Copyright © 2004 by the European Society of Cardiology.
Letter to the Editor
Coronary artery plaque temperature: what do we measure?
Department of Cardiology, Athens Medical School, Hippokration Hospital, 9 Tepeleniou str., 15454, Paleo Psychico, Athens, Greece
* Corresponding author. Tel.: +30-1-671-8694; Fax: +30-210-6457230/7585039
E-mail address: cstefan{at}cc.uoa.gr
To the Editor,
An interesting study was recently published in the Journal regarding the effect of blood flow on temperature measurements.1 The authors correlated the temperature measurements in normal porcine coronary arteries with blood flow alterations. These results confirm partly our findings in human coronary arteries in which we demonstrated the `cooling effect' of blood flow on normal wall and plaque temperatures.2
The authors raise a concern for coronary plaque temperature measurements when blood flow is completely interrupted. They speculate that in inflamed atheromatous plaques when blood flow is completely interrupted there might be a risk of false temperature measurements. They try to explain their hypothesis by a mathematical model after making several assumptions. Firstly, that heat generation inside the plaque is homogenous, although Casscells et al.3 have shown ex vivo significant heterogeneity within the plaques. Secondly, the atheromatous plaque is considered as solid rather than a biologic material with completely different properties being difficult to be interpreted by the Newton's Law which is valid for inorganic solids and liquids. Physics suggest that any dynamic change of the measurement conditions, most important of all being the blood flow, reduces the heat transferred to the sensing element (thermistor) leading to underestimation of plaque temperature. Therefore, by blood flow obstruction this limitation is eliminated and in addition the influence of friction locally is avoided.
In the clinical setting, we need to know whether an increase of temperature is indicative of a hot plaque with inflammatory involvement. The current data from experimental4 and clinical3 studies showed that there is correlation between thermal heterogeneity and macrophage content. A discrepancy however between ex vivo3,4 and in vivo5–7 plaque temperature measurements is observed. The `cooling effect' of blood flow leading to underestimation of the temperature measurements is a potential interpretation for this discrepancy. In our study2 there is a criticism from the authors regarding the complete attachment of the thermistor to the atherosclerotic plaque and the possible effect of normal saline at 37 °C used for balloon inflation that may had affected the measurements. However, in a study8 from our institution with a balloon-thermography catheter, which ensures the full attachment of the thermistor to the plaque by inflation of the balloon by carbon dioxide, similar results were found without the mentioned possible limitations. Additionally, from our experience temperature is not increased in all lesions, in which complete interruption of flow is accomplished. Thus by flow interruption more reliable temperature measurements are obtained. Diamantopoulos et al. recently presented their experience in an atheromatic porcine model and they observed that plaques with an increase of temperature during blood flow interruption had higher macrophage concentration.9 This study documented that by complete interruption of flow the real temperature of atheromatous plaque is approximated and the inflammatory substrate is identified. Interestingly, these results do not support the hypothesis that flow reduction threatens the accuracy of intravascular thermography,1 but instead that by flow obstruction we approximate the real plaque temperature. Finally, we have to recognize that temperature measurements are influenced by several biological and mechanical factors and we need more studies in our search for the pathophysiologic insights of plaque heat generation.
References
- Diamantopoulos L, Liu X, De Scheerder I et al. The effect of reduced blood-flow on the coronary wall temperature. Are significant lesions suitable for intravascular thermography. Eur. Heart J. 2003;24:1788–1795.
[Abstract/Free Full Text] - Stefanadis C, Toutouzas K, Tsiamis E et al. Thermal heterogeneity in stable human coronary atherosclerotic plaques is underestimated in vivo: the "cooling effect of blood flow. J. Am. Coll. Cardiol. 2003;41:403–408.
[Abstract/Free Full Text] - Casscells W, Hathorn B, David M et al. Thermal detection of cellular infiltrates in living atherosclerotic plaques: possible implications for plaque rupture and thrombosis. Lancet. 1996;347:1447–1451.[CrossRef][Web of Science][Medline]
- Verheye S, De Meyer GR, Van Langenhove G et al. In vivo temperature heterogeneity of atherosclerotic plaques is determined by plaque composition. Circulation. 2002;105:1596–1601.
[Abstract/Free Full Text] - Stefanadis C, Toutouzas K, Vavuranakis M et al. Statin treatment is associated with reduced thermal heterogeneity in human atherosclerotic plaques. Eur. Heart J. 2002;23:1664–1669.
[Abstract/Free Full Text] - Stefanadis C, Diamantopoulos L, Vlachopoulos C et al. Thermal heterogeneity within human atherosclerotic coronary arteries detected in vivo: A new method of detection by application of a special thermography catheter. Circulation. 1999;99:1965–1971.
[Abstract/Free Full Text] - Naghavi M, Madjid M, Gul K et al. Thermography basket catheter: in vivo measurement of the temperature of atherosclerotic plaques for detection of vulnerable plaques. Catheter. Cardiovasc. Interv. 2003;59:52–59.[CrossRef][Web of Science][Medline]
- Stefanadis C, Toutouzas K, Vavuranakis M et al. New balloon-thermography catheter for in vivo temperature measurements in human coronary atherosclerotic plaques: a novel approach for thermography. Catheter. Cardiovasc. Interv. 2003;58:344–350.[CrossRef][Web of Science][Medline]
- Diamantopoulos L, Liu X, De Scheerder I. The effect of blood-flow on the arterial wall temperature. In-vivo evaluation on an inflammation model. Eur Heart J 2003;24 [Abstract].
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