2004 Fiscal Year Final Research Report Summary
Ultrasound imaging of extracellular matrix remodeling for assessing congestive heart failure
| Project/Area Number |
15300184
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Medical systems
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| Research Institution | Hyogo College of Medicine (2004)
Osaka University (2003) |
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Principal Investigator |
MASUYAMA Tohru Hyogo College of Medicine, Faculty of Medicine, Professor, 医学部, 教授 (70273670)
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| Co-Investigator(Kenkyū-buntansha) |
TSUJINO Takeshi Hyogo College of Medicine, Faculty of Medicine, Associate Professor, 医学部, 助教授 (90283887)
NAKAO Shinji Hyogo College of Medicine, Faculty of Medicine, Research Associate, 医学部, 助手 (80309450)
YAMAMOTO Kazuhiro Osaka University, School of Medicine, Assistant Professor, 医学研究科, 助手 (90303966)
SHIOZAKI Akira Osaka Prefectural University, School of Engineering, Professor, 工学研究科, 教授 (40103345)
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| Project Period (FY) |
2003 – 2004
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| Keywords | Heart Failure / Cardiac Hypertrophy / Remodeling / Ultrasound / レニン・アンジオテンシン系 |
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| Research Abstract |
We have developed a system that analyzes ultrasound radiofrequency signals on the basis of chaos theory. This system was used to analyze the ultrasound signals derived from the human myocardium to show (1)that ultrasound signals show quasiperiodic rather than chaotic nature in the myocardium in patients with cardiomyopathy, and that (2)the quasiperiodic nature changes to chaotic nature following long-term administration of aldosterone blocker in patients with cardiac hypertrophy. Because aldosterone blocker is well known to reduce myocardial fibrosis, our data were may be interpreted that the analysis of ultrasound radiofrequency signals on the basis of chaos study provides a useful index of myocardial fibrosis.
In order to establish the value of the assessment of myocardial fibrosis in the hypertensive failing hearts, we developed a model in which myocardial fibrosis causes in left ventricular systolic and diastolic dysfunction. In this model, myocardial fibrosis was associated with inflammatory changes in the myocardium and with the increase in reactive oxygen species. These changes were hampered by long-term angiotensin II blockade through the activation of the enzymes that facilitate the degradation of extracellular matrix. This was particularly important in those with left ventricular remodeling (dilatation). Thus, myocardial fibrosis appeared to be an important determinant of cardiac function as well as of cardiac geometry, indicating that assessment of myocardial fibrosis is particularly important in hypertensive heart failure.
Currently, our system is not applicable to small animals because of the limitation of the size of region of interest, and therefore, we are attempting to improve the system from the technical aspect.
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