Assessment of Culprit Plaque Temperature byIntracoronary Thermography Appears Inconclusive in

Patients With Acute Coronary SyndromesŁukasz Rzeszutko, Jacek Legutko, Grzegorz L. Kałuza, Marcin Wizimirski, Angela Richter,

Michał Chyrchel, Grzegorz Heba, Jacek S. Dubiel, Dariusz Dudek

Objective—Safety and feasibility evaluation of intracoronary temperature measurements in patients with acute coronarysyndromes (ACS) using a catheter based thermography system.

Methods and Results—Thermography was performed in 40 patients with ACS. A 3.5-F thermography catheter containing5 thermocouples measuring vessel wall temperature, and 1 thermocouple measuring blood temperature (accuracy0.05°C) was used. Gradient (�Tmax) between blood temperature (Tbl) and the maximum wall temperature duringpullback was measured. The device showed satisfactory safety in ACS. Only in 16 patients (40%) �Tmax was �0.1°C.In 23 patients (57.5%) the highest �Tmax was found in the culprit segment. �Tmax between culprit and adjacentnon-culprit segments was observed in patients with transient blood flow interruption during thermography (0.11�0.03versus 0.08�0.01; P�0.04), in contrast to patients with preserved flow (0.07�0.03 versus 0.06�0.02; P�0.058).

Conclusions—The novel, technically sophisticated intracoronary thermography proved its safety and feasibility. However,we were not able to convincingly and consistently differentiate between different lesions at risk, despite a selection oflesions that should appear most distinct to differentiate. A systematic interruption of flow may be necessary to achievediagnostic results consistently, although such requirement may unfavorably change the risk-to-benefit ratio of thisdeveloping technology. (Arterioscler Thromb Vasc Biol. 2006;26:1889-1894.)

Key Words: infarction � ischemia � plaque � temperature � thermography

Several studies have demonstrated increased temperaturesof atherosclerotic plaques in patients with coronary artery

disease, especially acute coronary syndromes (ACS).1–3 Inthese studies catheters with a single sensor were used andmeasurements were taken at several points of the culpritlesion and adjacent segments.1–3 Multisensor catheters andmeasurements at multiple sites along the vessel provide apossibility of building a detailed thermal map of the vessel.4

In the present study we used a novel intracoronary thermog-raphy system to assess the safety and feasibility of thermo-graphic measurements and to analyze thermal maps of theculprit artery in patients with ACS.

MethodsStudy PopulationPatients admitted to the Department of Hemodynamics and Angio-cardiography of the Jagiellonian University Hospital for emergentpercutaneous coronary intervention (PCI) on a 24-hour basis wasenrolled in the study. Entry criteria were: acute myocardial infarctionwithin 12 hours of chest pain onset or unstable angina pectoris classIIIB or IIIC in Braunwald’s classification. Patients with TIMI 3 flowin the infarct-related artery were selected for the study and the

reference diameter of segments for thermographic measurements hadto be 2.5 to 4.0 mm. Patients with cardiogenic shock, significantrhythm or conduction disorders, co-morbid states, especially chronicinflammatory and neoplastic condition, pregnancy, under medicationwith corticosteroids or nonsteroid anti-inflammatory drugs exceptfor aspirin were excluded from the study. Angiographic exclusioncriteria were tortuous vessels or blood clot in the culprit artery.

The study was approved by the Institutional Review Board of theJagiellonian University and each patient provided written informedconsent.

Intracoronary Thermographic SystemThe intracoronary thermography system (Volcano Corporation, Ran-cho Cordova, Calif) was designed for the measurement and graphicrecording of vessel wall and blood temperature. Measurements weretaken using a 3.5-F catheter tipped with a 19.4-mm self-expandingbasket with 5 nitinol arms. Nitinol has elastic properties ensuring thatbasket arms are in contact with all segments of the wall, if the vesselhas a diameter of 2.5 to 4.0 mm. The catheter, compatible withguides 6-F or larger, was used to insert the folded basket over a long0.014� guide wire. The basket could easily be expanded whenpositioned at the distal vessel segment. Five thermocouples placedon each nitinol arms to measure the vessel wall temperature and onecentral thermocouple measuring the blood temperature transformedthe heat energy into electric signals. The signals were then analyzed

Original received January 23, 2006; final version accepted May 10, 2006.From II Department of Cardiology (L.R., J.L., M.W., M.C., G.H., J.S.D., D.D.), Institute of Cardiology, Jagiellonian University, Krakow, Poland; The

Methodist Hospital Research Institute (G.L.K.), Houston, Tex; Volcano Europe (A.R.), Zaventem, Belgium.Correspondence to Dariusz Dudek, II Department of Cardiology, Institute of Cardiology, Jagiellonian University, Kopernika 17th str, 31-501 Krakow,

Poland. E-mail mcdudek@cyf-kr.edu.pl© 2006 American Heart Association, Inc.

Arterioscler Thromb Vasc Biol. is available at http://www.atvbaha.org DOI: 10.1161/01.ATV.0000232500.93340.54

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within the computer based console providing absolute and relativetemperatures, for 5 arms and blood temperature simultaneously.Measurements were taken along the vessel axis every 0.5 mm. Thisway a thermal map of the scanned vessel segment could be obtained.The system was manufactured to detect temperature differences of0.05°C.

BiochemistryBlood was drawn at baseline to determine lipid levels, high-sensitivity C-reactive protein (hsCRP) (Dade Behring, Inc.), markersof myocardial injury, ie, CK, CK-MB, and Troponin T.

ProcedurePatients received unfractionated heparin to achieve ACT of at least250 s or 200 s in patients previously treated with an intravenousplatelet IIB/IIIA glycoprotein receptor inhibitor (abciximab). ACTwas controlled every 30 minutes and, if needed, heparinization wasrepeated. After coronary angiography a 7-F sheath was inserted inthe femoral artery and 7-F guiding catheter positioned in thecoronary ostium. A 300-cm-long 0.014-inch angiographic guide wirewas inserted into the culprit artery, and then the thermographycatheter was advanced beyond the lesion site. The expansion of thebasket was controlled by fluoroscopy and angiography was per-formed to assess blood flow. Temperature was measured during anautomatic pullback with a speed of 0.5 mm/s. Every 20 s, theposition of the thermography catheter was recorded by cine-angiography to allow a retrospective correlation of temperaturereadings with vessel segments. After the procedure repeat coronaryangiography was performed to confirm that there were no device-related adverse effects. Then standard percutaneous coronary inter-vention was performed. Patients were routinely treated andfollowed-up at the coronary care unit.

Angiographic MeasurementsAngiograms before and after the thermography procedure wereobtained in multiple projections after intracoronary injections of 0.2mg of nitroglycerin and recorded on CDs. Angiograms were ana-lyzed at an independent core laboratory using Sanders Data Systemsoftware (Palo Alto, Calif). Computerized quantitative analysis wasperformed according to edge-detection algorithms, with the guidingcatheter diameter used as reference. Reference lumen diameter,minimum lumen diameter, and percent diameter stenosis weremeasured at baseline. Flow analysis as well as qualitative analysisafter thermography procedure was performed to assess possiblecatheter related adverse events.

Statistical AnalysisContinuous variables were expressed as mean�SD. Variables weretested for normal distributions with Kolmogorov-Smirnov andShapiro-Wilk tests. Categorical variables were expressed as percentof the study population. Thermography analysis was based on �Tmax defined as the maximum difference between the vessel walltemperature, as measured by 5 thermocouples, and the bloodtemperature. Because of nonparametric distributions, Whitney-MannU test was used to compare mean �T max in the culprit segment andmean �T max in healthy adjacent vascular segments (identified byangiography). Bivariate correlation coefficients were calculated withPearson’s product moment method for continuous variables orSpearman’s rank method for discrete variables when appropriate toanalyze correlation between �T max and various variables. Whitney-Mann U test was also used to compare �T max for adjacent segmentsin patients with patent and occluded arteries during thermography.Angiographic data were analyzed by an independent core laboratory.

ResultsForty patients aged 57�10 with ACS were enrolled in thestudy, including 16 without and 24 patients with ST-segmentelevation in the ECG. Table 1 summarizes the patientcharacteristics. In STEMI patients normal blood flow in the

culprit artery was restored with combination of fibrinolysisand platelet inhibition (reduced tPA dose and full dose ofabciximab) used routinely in our center to facilitate PCI inpatients from remote hospitals with expected transport time toour cathlab exceeding 90 minutes. Intracoronary thermogra-phy was performed in 39 patients; in 1 patient temperaturescould not be measured because of software failure after studycatheter advancement to the vessel.

The thermography catheter was advanced beyond thelesion site in all patients; however, in 6 of them low-pressurepre dilatation with a 2.5-mm balloon was required to advancethe catheter through the tightly narrowed vascular segment. In2 patients there were difficulties with expanding the nitinolbasket; withdrawal backwards facilitated its expansion in 1patient, in the remaining 1 a new thermography catheter hadto be used.

In 11 patients, after the catheter crossed a tight lesion,blood flow interruption in contrast angiography at the start ofthe thermography pullback, as well as transient ST-segmentelevation in the ECG were observed. In all these patientsST-segment changes in the ECG were resolved once thebasket was withdrawn through the lesion.

In one patient in whom thermography was completedcoronary angiography revealed slight vessel contraction,which was relieved with an intracoronary infusion of 200 �g

TABLE 1. Patient Baseline Characteristics

Characteristic No. (%), No.�SD

Age, y 57�10

Female 7 (17.5%)

STEMI 24 (60%)

Cardiac enzymes atbaseline

CK total, U/L 1118�1458

CK-MB, U/L 115�141

Troponin I, U/L 5.5�13

Unstable angina (NSTACS) 16 (40%)

Cardiac enzymes atbaseline

CK total, U/L 300�728

CK-MB, U/L 30�70

Troponin I , ug/L 2.7�6

Risk Factors

Hypertension 5 (12.5%)

Diabetes 5 (12.5%)

Hyperlipidemia 8 (20%)

Total cholesterol, mmol/L 5.1�1.2

LDL, mmol/L 3.2�1.1

HDL, mmol/L 1.1�0.3

TG, mmol/L 1.7�0.8

Previous statin treatment 10 (25%)

hsCRP, mg/L 11.7�26

hsCRP �3 mg/L, % 23 (57.5%)

HDL indicates high-density lipoprotein; LDL, low-density lipoprotein; SD,standard deviation, STEMI, ST segment elevation myocardial infarction; TG,triglycerides.

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nitroglycerin. In the second patient slight deterioration ofblood flow was observed. No other device-related adverseeffects were observed. Angiographic measurements beforeand after thermography are placed in Table 2.

Mean blood temperature Tbl was 36.7�0.7°C. Mean max-imum difference between vessel wall and blood temperatures�Tmax was 0.093�0.032°C for the whole group, reflecting 4patients with �Tmax ranging from 0°C to 0.05°C, 19 patientsfrom 0.06°C to 0.09°C, and 16 patients in whom the differ-ence was at least 0.1°C (the highest �T max was 0.28°C). In23 patients (57.5%) the highest �T max was recorded in theculprit segment. In the remaining 16 patients the highest �Tmax was detected distally (11 patients) or proximally (4patients) to the lesion. Mean �T max at the lesion site relativeto mean �T max in the adjacent segments was significantlyhigher (0.092�0.03°C versus 0.062�0.01°C; P�0.0006)(Table 3 shows averaged temperatures measurements inculprit and non culprit segments). In patients with STEMI andunstable angina �Tmax at the culprit segment did not differ

(0.07�0.02 versus 0.09�0.04; P�0.2, respectively). Therewas no difference between �Tmax in the culprit segment inpatients with elevated hsCRP level and patients with hsCRP�3 mg/mL (0.09�0.04 versus 0.07�0.02 versus; P�0.2,respectively). There was also no significant correlation be-tween �Tmax and LDL cholesterol levels, previous treatmentwith statins, diabetes and duration of clinical symptoms eitherin STEMI or in unstable patients. An inverse correlationbetween �Tmax at the lesion site and vessel patency duringthermography was found (r��0.48354; P�0.02). In patientswith blockage of blood flow at the start of the pullbacktemperature difference between culprit and adjacent noncul-prit segments was observed (�Tmax: 0.11�0.03 versus0.08�0.01; P�0.04), whereas in patients with flow main-tained temperatures at culprit segments did not differ fromadjacent nonculprit segments (�Tmax: 0.07�0.03 versus0.06�0.02; P�0.058) (Figures 1 and 2).

DiscussionIn patients with ACS presenting as myocardial infarction andunstable angina pectoris a new catheter-based, thermographysystem detected the highest temperatures in culprit plaques in57.5% of patients. The difference between the lesion and thehealthy segments was statistically significant. Blood flowduring thermography was found to affect the temperaturereadings significantly. In patients with transient blood flowinterruption when the catheter was at the tight lesion site thedifference between temperatures of the plaque and healthysegments was significantly higher, whereas in patients withpreserved blood flow there was only a tendency towardhigher temperatures in the culprit segment.

The idea of measuring coronary wall temperatures is basedon the hypothesis that vascular inflammation may be identi-fied through detection of heat released by inflammatory cellsinfiltrating the plaque. In vitro studies confirm the significantcorrelation between plaque temperature and inflammatorycell accumulation.5 In vivo measurements of temperaturepose technical difficulties related to physical properties ofheat energy and the movement of bloodstream.4,6 Stefanadiset al developed an in vivo technique of blood temperaturemeasurements in human coronary arteries. Temperature wasfound to increase progressively in patients with myocardialischemia with highest values in AMI patients.

Our study contests previous findings with intracoronarythermography in multiple areas. This is not surprising giventhe fact that most of experience with thermography publishedto date has been acquired with 1 thermography system at asingle center, and our study evaluates for the first time to our

TABLE 2. Baseline and Post-ThermographyAngiographic Analysis

Characteristic No. (%), No.�SD

Culprit vessel

LAD 18 (45%)

Cx 7 (17.5%)

RCA 15 (37.5%)

QCA of culprit lesion (before procedure)

Lesion length, mm 17.4�6.8

Reference diameter, mm 3.0�0.3

Minimal lumen diameter, mm 0.7�0.3

Percent diameter stenosis, % 77.2�11

Flow analysis

Before procedure

TIMI 3 39/40

TIMI 2 1/40

After thermography

TIMI 3 39/40

TIMI 2 1/40 (2.5%)

Quantitative analysis afterthermography

Perforation 0/40

Dissection 0/40

Distal embolization 0/40

Coronary spasm 1/40 (2.5%)

QCA indicates quantitative coronary angiography.

TABLE 3. Temperature Measurements in the Culprit and Nonculprit Segments Guided by Angiography

Proximal AdjacentSegment

CulpritSegment P*

Distal AdjacentSegment P†

All NonculpritSegments P‡

Tbl, °C 36.7�0.6 36.7�0.6 NS 36.7�0.6 NS 36.7�0.6 NS

�Tmax 0.068�0.02 0.092�0.03 0.003 0.076�0.02 NS 0.062�0.02 0.01

*P for difference between culprit and proximal adjacent segment.†P for difference between culprit and distal adjacent segment.‡P for culprit vs averaged temperature values from all non culprit segments.

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knowledge the measurements derived from a fundamentallydifferent technology.

First, in the early published experience with intracoronarythermography, temperature differences between atheroscle-rotic plaque and healthy vessel wall exceeded even 1°C.1 Thisis easily explained by the fact that in the previous studiesyielded measurements of absolute temperatures without rela-tion to blood, whereas in our study vessel wall temperaturewas expressed as �Tmax, ie, the highest difference between

temperatures of vessel wall and blood. Consequently, thedifferences were markedly smaller and only in 40% of thepatients the maximum difference between vascular walltemperature and blood temperature exceeded 0.1°C. Also,accuracy and reproducibility of measurements taken withmultiple thermocouples should be higher than those takenwith a single sensor tipped catheter used in earlier studies.The system used in our study is able to detect quicktemperature changes according to manufacturer; however

Figure 1. Two different patterns of temperatures readings regarding blood flow during thermography. A, Thermographic readings of leftanterior descending artery in patient T.P. with blockage of flow in angiography at the start of the pullback. Higher temperatures in distaland culprit segments and lower in proximal segments. B, Thermography of right coronary artery in patient J.D. with preserved flow inangiography at the start of the pullback. Temperature curves without significant changes during pullback.

Figure 2. Differences between �Tmax. at culprit segment vs nonculprit segments regarding flow during procedure. A, Patients withmaintained blood flow: differences between �Tmax at culprit versus non culprit segments not significant (0.07�0.03 vs 0.06�0.02;P�0.058). B, Patients with blood flow blockade: significant difference between culprit vs nonculprit segments (0.11�0.03 vs 0.08�0.01;P�0.04).

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time to steady-state measurement of the temperature isunknown. However, it is also possible that sensor movementalong the luminal surface with speed of 0.5 mm per second istoo fast to localize “hot spots” in areas of inflammatory cellsaccumulation.

Second, in our study we compared plaque temperaturerelative to healthy vessel segments using averaged �Tmax inangiographically unchanged adjacent segments. In contrast,previous reports related plaque temperatures to “representa-tive” (which probably means arbitrary) temperatures mea-sured in the nonculprit segment.1

Third, we did not find significant temperature differencesbetween patients with ST segment elevation myocardialinfarction and unstable angina. In contrast, Stefanadis et alobserved plaque temperatures twice as high in patients withacute myocardial infarction than in patients with unstableangina (0.683�0.347 versus 1.472�0.691).1 The reason forthese discrepancies may lie in the differences in time elapsingfrom angioplasty to measurement. In the present studymeasurements were taken before PCI in the entire group(except for 6 patients in whom low-pressure predilatation wasperformed after unsuccessful advancement of the thermogra-phy catheter through the critical stenosis). In contrast, previ-ously reported temperature measurements were taken beforePCI in patients with unstable angina and after balloonangioplasty in patients with myocardial infarction.1 Moreimportantly, available evidence indicates that functional andmorphological changes in the plaque in patients with myo-cardial infarction and unstable angina pectoris are similar,whereas clinical manifestations in ACS are related to theseverity of luminal occlusion by the forming thrombus in thecoronary artery.7 In other words, morphological features ofatherosclerotic plaque cannot differentiate patients with myo-cardial infarction from patients with unstable angina. Assuch, they should not be expected to demonstrate signifi-cantly different findings in thermography.

Last but not least, the most important observation from thispilot study appears to be the impact of blood flow on thethermography readings. In patients with transient blood flowinterruption we recorded lower temperatures (cooling) inproximal reference segments. Averaged values recorded inproximal and distal reference segments blunted the differencebetween temperatures of the plaque and these segments.Moreover, there was a significant inverse correlation betweenplaque temperature and the presence of blood flow at thebeginning of thermographic evaluation. The effect of blood-stream on vessel wall temperature has been investigated invitro and in vivo, as well as by mathematical modeling.8

Verheye et al observed more pronounced temperature differ-ences when blood flow was stopped by balloon occlusion inrabbit aorta.6 Diamantopolous et al demonstrated in an animalmodel that small changes in blood flow did not determinevascular wall temperature and only a significant reduction ofblood flow (average peak velocity �4 cm/s) resulted in theincrease of wall temperature but this study was conducted innormal porcine coronary arteries.9 Stefanadis et al demon-strated that vessel occlusion by the balloon catheter duringmeasurements in patients with stable angina pectoris signif-icantly affected vessel wall temperature leading to its increase

by a mean of 60.5% as compared with baseline values. Therestoration of blood flow restored the baseline values.10

Stefanadis described these relationships as cooling of theplaque by the bloodstream. It seems that in our study thiscooling effect could have a decisive impact on temperaturevalues. It is noteworthy that in patients with preserved bloodflow during thermography, the temperature differences be-tween vessel wall and blood were close to the detectionthreshold, which is 0.05°C for the catheter we used.

Study LimitationsAmong study patients with unstable angina the time from theonset of symptoms varied significantly. Moreover, in 3patients postinfarctional angina (Braunwald III C) was recog-nized at inclusion to the study. In this population bothinflammatory processes expressed by CRP level as well astemperature measurements could be influenced by myocar-dial necrosis. In our study contrast injection at start of thepullback of the catheter was mandated for visualization of theblood flow for safety reasons. These contrast media injectionshave unknown temperature and it is unclear whether theymight have an impact on the temperature readings. Similarly,predilatation of the culprit lesion was performed per protocolin 6 of 40 patients to advance the thermography probe, andthe impact of this intervention on the thermography result isunclear. It may be a confounder but it is most likely to occurreproducibly in every attempt to characterize lesions respon-sible for myocardial infarction and ACS since a number ofthem will inevitably first present as total or subtotalocclusions.

In conclusion, measurements of the vessel wall tempera-ture in coronaries of patients with ACS using a novelintracoronary thermography system were safe. The tempera-ture difference between culprit and adjacent nonculprit seg-ments was lower than previously reported and only observedwhen the blood flow was interrupted during thermography.Overall, this early experience seems to show that temperaturemeasurements with the novel, technically sophisticated intra-coronary thermography system (Volcano Corporation) failsto convincingly and consistently differentiate between differ-ent lesions at risk, despite a selection of lesions that shouldappear most distinct to differentiate (myocardial infarctionand unstable angina). The mere numbers have demonstratedsome trends or even statistically significant differences.However, the difficulty to interpret the data and the myriad ofconfounding factors, eg, impact of blood flow, make themethod’s practical application difficult to imagine in a dailypractice. Experience from different studies suggests that asystematic interruption of flow in the interrogated segmentmay be proposed to achieve diagnostic results consistently.However, such requirement has unfavorably changed therisk-to-benefit ratio of this technology in development andwould have to be specifically addressed in future studies.

Sources of FundingL.R. received scientific grant from Volcano Therapeutics. J.L.received scientific grant from Volcano Therapeutics. A.R. is Directorof Clinical Affairs Volcano Europe. D.D. received scientific grantfrom Volcano Therapeutics.

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DisclosuresNone.

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Michal Chyrchel, Grzegorz Heba, Jacek S. Dubiel and Dariusz DudekLukasz Rzeszutko, Jacek Legutko, Grzegorz L. Kaluza, Marcin Wizimirski, Angela Richter,

Inconclusive in Patients With Acute Coronary SyndromesAssessment of Culprit Plaque Temperature by Intracoronary Thermography Appears

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