Reply to Letter to the Editor

We thank (the authors of the letter) for their comments about our study in the Journal,¹ and it seems they essentially agree with our conclusions. However, they raise some specific points to add weight to the argument that the main reason we did not identify an increase in plaque temperature was primarily due to limitations with the lesion criteria for enrollment. Furthermore, they suggest that against the weight of previous data showing an increase in plaque temperature in similar cohorts, our data should be interpreted with caution.
With regard to these points, we think the following should be clarified. The authors of the letter suggest that we used FFR to enroll patients and identify lesion severity. We did not. It is clearly stated in the Methods section that angiographic lesion severity needed to be in excess of 70%, among other high-risk enrollment features.¹ We provide the FFR data pre-PCI, but this was not part of the enrollment criteria. We clearly used a cohort of patients with acute coronary syndromes and severe coronary stenoses, giving us the best opportunity to get contact between the RADI wire and the atherosclerotic plaque.
We have some concerns with the quoting of 4 studies contradicting our data: “...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 In fact, 3 of these 4 studies are not published in peer-reviewed journals, but are abstracts from meetings.^2–4 The only published manuscript the authors mention is referenced in our manuscript, and it showed an unimpressive 0.07ºC elevation.⁵ However, it is not published in an English-language journal, and thus it is difficult to assess in further detail.
There are potential explanations that we and the authors of the letter explain for not finding a temperature increase in the lesions of the patients enrolled in our study. We do need to remind ourselves that we should not discount one important potential explanation: that in these patients, there was no increase in plaque temperature.

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.