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

摘要 只有50%的高血压患者的血压控制在目标水平，这表明目前的高血压患者的血压水平仍然很低。 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，以及减少脉搏波的阻尼， 外周微血管系统，较高水平的主动脉僵硬度导致收缩压升高， 易受影响的血管床中的终末器官损伤。因此，假设主动脉僵硬是一种潜在的 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，以及目前的假设是否围绕 主动脉僵硬及其后果受到与血压相关的其他主要血管床的影响 调节，从而影响左心室结构和功能。由此，我们假设颈动脉和 锁骨下动脉与这些关联尤其相关。为了验证上述假设， 以及本申请中概述的其他数据和资源，我们建议使用多民族 评估胸主动脉、颈动脉僵硬度与动脉粥样硬化相关性的研究 整个右上肢，血管钙化本身，以及体积和密度 对应的钙化动脉段此外，我们还将确定不同动脉床的僵硬程度 与血压以及左心室结构和功能的几项指标相关，如果 这些由来自不同动脉段的血管钙的体积或密度混淆/介导。 为了做到这一点，我们将利用上述血管床中动脉硬度的不同测量值，血液 双臂压力和左心室结构和功能的测量。我们将添加到这些， 询问胸部的现有计算机断层扫描，以确定是否存在/程度、体积和密度 升/弓/降胸主动脉以及颈总动脉中的血管钙， 锁骨下动脉拟议的项目反映了一种新的和合理的进步，以解决目前的差距 动脉硬度与高血压和心力衰竭相关性的当前科学（维斯维斯左 心室结构和功能），以及颈动脉（压力感受器的部位）中的疾病 调节）和锁骨下（臂中血压测量的邻近血管床）动脉可以 贡献.

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.