Study for the mechanism of mechanical alternans
Study for the mechanism of mechanical alternans
批准号:
18590763
负责人:
KODAMA Makoto
金额:
$2.55万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2006
资助国家:
日本
项目状态:
已结题
起止时间:
2006 至 2007
中文摘要
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英文摘要
Mechanical alternans is a poorly-understood phenomenon of alternating strong and weak beats with a constant beat-to-beat interval. It is a possible linker between failing myocardium and ventricular fibrillation in patients with chronic heart failure. Interval-force relationship, so-called mechanical restitution, is an intrinsic regulatory principle of myocardial contractility depending on sarcoplasmic reticulum (SR)Ca^(2+) cycling. Force-frequency relationship is also considered to reflect Ca^(++) handling of SR. We analyzed interval-force relationship and force frequency relationship in patients with chronic heart failure. In patients with atrial fibrillation, mechanical restitution curves were able to be obtained from beat by beat variance of left ventricular contractility adjusted by pre-preceding coupling intervals. We estimated mechanical restitution curves by fitting to monoexponential curves. Tau of the mechanical restitution curve increased in accord with the decrease of ejection fraction. We analyzed force-frequency relationship. In patients with chronic heart failure, peak force rate shifted to lower heart rate. The force gain of patients was little. A force gain was correlated to the left ventricular ejection fraction. We were able to obtain adequate mechanical restitution curves after both strong beats and weak beats from some patients. Mechanical restitution curves after weak beats steeply rose compared with those after strong beats. The time constant after weak beats were shorter than those after strong beats. Thus mechanical restitution properties were different after strong beats and weak beats during mechanical alternans. This implies that mechanical alternans originates from alternating changes of myocardial Ca^(2+) cycling property.
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DOI:
10.1253/circj.71.343
发表时间:
2007-02
期刊:
Circulation journal : official journal of the Japanese Circulation Society
影响因子:
--
作者:
[W. Mitsuma;M. Kodama;S. Hirono;M. Ito;M. Ramadan;Komei Tanaka;Makoto Hoyano;T. Saigawa;T. Kashimura;K. Fuse;Y. Okura;Y. Aizawa]
通讯作者:
W. Mitsuma;M. Kodama;S. Hirono;M. Ito;M. Ramadan;Komei Tanaka;Makoto Hoyano;T. Saigawa;T. Kashimura;K. Fuse;Y. Okura;Y. Aizawa
DOI:
10.1536/ihj.49.39
发表时间:
2008-01-01
期刊:
INTERNATIONAL HEART JOURNAL
影响因子:
1.5
作者:
[Watanabe, Hiroshi, Okamura, Kazuki, Aizawa, Yoshifusa]
通讯作者:
Aizawa, Yoshifusa
Angiopoietin-1, Angiopoietin-2 and Tie-2 in the Coronary Circulation of Patients with and without Coronary Collaterai Vessels.
有或没有冠状动脉侧支血管的患者冠状动脉循环中的血管生成素-1、血管生成素-2 和 Tie-2。
DOI:
--
发表时间:
2007
期刊:
Circ J 71
影响因子:
--
作者:
[Wataru Mitsuma, 他]
通讯作者:
他
Impact of percutaneous coronary intervention on the levels of interleukin-6 and C-reactive protein in the coronary circulation a subjects with coronary artery disease.
经皮冠状动脉介入治疗对冠状动脉疾病患者冠状动脉循环中白细胞介素 6 和 C 反应蛋白水平的影响。
DOI:
--
发表时间:
2006
期刊:
Am J Cardiol 98
影响因子:
--
作者:
[Malimoud M Ramadan, Makoto Kodama, et al.]
通讯作者:
et al.
Left ventricular pressure-volume loops during mechanical alternans in a patient with dilated cardiomyopathy
扩张型心肌病患者机械交替期间的左心室压力-容量环
DOI:
--
发表时间:
2007
期刊:
Heart 93
影响因子:
--
作者:
[Kashimura, T, Kodama, M, Aizawa, Y]
通讯作者:
Y
共 17 条
Analysis of regulatory T cells and helper T cells in myocarditis and its application to the therapy for inflammatory cardiovascular diseases.
-
批准号:22590805
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.91万
-
财政年份:2010
-
负责人:KODAMA Makoto
-
依托单位:
Analysis of T-cell receptor β-chain complementarity-determining region 3 motifs of infiltrating T cells in the inflammatory lesions from human myocarditis
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批准号:10670636
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项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$1.09万
-
财政年份:1998
-
负责人:KODAMA Makoto
-
依托单位:
海外基金