2001 Fiscal Year Final Research Report Summary
Development of Parametric Imaging of Myocardial Perfusion Using Ultrasonic Microbubble Destruction
| Project/Area Number |
12670675
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Kagawa Medical University |
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Principal Investigator |
OHMORI Koji Kagawa Medical University, Second Department of Internal Medicine, Lecturer, 医学部・附属病院, 講師 (00263913)
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| Co-Investigator(Kenkyū-buntansha) |
NOZAKI Shiro Kagawa Medical University, Second Department of Internal Medicine, Assistant Professor, 医学部・附属病院, 助手 (80243773)
MIZUSHIGE Katsufumi Kagawa Medical University, Second Department of Internal Medicine, Associate Professor, 医学部, 助教授 (90166009)
SENDA Shoichi Kagawa Medical University, Second Department of Internal Medicine, Professor, 医学部・附属病院, 教授 (30145049)
WADA Yoshihiro Kagawa Medical University, Second Department of Internal Medicine, Assistant Professor, 医学部・附属病院, 助手 (00314930)
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| Project Period (FY) |
2000 – 2001
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| Keywords | microbubble / myocardial perfusion / Myocardial contrast echocardiography / intermittent imaging / ultrasound / dipyridamole / microsphere |
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| Research Abstract |
We devised a new intermittent imaging employing an ultrasound pulsing sequence that utilized ultrasonic microbubble destruction to quantitate myocardial blood flow (MBF).
We devised a new intermittent imaging employing an ultrasound pulsing sequence that utilized ultrasonic microbubble destruction to quantitate myocardial blood flow (MBF). We found that abrupt shortening of ultrasound pulsing interval (PI) in myocardial contrast echocardiography during intravenous microbubble infusion produces a decay of contrast intensity (CI) along frame number (f), which fit tell to a decay function SI=α×exp(-β×f)+γ. Our study in vitro using a flow model revealed that α and β thus obtained reflect flow transit velocity. Subsequently, we performed an in vivo study in which MBF in rats was successfully quantitated with the new parameters derived from this formula. By defining myocardial velocityas Vel=1/(β/HR), where HR is heart rate, and myocardial blood volume as Vol=α+γ, MBF is determined as VelxVol
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= [1/(β/HR)](α+γ). MBF thus determined exhibited a close correlation with microsphere-derived MBF at baseline, during pharmacological hyperemia, and during coronary stenoses.
Finally, we validated this method in clinical settings. The parameters obtained with harmonic power Doppler and commercially available microbubbles for clinical use, we examined the usefulness of the pulsing sequence. The extent of CI decay produced by PI shortening from 1:10 to 1:1 end-systolic ECG trigger during intravenous microbubble infusion exhibited a similar decay. The extent of CI decay:α/(α+γ) was found useful in quantification of coronary vasodilator reserve, which allowed defection of significant coronary stenoses with a sensitivity of 93 % and a specificity of 85%. In addition, multi-frame trigger that emitted a burst of 4 rapid pulses was found useful in standardizing microbubble concentration in the myocardium. The time duration from the beginning of segmental myocardial opacification after bolus microbubble injection to the burst in which the last pulse resulted in no opacification was correlated with myocardial blood volume, and thus the myocardial viability evaluated by 201-thallium uptake in infarcted segments inpatients. Less
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