CLINICAL APPLICATION OF END SYSTOLIC P-V RELATIONS

这项研究计划的长期目标是确定一个时间， 慢性左心室容量超负荷的外科治疗 主动脉瓣返流（AR）或二尖瓣返流（MR），以保持或 恢复正常的LV尺寸和性能。 左心室容积的自然史 过载遵循潜在可识别的血流动力学过程 特征为代偿性LV肥大，随后为LV收缩期 在没有心肌功能障碍的情况下发生功能障碍，最后， 不可逆性心肌功能障碍。 常用的临床、非临床 侵入性和侵入性指标倾向于识别晚期AR和MR患者 在不可逆性心肌功能不全时血流动力学过程中 占主导地位。 相比之下，这个实验室的初步数据 强有力地支持了这样的假设，即在没有左室收缩功能障碍的情况下， 在AR和MR患者中， 应用最大时变弹性和心肌硬度 在这种情况下，LV收缩功能障碍是以下因素的结果： 左心室肥大不充分和球形几何形状，以及 此时左心室容量超负荷手术将逆转这些有害的 血流动力学过程，从而保持或恢复正常的LV大小， 性能 因此，本研究提案的具体目标是： 1)使用以下方法表征LV腔室性能和心肌特性 正常人时变弹性和心肌硬度的概念 患者并与AR或MR患者进行对比; 2） 在存在以下情况下建立异常LV腔室弹性的机制： 正常心肌特性; 3）建立AR患者亚组 或MR，基于是否存在或正常LV腔室弹性， 心肌性质; 4）确定变化的程度和时间过程 在AR和MR手术后一年内的LV尺寸和性能， 和5）表征AR和MR手术对 左心室腔室弹性和心肌特性。 本研究提案 因此，代表了复杂的血液动力学和 这些方法被整合，重点是提供新的数据， 在缺乏心肌收缩功能障碍的情况下， AR和MR患者的功能障碍和手术时间， 或恢复正常的左心室大小和性能。

The long-term goal of this research proposal is to define a time for surgery in chronic left ventricular (LV) volume overload resulting from aortic regurgitation (AR) or mitral regurgitation (MR) to preserve or restore normal LV size and performance. The natural history of LV volume overload follows a potentially identifiable hemodynamic course characterized by compensated LV hypertrophy, followed by LV systolic dysfunction in the absence of myocardial dysfunction, and finally, irreversible myocardial dysfunction. The commonly employed clinical, non- invasive, and invasive indices tend to identify patient with AR and MR late in their hemodynamic course when irreversible myocardial dysfunction predominates. In contrast, the preliminary data from this laboratory strongly support the hypotheses that LV systolic dysfunction in the absence of myocardial dysfunction can be identified in patients with AR and MR by applying both the maximum time-varying elastance and myocardial stiffness concepts, that LV systolic dysfunction in this setting is the result of inadequate LV hypertrophy and assumption of spherical geometry, and that surgery for LV volume overload at this time will reverse these detrimental hemodynamic processes and, thereby, preserve or restore normal LV size and performance. Therefore, the specific aims of this research proposal are: 1) to characterize LV chamber performance and myocardial properties using the time-varying elastance and myocardial stiffness concepts in normal patients and contrast them with those in patients with AR or MR; 2) to establish mechanisms for abnormal LV chamber elastance in the presence of normal myocardial properties; 3) to establish subgroups of patients with AR or MR based upon the presence or absence or normal LV chamber elastance and myocardial properties; 4) to define the extent and time course of changes in LV size and performance during the year following surgery for AR and MR, and 5) to characterize the independent effects of surgery for AR and MR on LV chamber elastance and myocardial properties. This research proposal represents, therefore, a unique combination of sophisticated hemodynamic approaches that are integrated to focus on providing new data to define the mechanisms for LV systolic dysfunction in the absence of myocardial dysfunction and a time for surgery in patients with AR and MR to preserve or restore normal LV size and performance.