MECHANISMS OF SYSTOLIC CARDIAC DEFORMATION

心肌纤维在心外膜内呈倾斜方向，并经历 穿过横跨的左室壁的方向转变 大约100度。尽管纤维解剖学已经在 详细说明了至少300年来，这一现象的功能后果 错综复杂的安排还没有完全理解。纤维连接在一起 一起在结缔组织基质中，并且每个都可以在功能上 被拴在近邻或远邻的。事实上，最近的研究已经 提示拴系可使心肌缩短发生在 纤维的方向，也垂直于纤维。这 “交叉纤维”的缩短可能会导致心壁 向两个方向缩短，在第三个方向广泛增厚，是一种强有力的 喷出血液的机制。 磁共振成像组织标记法是一种新的成像方法 允许将短寿命的磁性标记以非手术方式放置到 心肌，从而允许通过心脏追踪组织 循环，并精确测量整个左侧的局部变形 脑室。在该方案中，使用标注来刻画区域 左心室收缩时的正常应变和剪切应变。 为了定义心脏的架构如何实现广泛的增厚 发生在收缩时，我们首先会确定心脏的各层是否 每一面墙都是通过关联最大角度 组织学纤维角度缩短，在多个区域 左心室。我们将通过以下方式详细描述心肌变形 测量与左心室纤维角相关的左心室应变 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变来缩短收缩压增厚 从左心室的区域到另一个区域。心外膜的作用 纤维上的垂直心内膜纤维会变形 通过用液体选择性破坏心外膜层来评估 氮气，并测量其对心内膜压力的影响。 我们的发现将与疾病状态的研究相关，例如 心肌病和缺血，其中紊乱的相互作用 纤维可能影响增厚并导致心功能不全。

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.