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| Statin cools down temperature of athrosclerotic plaque in patient with coronary artery disease: temperature measurement and intravascular ultrasound study |
| Department of cardiology, Ajou University School of Medicine |
| So-Yeon Choi, Byoung-Joo Choi, Seung-Jea Tahk, Myeong-Ho Yoon, Sung-Gyun Ahn, Zhen-Guo Zheng, Hong-Seok Lim, Jung-Hyun Choi, Soo-Jin Kang, Gyo-Seung Hwang, Joon-Han Shin |
Background: Because the increased temperature is considered associated with expression of aggressive inflammation in plaque, the measurement of plaque temperature might be used to assess plaque vulnerability. This study was planed to investigate the effect of statin on stability of plaque by assessing temperature using RADI pressure-temperature measurement wire that reveals the temperature difference (ΔT) between the atherosclerotic plaque and the healthy vessel wall. Methods: We included angina patients who were planed to take coronary intervention, had significant stenosis on diagnostic coronary angiogram performed by radial artery approach in out-patient clinic and then evenly randomized into two groups: statin (pravastatin 40mg/d) or control group. The temperature measurement and IVUS study were performed during diagnostic angiogram (baseline) and just before intervention (follow-up). All patients had taken same medications except statin during study period. Results: 19 angina patients (age range, 48-70; 63% men; 63% unstable angina) were enrolled (10 in statin group, 9 in control group). The average time interval between baseline and follow-up was 21±6 days. On IVUS study, there were no significant changes of quantitative and qualitative parameters between baseline and follow-up in both groups. The baseline ΔT was not significantly different between two groups (statin: 0.25±0.12°C vs. control: 0.22±0.12°C, P=0.599), however statin group had a trend of lower follow-up ΔT than control group (statin: 0.13±0.06 °C vs. control: 0.21±0.13 °C, p=0.120) and the reduction of ΔT (follow-up ΔT- baseline ΔT) was significantly greater in statin group compared to the control group (-0.12±0.09 °C vs. -0.01±0.07 °C, p=0.010, respectively). Conclusion: Even though a major limitation of this study is the very small number of enrolled patients, it provides evidence in support of the anti-inflammatory effect of statins in human coronary plaque and also reveals that physiologic change like a decrease of temperature procedes any morphologic change in processing reduction of plaque vulnerability. A study to evaluate dose-dependent effect of statin has been underway.
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