MECHANISMS OF SYSTOLIC CARDIAC DEFORMATION
心脏收缩变形的机制
基本信息
- 批准号:2222749
- 负责人:
- 金额:$ 25.93万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1992
- 资助国家:美国
- 起止时间:1992-02-27 至 1995-01-31
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Myocardial fiber orientation is oblique in the epicardium and undergoes a
transition in direction through the left ventricular wall that spans
approximately 100 degrees. Although fiber anatomy has been studied in
detail for at least 300 years, the functional consequences of this
intricate arrangement are not fully understood. Fibers are joined
together in a connective tissue matrix, and each may be functionally
tethered to near or distant neighbors. indeed, recent studies have
suggested that tethering may allow myocardial shortening to occur both in
the direction of the fibers and also perpendicular to them. This
"cross-fiber" shortening could result in the ability of the heart wall to
shorten in two directions and thicken extensively in the third, a potent
mechanism for ejection of blood.
Magnetic Resonance Imaging tissue tagging is a new imaging method which
allows the nonsurgical placement of short-lived magnetic markers into
myocardium, and thus permits the tracking of tissue through the cardiac
cycle, and accurate measurement of local deformations in the entire left
ventricle. In this proposal, tagging is used to characterize regional
left ventricular normal and shear strains during systole.
To define how the heart's architecture enables extensive thickening to
occur in systole, we will first determine whether the layers of the heart
wall are tethered to each by correlating the angle at which maximum
shortening occurs to the histologic fiber angle, at multiple regions in
the left ventricle. We will describe myocardial deformation in detail by
measuring left ventricular strains with respect to the fiber angle of
each layer. This will allow us to define the importance of crossfiber
shortening for systolic thickening by determining whether they co-vary
from region to region of the left ventricle. The effect of epicardial
fibers on the deformation of the perpendicular endocardial fibers will be
assessed by selectively destroying epicardial layers with liquid
nitrogen, and measuring the consequences on endocardial strains.
Our findings will have relevance to the study of disease states such as
cardiomyopathy and ischemia, in which a disturbed interaction between
fibers may affect thickening and result in ventricular dysfunction.
心肌纤维在心外膜中的取向是倾斜的,并且经历了
穿过左心室壁的方向转变
大约100度。 尽管纤维解剖学已被研究
至少 300 年的细节,这一功能的后果
错综复杂的安排尚未完全理解。 纤维已连接
一起在结缔组织基质中,并且每个都可以在功能上
与近或远的邻居拴在一起。事实上,最近的研究表明
表明束缚可能使心肌缩短发生在
纤维的方向,也垂直于它们。 这
“交叉纤维”缩短可能会导致心壁的能力
在两个方向上缩短并在第三个方向上广泛增厚,这是一种有效的
血液喷射的机制。
磁共振成像组织标记是一种新的成像方法,
允许非手术地将短寿命的磁性标记放置到
心肌,从而允许通过心脏追踪组织
周期,精确测量整个左侧的局部变形
心室。 在本提案中,标签用于表征区域
收缩期左心室正常应变和剪切应变。
定义心脏结构如何实现广泛增厚
发生在收缩期时,我们首先要判断心脏的各层是否
墙壁通过关联最大角度来连接到每个墙壁
组织学纤维角在多个区域发生缩短
左心室。 我们将详细描述心肌变形
测量左心室应变相对于纤维角度
每一层。 这将使我们能够定义交叉纤维的重要性
通过确定它们是否共同变化来缩短收缩期增厚
从左心室的一个区域到另一个区域。 心外膜的作用
垂直心内膜纤维变形的纤维将是
通过用液体选择性破坏心外膜层进行评估
氮,并测量对心内膜应变的影响。
我们的研究结果将与疾病状态的研究相关,例如
心肌病和缺血,其中相互作用受到干扰
纤维可能会影响增厚并导致心室功能障碍。
项目成果
期刊论文数量(0)
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{{ truncateString('EDWARD P SHAPIRO', 18)}}的其他基金
Mechanisms of Age-related Diastolic Dysfunction in Human
人类年龄相关舒张功能障碍的机制
- 批准号:
7485716 - 财政年份:2004
- 资助金额:
$ 25.93万 - 项目类别:
Mechanisms of Age-related Diastolic Dysfunction in Human
人类年龄相关舒张功能障碍的机制
- 批准号:
6870491 - 财政年份:2004
- 资助金额:
$ 25.93万 - 项目类别:
Mechanisms of Age-related Diastolic Dysfunction in Human
人类年龄相关舒张功能障碍的机制
- 批准号:
7277742 - 财政年份:2004
- 资助金额:
$ 25.93万 - 项目类别:
Mechanisms of Age-related Diastolic Dysfunction in Human
人类年龄相关舒张功能障碍的机制
- 批准号:
6950349 - 财政年份:2004
- 资助金额:
$ 25.93万 - 项目类别:
Mechanisms of Age-related Diastolic Dysfunction in Human
人类年龄相关舒张功能障碍的机制
- 批准号:
7098781 - 财政年份:2004
- 资助金额:
$ 25.93万 - 项目类别:
MECHANISMS OF SYSTOLIC AND DIASTOLIC CARDIAC DEFORMATION
收缩期和舒张期心脏变形的机制
- 批准号:
6030623 - 财政年份:1992
- 资助金额:
$ 25.93万 - 项目类别:
MECHANISMS OF SYSTOLIC AND DIASTOLIC CARDIAC DEFORMATION
收缩期和舒张期心脏变形的机制
- 批准号:
2696592 - 财政年份:1992
- 资助金额:
$ 25.93万 - 项目类别:
MECHANISMS OF SYSTOLIC AND DIASTOLIC CARDIAC DEFORMATION
收缩期和舒张期心脏变形的机制
- 批准号:
6389165 - 财政年份:1992
- 资助金额:
$ 25.93万 - 项目类别:
MECHANISMS OF SYSTOLIC AND DIASTOLIC CARDIAC DEFORMATION
收缩期和舒张期心脏变形的机制
- 批准号:
2222750 - 财政年份:1992
- 资助金额:
$ 25.93万 - 项目类别:
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