The Relevance of Arterial Stiffness and Vascular Calcium to Blood Pressure and LV Structure and Function.

摘要 接受高血压治疗的患者中只有50%被控制在目标水平，这表明目前的 治疗可能不会影响血压升高的所有潜在机制。通过增加 反射脉搏波的速度和幅度，以及将脉搏波的衰减降低到 外周微血管系统，较高水平的主动脉僵硬会导致收缩压和 易感血管床的终末器官损害。因此，主动脉僵硬被认为是一种潜在的 高血压治疗失败的机制。在这方面，有必要进一步了解 僵硬和动脉粥样硬化之间的相互关系，以及目前的假说是否围绕 主动脉僵硬及其后果受其他与血压有关的主要血管床的影响 从而调节左心室的结构和功能。由此，我们假设颈动脉和 锁骨下动脉将与这些联系特别相关。检验上面所暗示的假设，如 和本申请中概述的其他内容一样，我们建议使用来自多种族的现有数据和资源 评价胸主动脉、颈动脉僵硬与动脉粥样硬化关系的研究 横跨右上肢，血管钙化本身，以及血管的体积和密度 相应的钙化动脉节段。此外，我们将确定不同动脉床的僵硬程度 与几项血压测量以及左心室结构和功能有关，如果 这些受来自不同动脉段的血管钙的体积或密度的影响。 为此，我们将使用上述血管床、血液中动脉硬度的不同测量方法。 双臂压力和左心室结构和功能的测量。我们将通过以下方式增加这些功能 询问现有的胸部CT扫描是否存在/范围、体积和密度 升主动脉/弓/降主动脉以及颈总动脉和降主动脉内的血管钙。 锁骨下动脉。拟议的项目反映了一种新颖和合理的进展，以解决目前在 关于动脉僵硬与高血压和心力衰竭的相关性的现代科学(与左 心室结构和功能)，以及颈动脉疾病(压力感受器的位置) 调节)和锁骨下动脉(臂中连续的血管床对血压的测量)可以 贡献力量。

ABSTRACT Only 50% of those treated for hypertension are controlled to target levels, suggesting that the current treatments may not be affecting all of the potential mechanisms for elevations in blood pressure. By increasing the velocity and amplitude of reflected pulse waves, as well as decreasing the dampening of pulse waves into the peripheral microvasculature, higher levels of aortic stiffness cause increases in systolic blood pressure and end-organ damage in susceptible vascular beds. As such, aortic stiffness is hypothesized to be a potential mechanism for hypertension treatment failure. In this regard, it is essential to further understand the interrelationships between stiffness and atherosclerosis, and whether the current hypotheses surrounding aortic stiffness and its consequences are influenced by other major vascular beds linked to blood pressure regulation and, thereby, left ventricular structure and function. From this, we hypothesize that the carotid and subclavian arteries will be particularly relevant to these associations. To test the hypotheses implied above, as well as others outlined in this application, we propose to use existing data and resources from the Multi-Ethnic Study of Atherosclerosis to assess associations between stiffness in the thoracic aorta, carotid arteries and across the right upper extremity, with vascular calcification per se, as well as the volume and density of corresponding calcified arterial segments. Moreover, we will determine if stiffness in the different arterial beds is associated with several measures of blood pressure, as well as left ventricular structure and function, and if these are confounded/mediated by the volume or density of vascular calcium from distinct arterial segments. To do so, we will utilize different measurements of arterial stiffness in the aforementioned vascular beds, blood pressure in both arms and measures of left ventricular structure and function. We will add to these by interrogating existing computed tomography scans of the chest for the presence/extent, volume and density of vascular calcium in the ascending/arch/descending thoracic aorta, as well as the common carotid and subclavian arteries. The proposed projects reflect a novel and rational advance to address current gaps in the current science on the relevance of arterial stiffness to both hypertension and heart failure (vis-à-vis left ventricular structure and function), and how disease in the carotid (the site of baroreceptors for pressure regulation) and subclavian (contiguous vascular bed to blood pressure measurement in the arm) arteries may contribute.