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

动脉僵硬度和血管钙与血压以及左心室结构和功能的相关性。

• 批准号: 10188614
• 负责人: Matthew A Allison
• 金额: $ 65.05万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2019
• 资助国家: 美国
• 起止时间: 2019-07-01 至 2024-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10188614
• 关键词: Address; Adherence; Affect; Antihypertensive Agents; Aorta; Area; Arteries; Atherosclerosis; Attenuated; Beds; Blood Pressure; Blood Vessels; Calcium; Cardiovascular Diseases; Carotid Arteries; Chest; Clinical; Common carotid artery; Coronary artery; Cross-Sectional Studies; Deposition; Diagnosis; Diastolic blood pressure; Disease; Distal; Glucose; Heart failure; Hypertension; Individual; Ipsilateral; Left Ventricular Mass; Left ventricular structure; Link; Measurement; Measures; Mediating; Multi-Ethnic Study of Atherosclerosis; Muscle function; Organ; Peripheral; Physical activity; Physiologic pulse; Population Attributable Risks; Pressoreceptors; Process; Pulse Pressure; Regulation; Research; Risk; Risk Assessment; Scanning; Science; Site; Smoking; Structure; Structure of subclavian artery; Systolic Pressure; Techniques; Testing; Thoracic aorta; Treatment Failure; Unhealthy Diet; Upper Extremity; Vascular Diseases; Vascular blood supply; Vascular calcification; X-Ray Computed Tomography; arm; arterial stiffness; base; blood pressure regulation; calcification; cohort; data resource; density; heart function; hypertension treatment; longitudinal analysis; novel; pressure; vascular bed

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.

抽象的 只有50％的接受高血压治疗的人被控制为目标水平，这表明当前 治疗可能不会影响血压升高的所有潜在机制。通过增加 反射脉冲波的速度和振幅，并减少脉搏波的阻尼 周围微脉管系统，较高水平的主动脉僵硬导致收缩压和 易感血管床的最终器官损伤。因此，假设主动脉刚度是潜力 高血压治疗失败的机制。在这方面，必须进一步了解 刚度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有关的其他主要血管床的影响 调节，从而左心室结构和功能。由此，我们假设颈动脉和 锁骨下动脉将与这些关联特别相关。测试上面暗示的假设，如 就像本应用程序中概述的其他人一样，我们建议使用多种族的现有数据和资源 研究动脉粥样硬化，以评估胸主动脉，颈动脉和 在右上端，本身具有血管计算，以及 相应计算的动脉片段。此外，我们将确定不同动脉床的刚度是否 与血压的多种指标以及左心室结构和功能有关，以及 这些是由不同伪影的血管钙的体积或密度混淆/介导的。 为此，我们将利用近似血管床中动脉刚度的不同测量 手臂的压力以及左心室结构和功能的度量。我们将通过 询问胸部现有的计算机断层扫描，以了解存在/程度和密度 上升/拱/降胸主动脉的血管钙，以及常见的颈动脉和 锁骨下动脉。拟议的项目反映了一种新颖而合理的进步，以解决当前差距 有关动脉僵硬与高血压和心力衰竭的相关性的当前科学（相对于剩余 心室结构和功能），以及颈动脉中的疾病（压力受体部位 调节）和锁骨下（手臂中血压测量的连续血管床）可能 贡献。