MECHANISMS OF SYSTOLIC CARDIAC DEFORMATION

心肌纤维在心外膜内的取向是倾斜的， 在穿过左心室壁的方向上的过渡， 大约100度。 虽然纤维解剖学已经在 至少300年的细节，这一功能的后果， 复杂排列并不完全清楚。 纤维连接 在结缔组织基质中一起，并且每一个可以在功能上 与近邻或远邻相连。事实上，最近的研究 表明栓系可能会使心肌缩短， 纤维的方向，也垂直于它们。 这 “交叉纤维”缩短可能导致心脏壁的能力， 在两个方向上缩短，在第三个方向上广泛缩短， 喷射血液的机制。 磁共振成像组织标记是一种新的成像方法， 允许将短寿命的磁性标记物非手术放置到 心肌，从而允许通过心脏跟踪组织 循环，并精确测量整个左侧的局部变形 脑室 在该建议中，标记用于表征区域 收缩期左心室正常应变和剪切应变。 为了确定心脏的结构如何使广泛的增厚， 发生在心脏收缩期，我们将首先确定心脏各层是否 墙被拴在每个相关的角度， 组织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， 测量左心室相对于纤维角的应变， 每一层。 这将使我们能够定义交叉光纤的重要性 收缩期增厚的缩短，通过确定它们是否共同变化 从左心室的一个区域到另一个区域。 心外膜的作用 纤维对垂直内皮纤维的变形将是 通过用液体选择性破坏心外膜层进行评估 氮，并测量对内生菌菌株的影响。 我们的发现将与疾病状态的研究相关， 心肌病和缺血，其中一个干扰的相互作用， 纤维可影响增厚并导致心室功能障碍。

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.