MECHANISMS OF SYSTOLIC AND DIASTOLIC CARDIAC DEFORMATION

心脏壁中的心肌纤维形成了一个非凡的机械系统， 旨在将少量的肌节缩短放大为充满活力的 变稠，然后迅速回缩，允许突然、快速填充。 这个项目是为了继续我们的项目相关的当地 变形到全局参数的函数，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有创跟踪，并准确 测量整个LV的局部变形。与世隔绝的血液 灌流犬心脏模型是一种我们已经适应的准备工作 磁性环境，允许计算机驱动的精密伺服泵 预载、后载和空腔体积的控制。 在我们之前的工作中，我们演示了交互的重要性 心壁各层之间的收缩变形。我们现在扩展 我们的调查是为了舒缓。当心室排出时，它表现出一种 扭动的动作，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期反冲，这主要发生在 在腔体积固定时的等容松弛过程中，可能会产生 抽吸以帮助早期舒张期充盈。我们现在的目标是将 这种反冲的速度和时间与早期舒张期的有效性 填写一组已知存在填充异常的患者： 高血压。我们还将研究高血压，因为分离的心脏 该模型允许测量整体舒张期吸力。我们会 阐明间质结缔组织基质在血管生成中的作用 心脏在协调收缩、变形和发育中的作用 使用结缔组织功能障碍模型的舒张期吸力 (放荡主义)。在其他研究中，我们将描述负载依赖关系 扭转的影响，以及改变间隔几何形状对变形的影响。 这一结果将对表征的过程具有重要的意义 通过减少早期舒张期充盈，我们怀疑这与 收缩期畸形的反冲异常。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一些方面 以胶原蛋白异常为特征，包括心肌病、心肌梗死 梗塞、扩张和眩晕。他们将增加了解 在改变心室几何形状的疾病过程中的左心功能障碍， 比如右室负荷过重的状态。

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.