Ultrasound imaging of extracellular matrix remodeling for assessing congestive heart failure

细胞外基质重塑的超声成像评估充血性心力衰竭

基本信息

项目摘要

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.
我们已经开发了一个系统,分析超声射频信号的基础上混沌理论。该系统被用于分析来自人类心肌的超声信号,以显示(1)在心肌病患者的心肌中超声信号显示准周期性而不是混沌性质,以及(2)在心脏肥大患者中长期施用醛固酮阻滞剂之后准周期性质改变为混沌性质。由于醛固酮受体阻滞剂可以减轻心肌纤维化,我们的数据可以解释为基于混沌研究的超声射频信号分析提供了一个有用的心肌纤维化指标。为了建立心肌纤维化在高血压衰竭心脏中的评估价值,我们建立了一个心肌纤维化导致左心室收缩和舒张功能障碍的模型。在该模型中,心肌纤维化与心肌炎性变化和活性氧增加相关。这些变化受到长期血管紧张素II阻断剂通过激活促进细胞外基质降解的酶的阻碍。这在左心室重构(扩张)的患者中尤为重要。因此,心肌纤维化似乎是心脏功能以及心脏几何形状的重要决定因素,表明心肌纤维化的评估在高血压性心力衰竭中尤为重要。目前,由于感兴趣区域的大小限制,我们的系统不适用于小动物,因此,我们正在尝试从技术方面改进该系统。

项目成果

期刊论文数量(29)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
N-methylethanolamine attenuates cardiac fibrosis and improves diastolic function: inhibition of phospholipase D as a possible mechanism.
  • DOI:
    10.1016/j.ehj.2004.05.003
  • 发表时间:
    2004-07
  • 期刊:
  • 影响因子:
    39.3
  • 作者:
    Kazuhiro Yamamoto;Yoshito Takahashi;T. Mano;Y. Sakata;N. Nishikawa;Junichi Yoshida;Y. Oishi;M. Hori;T. Miwa;S. Inoue;T. Masuyama
  • 通讯作者:
    Kazuhiro Yamamoto;Yoshito Takahashi;T. Mano;Y. Sakata;N. Nishikawa;Junichi Yoshida;Y. Oishi;M. Hori;T. Miwa;S. Inoue;T. Masuyama
Junich Yoshida: "ATI RECEPTOR BLOCKER ADDED TO ACE INHIBITOR PROVIDES BENEFITS AT ADVANCED STAGE OF HYPERTENSIVE DIASTOLIC HEART FAILURE"Hypertension. (in press). (2004)
Junich Yoshida:“ATI 受体阻滞剂添加到 ACE 抑制剂可在高血压舒张性心力衰竭的晚期阶段提供益处”高血压。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
ACE Inhibitor and angiotensin II type I receptor blocker differently regulate ventricular fibrosis in hypertensive diastolic heart failure
ACE抑制剂和血管紧张素II I型受体阻滞剂不同地调节高血压舒张性心力衰竭的心室纤维化
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Shirakawa他;E.Ishii他;R.Shirakawa et al.;E.Ishii et al.;E.Ishii他;T.Higashi他;R.Shirakawa他;T.Higashi et al.;Kazuhiro Yamamoto;R.Shirakawa et al.;Kazuhiro Yamamoto;T.Higashi他;Kazuhiro Yamamoto
  • 通讯作者:
    Kazuhiro Yamamoto
Tissue characterization identifies subjects with high risk of cardiovascular diseases
ACE inhibitor and angiotensin II type 1 receptor blocker differently regulate ventricular fibrosis in hypertensive diastolic heart failure
  • DOI:
    10.1097/00004872-200502000-00022
  • 发表时间:
    2005-02-01
  • 期刊:
  • 影响因子:
    4.9
  • 作者:
    Yamamoto, K;Mano, T;Masuyama, T
  • 通讯作者:
    Masuyama, T
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MASUYAMA Tohru其他文献

MASUYAMA Tohru的其他文献

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{{ truncateString('MASUYAMA Tohru', 18)}}的其他基金

Role of Duodenal Iron Transporters in Cardio-Renal Anemia Syndrome
十二指肠铁转运蛋白在心肾贫血综合征中的作用
  • 批准号:
    24590907
  • 财政年份:
    2012
  • 资助金额:
    $ 10.62万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Ultrasound imaging for tissue characterization to assess cardiovascular involvement in diabetes
用于组织表征的超声成像以评估糖尿病的心血管参与情况
  • 批准号:
    17300177
  • 财政年份:
    2005
  • 资助金额:
    $ 10.62万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Acquirement of the Ischemic Cardioprotection and ecto-5'-nucleotidase : Investigation of the Receptor Activation and Subsequent Signal Transduction
缺血性心脏保护和 ecto-5-核苷酸酶的获得:受体激活和随后信号转导的研究
  • 批准号:
    12470153
  • 财政年份:
    2000
  • 资助金额:
    $ 10.62万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Examination of the mechanism of the transition to isolated diastolic heart failure
向孤立性舒张性心力衰竭转变的机制研究
  • 批准号:
    10670653
  • 财政年份:
    1998
  • 资助金额:
    $ 10.62万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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Energetic State and Metabolic Remodeling in Cardiac Hypertrophy and Failure
心脏肥大和衰竭的能量状态和代谢重塑
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    10522598
  • 财政年份:
    2022
  • 资助金额:
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  • 项目类别:
Energetic State and Metabolic Remodeling in Cardiac Hypertrophy and Failure
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致命性心脏肥大中的 T 管重塑和钙处理功能障碍
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    2020
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Role of miR-574-Fam210a axis in cardiac hypertrophy and remodeling
miR-574-Fam210a 轴在心脏肥大和重塑中的作用
  • 批准号:
    10251906
  • 财政年份:
    2018
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    $ 10.62万
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Myocardial Metabolic Remodeling in Cardiac Hypertrophy
心脏肥大中的心肌代谢重塑
  • 批准号:
    9281869
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心脏肥大电重塑的分子机制
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    2008
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Molecular mechanisms of electrical remodeling in cardiac hypertrophy
心脏肥大电重塑的分子机制
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    7765574
  • 财政年份:
    2008
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    $ 10.62万
  • 项目类别:
Molecular mechanisms of electrical remodeling in cardiac hypertrophy
心脏肥大电重塑的分子机制
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    7623869
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    2008
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Molecular mechanisms of electrical remodeling in cardiac hypertrophy
心脏肥大电重塑的分子机制
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Molecular mechanisms of electrical remodeling in cardiac hypertrophy
心脏肥大电重塑的分子机制
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