The Radi PressureWire® Thermistor for
Intracoronary Thermography
Re: J Invasive Cardiol 2006;18:528–531 (November)

We read with great interest the article recently published in the Journal by Worthley et al regarding the use of the Radi PressureWire^® high-sensitivity thermistor (Radi Medical Systems, Inc., Uppsala, Sweden) for the detection of culprit lesion temperature.¹ The authors used this system in patients with acute coronary syndromes and measured the temperature at the culprit lesions in 20 patients with significant stenosis, as evaluated by the fractional flow reserve (FFR). They concluded that the specific guidewire is unable to detect a local increase in culprit site temperature relative to the reference coronary site.
We fully agree with the possible explanations for the results of this study and we would like to add some specific comments. The Radi wire is not dedicated to atheromatous plaque temperature measurements, but rather for the blood temperature measurement within the coronary arteries. The contact of the thermistor with the atheromatous plaque is not ensured in any case, especially in intermediate stenoses. Worthley et al used the FFR as an index for the severity of the stenosis.¹ However, FFR is not linearly correlated with the degree of stenosis and therefore is not indicative of the contact of the thermistor with the atheromatous plaque. Thus, contact of the Radi wire thermistor with the plaque seems to be incidental, or the selection of really high-grade stenoses based on quantitative coronary angiography would counteract this limitation. These observations may explain the conflicting results of the present study with other studies using the Radi wire for temperature measurements. These 4 studies including 169 patients and 206 lesions demonstrated an elevation of temperature in a range of 0.07–0.34ºC in patients with acute coronary syndromes.^2–5 We also agree with the comment of the authors regarding the comparison of the Radi wire with intracoronary thermography (ICT) catheters. It is rather difficult, if not prohibitive, to compare the Radi wire with an ICT catheter in humans in vivo, unless full contact of both systems with the target lesion could be confirmed. Regarding their comment on the magnitude of temperature elevations reported in the first studies performed almost a decade ago,⁶ we have to mention that these differences may be caused in part by the cooling effect of blood flow,⁷ the discrepancies in the use of various medications (e.g., statins, aspirin) which may stabilize “hot” plaques,⁸ the different ICT devices,⁹ and most importantly, the industrialized production of variably-sized ICT catheters used in the subsequent studies.¹⁰
Therefore, the conclusion of the authors regarding the usage of the Radi wire for atheromatous plaque temperature measurements needs to be interpreted in light of the mentioned limitations. ICT is a method for the identification of local inflammation in atheromatous plaques, despite the current shortcomings of the technology. The prognostic value of dedicated catheters for ICT needs to be evaluated in long-term studies with a large number of patients, such as the forthcoming studies VIP-1 and VIP-2.

(See reply to this letter from Stephen G. Worthley, MBBS, PhD, Matthew I. Worthley, MBBS, PhD, and Ian T. Meredith, MBBS, PhD on page 152 of this issue) 

References

1. Worthley S, Farouque MO, Worthley M, et al. The RADI PressureWire high-sensitivity thermistor and culprit lesion temperature in patients with acute coronary syndromes. J Invasive Cardiol 2006;18:528–531.
2. Akasaka T, Koyama Y, Neishi Y, et al. Increase in plaque temperature reflects macrophage infiltration in coronary stenotic lesions: Intracoronary temperature measurement and histological assessment. Circulation 2005;112(Abstr):1740.
3. Choi S, Tahk S, Choi B, et al. Temperature difference of atherosclerotic plaque and normal vessel wall predict distal embolization after percutaneous coronary stenting. Circulation 2005;112(Abstr):2918.
4. Leborgne L, Dascotte O, Jarry G, et al. Multi-vessel coronary plaque temperature heterogeneity in patients with acute coronary syndromes. First study with the Radi Medical System wire. Circulation 2005;112(Abstr):3092.
5. Shindo N, Tanaka N, Kobori Y, et al. [Intracoronary temperature in patients with coronary artery disease]. J Cardiol 2005;45:185–191.
6. 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.
7. 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.
8. 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.
9. Belardi JA, Albertal M, Cura FA, et al. Intravascular thermographic assessment in human coronary atherosclerotic plaques by a novel flow-occluding sensing catheter: A safety and feasibility study. J Invasive Cardiol 2005;17:663–666.
10. Madjid M, Willerson JT, Casscells SW. Intracoronary thermography for detection of high-risk vulnerable plaques. J Am Coll Cardiol 2006;47(8 Suppl):C80–C85.