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J Am Coll Cardiol, 2007; 50:2197-2203, doi:10.1016/j.jacc.2007.07.079
(Published online 14 November 2007). © 2007 by the American College of Cardiology Foundation |
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* Department of Cardiology, Kagoshima City Hospital, Kagoshima, Japan
Department of Cardiovascular, Respiratory, and Metabolic Medicine, Graduate School of Medicine, Kagoshima University, Kagoshima, Japan.
Manuscript received February 9, 2007; revised manuscript received July 5, 2007, accepted July 30, 2007.
* Reprint requests and correspondence: Dr. Shuichi Hamasaki, Department of Cardiovascular, Respiratory, and Metabolic Medicine, Graduate School of Medicine, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima City, 890–8520, Japan. (Email: hamasksh{at}m.kufm.kagoshima-u.ac.jp).
A portion of this study was presented at the 55th Annual Scientific Session of the American College of Cardiology, Atlanta, GA, March 11–14, 2006.
Objectives: The purpose of this study was to test the hypothesis that the maximal temperature (Tmax) site, as measured by thermal wire, coincides with the culprit plaque by intravascular ultrasound (IVUS) in patients with acute myocardial infarction (AMI).
Background: Subsequent thrombosis developing to the proximal region from the site of plaque rupture or erosion can potentially complicate the ability of coronary angiography to identify the accurate culprit plaque in patients with coronary total occlusion.
Methods: In 45 consecutive patients with a first anterior AMI, the Tmax site by thermal wire and the culprit plaque by IVUS were evaluated in the left anterior descending coronary artery (LAD).
Results: Twenty-five patients had LAD total occlusion, and the remaining 20 had LAD reperfusion. In both groups of patients, the Tmax site was significantly more distal to the angiographically most stenotic site or occlusive site (reperfusion: mean distance [MD] = 1.1 mm distal, 95% confidence interval [CI] 0.3 to 1.9 mm, p = 0.01; total occlusion: MD = 8.8 mm distal, 95% CI 8.0 to 9.6 mm, p < 0.0001). The culprit plaques by IVUS approximately coincided with those by angiography or thermal wire in patients with reperfusion. However, the angiographic occlusive site was significantly more proximal to the culprit plaque by IVUS (MD = 9.2 mm, 95% CI 7.9 to 10.6 mm, p < 0.0001), but the Tmax site coincided with the culprit plaque by IVUS (MD = 0.3 mm distal, 95% CI 0.3 mm proximal to 1.0 mm distal, p = 0.293) in patients with total occlusion.
Conclusions: Temperature measurement of coronary plaque enables accurate localization of the culprit plaque in AMI with coronary total occlusion.
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