MECHANISMS OF SYSTOLIC AND DIASTOLIC CARDIAC DEFORMATION

心壁中的心肌纤维形成了一个非凡的力学系统， 旨在将少量的肌节缩短放大为有力的 变厚，然后迅速弹回，允许突然，快速填充。 该项目旨在继续我们的项目， 变形到函数的全局参数，使用两个唯一的 方法论。 MRI组织标记是一种强大的新成像技术， 在我们的实验室开发，现在广泛使用，它允许非- 通过心动周期对组织进行侵入性跟踪， 测量整个LV上的局部变形。 分离的，血液 灌注的犬心脏模型是我们已经适应的准备， 磁环境，允许精确的计算机驱动伺服泵 预加载、后加载和腔体体积的控制。 在我们以前的工作中，我们证明了相互作用的重要性， 在心脏壁的各层之间进行收缩变形。 我们现在扩大 把我们的调查报告交给了达索。 当心室膨胀时， 扭转运动，称为“扭转”。 我们和其他人有证据表明 在这种扭转变形过程中可以储存势能，并且 左心室扭转的快速舒张回缩， 在等容松弛期间，当腔体积固定时， 抽吸以帮助舒张早期充盈。 我们现在的目标是将 这种反冲的速度和时间与舒张早期的有效性 填充一组已知存在充盈异常的患者： 高血压 我们还将研究高血压，因为离体心脏 模型允许测量整体舒张期吸力。 我们将 阐明间质结缔组织基质在 心脏在收缩期协调变形， 使用结缔组织功能障碍模型， （lathyrism）。 在其他研究中，我们将描述负载依赖性 的扭转，以及改变中隔几何形状对变形的影响。 结果将有重要的影响，在过程中的特点 舒张早期充盈减少，我们怀疑这与 收缩变形的异常回缩。 这些过程包括 高血压、充血性心力衰竭以及衰老本身。 他们 应阐明心肌疾病中室壁变形的各个方面 其特征在于异常的胶原蛋白，包括心肌病、心肌梗塞、心肌纤维化、纤维化、 梗塞扩张和昏迷 他们会加深对 在改变心室几何结构的疾病过程中的LV功能障碍， 例如右心室超负荷状态。

Myocardial fibers in the heart wall form a remarkable mechanical system, designed to amplify small amounts of sarcomere shortening into vigorous thickening, and then to recoil briskly, allowing sudden, rapid filling. This project is designed to continue our project relating local deformation to global parameters of function, using two unique methodologies. MRI tissue tagging is a powerful new imaging technique, developed in our laboratory and now widely used, which permits the non- invasive tracking of tissue through the cardiac cycle and accurate measurement of local deformation over the entire LV. The isolated, blood perfused canine heart model is a preparation that we have adapted to the magnetic environment, that allows precise computer driven servo-pump control of preload, afterload, and cavity volume. In our previous work, we demonstrated the importance of the interaction among layers of the heart wall for systolic deformation. We now expand our investigations to diastole. As the ventricle ejects, it exhibits a wringing motion, termed "torsion". We and others have evidence suggested hat potential energy may be stored during this torsional deformation, and that the rapid diastolic recoil of LV torsion, which occurs largely during isovolumic relaxation when cavity volume is fixed, may create suction to aid early diastolic filling. We now aim to correlate the speed and timing of this recoil with the effectiveness of early diastolic filling in a group of patients known to have filling abnormalities: hypertensives. We will also study hypertension since the isolated heart model allows the measurement of global diastolic suction. We will clarify the role of the interstitial connective tissue matrix in the heart in the coordination of deformation in systole, and the development of suction in diastole, using a model of connective tissue dysfunction (lathyrism). In other studies we will characterize the load dependence of torsion, and the effects of altered septal geometry on deformation. The results will have important implications in processes characterized by reduced early diastolic filling, which we suspect is related to abnormal recoil of systolic deformations. These processes include hypertension, congestive heart failure, and also aging itself. They should clarify aspects of wall deformation in myocardial diseases characterized by abnormal collagen including cardiomyopathy, myocardial infarction, expansion, and stunning. They will add to the understanding of LV dysfunction in disease processes that alter ventricular geometry, such as right ventricular overload states.