by IVUS) vessel
wall near the lesion were made. The dominant (most frequent)
temperature of these measurements was designated the background
temperature. In addition, measurements at 5 different lesion sites
(region of interest [ROI] for the atherosclerotic coronary
arteries) were made, scanning the whole lesion both longitudinally and
circumferentially (Figure 3). One
measurement was made in the proximal part of the lesion, 1 at the
distal, and 1 at the center. The other 2 measurements were made in
areas between the center and the ends of the plaque. In the SA or UA
patients in whom the thermography catheter could not cross the lesion,
measurements scanning the whole lesion were obtained again 5 minutes
after successful balloon angioplasty. In the AMI patients, measurements
were obtained only 5 minutes after angioplasty and verification by
IVUS of mechanical lysis of thrombus. In all patients, measurements
were obtained 5 minutes after any contrast infusion. For
coronary angioplasty, the balloon was dilated with a mixture of
contrast medium and normal saline at 37°C.
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Control Subjects
Absence of atherosclerosis was verified by IVUS.
After blood temperature measurement, 5 wall temperature measurements in
a region 1 cm long were obtained. This region was designated the
control region and its dominant temperature background temperature.
Subsequently, 5 temperature measurements were obtained in another
region of the same length (randomly selected distally or proximally to
the first lesion), which was designated the ROI. For control subjects,
the absolute values of the differences between ROI and background
temperature were taken for analysis.
Simultaneous with vessel wall measurements, mouth temperature was measured with a separate thermistor with the same specifications as the thermistor of the thermography catheter. All angiograms were examined by investigators who were unaware of the results of temperature measurements.
Statistical Analysis
Data are expressed as mean±SD. Variables were tested for
normal distribution with the Kolmogorov-Smirnov 1-sample test. Because
of nonnormal distributions, to detect significant differences regarding
the difference between ROI temperature and background temperature (all
5 differences in ROI measurements from background temperature in each
subject were taken into account in the analysis), the
difference between maximum ROI temperature and background temperature,
C-reactive protein, and fibrinogen between all groups, the
Kruskal-Wallis 1-way ANOVA was used. Pairwise testing for significant
differences between the groups regarding these variables was
performed with Dunn's test for multiple comparisons. To detect
significant differences between the groups regarding age, total
cholesterol, and ratio of total cholesterol to
HDL cholesterol, 1-way ANOVA was used. Pairwise testing for
significant differences between the groups regarding these
variables was performed with an independent-samples t
test. Frequency of the peak difference from background temperature
regarding its distribution in the 5 sites of measurement in the SA, UA,
and AMI patients was performed with the 
2
goodness-of-fit test. Bivariate correlation coefficients were
calculated with Pearson's product-moment method (continuous versus
continuous variables) or the Spearman's rank method (continuous
versus discrete variables) when appropriate.
Heterogeneity within the ROI was defined as the
presence of 1 measurement outside the range: mean of the 5
differences from background temperature ±0.1°C. Differences in the
heterogeneity within the plaque between SA, UA, and AMI
groups were tested with the 2 test. Pairwise
testing between these 3 groups of patients regarding
heterogeneity was done with Fisher's exact test. The
independent relations of the difference between maximum ROI temperature
and background temperature to its potential predictors (age, C-reactive
protein, fibrinogen, total cholesterol, ratio of total
cholesterol to HDL cholesterol, time of day
[day divided into 3 periods: midnight to 8 AM, 8
AM to 4 PM, and 4
PM to midnight], and time elapsed from onset of
symptoms to temperature measurement [AMI patients only]) were
analyzed with stepwise multiple regression analysis. To
detect differences in the differences between maximum lesion
temperature and background temperature values before and after
angioplasty, multiple linear regression analysis was performed
with the use of the intervention (angioplasty) and 29 dummy
variables as independent variables to adjust for intersubject
variability. Values of P<0.05 were considered statistically
significant. Analyses were performed with SPSS for Windows
(version 8.0) statistical software.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In Vitro and Experimental Testing
In in vitro testing, the thermistor was not in contact with the glass wall at resting conditions, but when blood was infused, it was driven against the wall and contacted its internal surface at any combination of flow velocity (range, 10 to 50 cm/s) and driving pressure (range 50 to 140 mm Hg).
In all experimental procedures, the catheter could be inserted and positioned without difficulties or complications. In gross inspection after each procedure, no thrombi were observed on the catheter. No embolic events were observed in any of the experimental pigs. Scanning electron and light microscopy disclosed no endothelial denudation, no thrombus formation, and no internal elastic lamina or deep wall damage.
Coronary wall temperatures in each pig were constant, varying by only 0.05°C. The SD of the 10 measurements for each pig ranged from 0°C to 0.0258°C.
In 4 of the 6 pigs in which the contact of the thermistor on the artery wall was tested, the thermistor was close to but not in direct contact with the intima during ligation of the coronary artery origin; during unobstructed flow, however, the thermistor was in direct contact with arterial intima. In 2 cases, the thermistor was in contact both during ligation and unobstructed flow.
Clinical Studies
Age and fibrinogen did not differ among the 4 groups. Total
cholesterol, ratio of total cholesterol to HDL
cholesterol, and C-reactive protein were different in the 4
groups (P<0.001 for all). For pairwise comparisons, see
Table 1.
Surface wall temperature was measured in 90 ROIs, 1 in each patient. Two left main coronary arteries, 37 left anterior descending arteries, 18 left circumflex arteries, and 33 right coronary arteries were studied. In the first 10 patients of our series in whom contact of the thermistor on the artery was tested, frame-by-frame analysis in 2 biplane views during washout of the contrast medium revealed that the radio-opaque thermistor was in contact with the edge of the vessel. The temperature of healthy vessel wall was 0.36±0.11°C higher than mouth temperature. Mean coronary artery stenosis was 83±8% for the SA patients and 81±7% for the UA patients (P=NS).
The 5 measurements obtained for determination of background temperature
were constant in each subject of the total study population, varying by
only 0.05°C (SD for each of the subjects ranged from 0 to 0.0263).
Temperature of blood and healthy vessel wall did not differ
(P=NS; in 78 patients, temperature was identical; in the
remainder, it ranged within the accuracy of the thermistor [in 7
patients, blood temperature was higher by 0.05°C; in 5, blood
temperature was lower by 0.05°C]). Coronary wall
temperatures in the ROI of each control subject were constant, varying
by only 0.05°C. SDs of ROI measurements for each control subject
ranged from 0°C to 0.0274°C. In the SA or UA patients, there was no
difference in the differences between maximum and background
temperatures before and after angioplasty (0.470±0.418°C versus
0.458±0.415°C, respectively; P=NS). Most atherosclerotic
plaques showed higher surface temperatures compared with normal vessel
wall (Figure 4). The difference between
maximum plaque and background temperatures did not correlate with
coronary artery stenosis in both SA and UA patients
(r=-0.10 and -0.09, respectively; P=NS for
both). Greater values in the differences between maximum plaque and
background temperatures were observed in UA (maximum, 1.55°C) and in
AMI (maximum, 2.60°C) patients. Differences between ROI and
background temperatures and between maximum ROI and background
temperatures were different among the 4 groups, increasing
progressively from SA to AMI patients (P<0.001 for both
parameters; for pairwise comparisons, see Table 2). Mean temperature differences between
ROI and background temperatures in each group were 0.004±0.009°C in
the control subjects, 0.106±0.110°C in SA patients, 0.683±0.347°C
in UA patients, and 1.472±0.691°C in AMI patients; mean temperature
differences between maximum ROI and background temperatures were
0.010±0.020°C in normal subjects, 0.153±0.134°C in SA patients,
0.787±0.360°C in UA patients, and 1.593±0.704°C in AMI patients
(Figure 5). There was no statistical
difference in the frequency of maximum plaque difference from
background temperature in terms of its distribution in the 5 sites of
measurement in the coronary artery disease patients.
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Heterogeneity within the ROI was shown in 20%, 40%, and 67% of the patients with SA, UA, and AMI, respectively, whereas no heterogeneity was shown in the control subjects. Heterogeneity within the plaque between SA, UA, and AMI patients was different (P<0.05), and pairwise comparisons revealed significant differences in heterogeneity between AMI and SA patients (P<0.05).
Multiple regression analysis revealed that C-reactive protein
was the only factor significantly associated with the differences
between maximum ROI temperature and background temperature values
(F=70.2, multiple r2=0.55,
B=0.28, P<0.001; Figure 6).
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Aspirin intake did not correlate with the difference between maximum ROI and background temperature values in the AMI group (r=-0.37, P=NS).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Plaque Rupture
Atherosclerotic plaque rupture is the main mechanism of acute ischemic syndromes,3 4 but despite improvements in established diagnostic techniques and the advent of new imaging modalities,11 12 13 neither plaque rupture nor plaque erosion can be predicted reliably in clinical practice. Inflammation at the immediate site of plaque rupture plays an important role in the destabilization of plaque because macrophages release enzymes that digest extracellular matrix and weaken the overlying fibrous cap.1 Furthermore, recent evidence suggests a possible role for infection in the pathogenesis of atherosclerosis.5 In addition, relative blood viscosity rises and aggregation of red cells increases with increases in temperature.6
Thermography of Arteries
Previous ex vivo studies by Casscells et al7
introduced the concept that detection of heat released by
activated inflammatory cells of atherosclerotic plaques may
predict plaque rupture and thrombosis. Consistent with the
development of other cardiac and vascular catheters,10 14
we have developed a catheter-based technique for the temperature
measurement of human arteries in vivo and demonstrated that there is
thermal heterogeneity within human atherosclerotic
coronary arteries. This heterogeneity is larger
in UA and AMI patients, implying that it may be related to the
pathogenesis of these syndromes.
The heterogeneity within the plaque that we observed in SA, UA, and AMI patients is in accordance with previous reports.7 Although detection of heterogeneity was not the main target of the study and optimally more measurements within the lesion should have been obtained, this finding is in accordance with the involvement of a localized process, such as clustering of mononuclear infiltrates, in the pathogenesis of plaque rupture.
Our technique or similar techniques, such as infrared thermography (which may provide additional information about the microstructure of the plaque),7 enhance the diagnostic approach for the detection of plaques that are prone to rupture and may prove useful in evaluating existing or future treatment modalities, thus intensifying effectiveness in avoiding potentially life-threatening plaque rupture. Similarly, thermal detection of atherosclerotic plaques may be useful in predicting inflamed lesions at high risk for restenosis after interventional procedures.7 Detection of temperature heterogeneity may also provide useful information in other cardiovascular conditions, such as myocarditis, valvulitis, aortitis, or even arrhythmogenic foci. Furthermore, the concept of thermal heterogeneity may be applied by other specialties with the detection of inflamed or malignant cells in other organs.
Specific Comments
Ideally, temperature should have been measured just before the
acute event. Indeed, temperature changes might result from the
structural changes of the plaque, such as fissuring or fracturing,
because the temperature might be different within the
arterial wall. Moreover, a possible incomplete or
intermittent contact of the thermistor with the vessel wall might
contribute to the temperature differences observed. In addition,
altered flow patterns (decreased flow may lead to decreased heat
transfer with the bloodstream and consequent local increase in
temperature at the lesion), the formation of thrombus, and the
possibility that the inflammatory response (which leads to the
increased temperature at the site of the lesion) is caused by the
rupture of the plaque rather than being a process preceding the rupture
of the plaque may also be considered confounding factors. However, if
temperature increase is merely a secondary phenomenon and not a finding
related to the process that leads to plaque rupture, then the SA
patients would be expected to have no temperature difference compared
with control subjects. On the contrary, the SA patients exhibited
increased plaque temperature, implying that the process that leads to
increased temperature is underway and precedes the occurrence of acute
syndromes. In cases of incomplete or intermittent contact of the
thermistor with the vessel wall because of the structure of the plaque,
one might expect equal temperature differences in SA, UA, and AMI
patients because all these syndromes have approximately the same degree
of atherosclerosis (and consequently anatomic
irregularity), as indicated by previous studies15 and the
similar percent stenosis of these patient groups in the
present study. On the contrary, we observed a progressive
temperature increase from SA to AMI patients. Moreover, even if the
whole surface of the thermistor was not in direct contact with a hard,
irregular, stable plaque, then the thermistor would underestimate
temperature differences because of either cooling by the bloodstream or
averaging of very small areas of higher temperature with areas of lower
temperature. In that case, the actual temperature differences would be
ever greater, thus reinforcing our findings. In addition, the
effectiveness of the thermography catheter in measuring vessel wall
temperature reliably is emphasized by the results that show no
differences between blood and healthy wall and differences between
blood and certain areas of the inflamed vessel. Regarding the possible
temperature released by thrombus formation and its contribution to the
findings of our study in the AMI group, it should be noted that in all
these patients, measurements were obtained after angioplasty and
verification by IVUS of thrombus lysis. In addition, as regards the
effect of flow patterns, we should stress that no differences in
temperature were observed before and after successful angioplasty.
Moreover, as demonstrated, this lack of difference before and after
angioplasty cannot be attributed to intersubject variability. Thus,
temperature increase in the lesion is not likely to result from
structural variation after angioplasty. In addition, the positive
correlation between levels of C-reactive protein (a sensitive
indica-tor of inflammation increasing in acute
ischemic syndromes16 ) and increased lesion
temperature supports the notion that an inflammatory process is
underlying heat release. Therefore, although our results cannot be
directly extrapolated to unstable plaques before rupture, they are
supportive of the concept that increased temperature precedes plaque
rupture. Nevertheless, larger prospective studies are required.
An interesting point is that the AMI patients were not significantly different from the UA patients in terms of total cholesterol, ratio of total cholesterol to HDL cholesterol, C-reactive protein, fibrinogen, and age, indicating that these factors do not account for the unequal temperature differences observed in these 2 groups.
The temperature differences we found in our study were not as high would be expected according to previous studies.7 Several reasons can explain this discrepancy. First, the presence of heat-delivering blood in vivo may act as a buffering pool that tends to decrease heat differences. Second, the original measurements in these studies were made 10 to 15 minutes after removal of the samples at room temperature. Therefore, areas with fewer heat-producing cells may have cooled faster than monocyte-populated areas that continued, even for a short period after removal, to release heat, thus magnifying an in vivo difference. A finding supportive of this explanation is the higher temperature differences observed in a hypothermic patient suffering from cardiogenic shock secondary to AMI.
There is a theoretical possibility that a hard plaque containing relatively large amounts of collagen and calcium would have a lower temperature than the metabolically active normal wall. However, this was not the case in any of our SA patients, rendering this possibility unlikely.
Flow through the rich vasa vasorum network in the atherosclerotic plaque in vivo might affect the temperature. However, a positive correlation exists between angiogenesis and inflammation,17 and both are considered to predispose to plaque rupture. Therefore, the concept of higher temperature indicating a higher risk of rupture is reinforced.
The negative correlation between the intake of aspirin before the event and lesion temperature in the AMI group was not statistically significant. This may be due to the small number of patients participating in the study. Future, specially designed studies are needed to clarify the role of aspirin or other anti-inflammatory drugs in the process of heat release.
Conclusions
Thermal heterogeneity exists within the
coronary arteries of coronary artery disease patients,
whereas temperature is constant within normal coronary
arteries. This heterogeneity increases progressively
from SA to UA and then to AMI patients, thus supporting the involvement
of temperature heterogeneity in the natural history of
these syndromes. This technique or other techniques that can localize
heat in clinical practice may prove useful in identifying plaques that
are prone to rupture or thrombosis.
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Acknowledgments |
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This study was supported by a grant from the Hellenic Heart Foundation.
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Footnotes |
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Guest Editor for this article was Valentin Fuster, MD, PhD, Mt Sinai Medical Center, New York, NY.
Received July 28, 1998; revision received January 5, 1999; accepted January 25, 1999.
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L. Marcu, M. C. Fishbein, J.-M. I. Maarek, and W. S. Grundfest Discrimination of Human Coronary Artery Atherosclerotic Lipid-Rich Lesions by Time-Resolved Laser-Induced Fluorescence Spectroscopy Arterioscler. Thromb. Vasc. Biol., July 1, 2001; 21(7): 1244 - 1250. [Abstract] [Full Text] [PDF]
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M. J. Kern and B. Meier Evaluation of the Culprit Plaque and the Physiological Significance of Coronary Atherosclerotic Narrowings Circulation, June 26, 2001; 103(25): 3142 - 3149. [Full Text] [PDF]
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