Race & Gender Differences In Arterial Velocity

本项目利用多普勒超声对巴尔的摩老年纵向研究参与者的颈动脉和脑内血流速度进行研究。目的是确定动脉解剖和生理特性与脑血管疾病和衰老的关系。我们目前正在研究BLSA中几种颈动脉测量与酒精使用之间的关系。我们发现轻度至中度饮酒与颈总动脉更大的动脉弹性和硬度降低有关。与动脉壁厚度和直径的相关性不明显。这些变化与血压和年龄无关。动脉对酒精使用的反应可能代表了它对心血管疾病的保护作用的一种机制。在之前的研究中，我们已经表明，绝经后妇女使用雌激素替代与动脉僵硬度降低有关。众所周知，男性性激素会随着年龄的增长而下降，并与动脉粥样硬化疾病和动脉粥样硬化的危险因素有关。我们研究了雄激素和动脉硬度（β硬度指数）之间的关系。睾酮和游离睾酮（以游离睾酮指数衡量）与年龄、脉压和僵硬指数呈负相关，SHBG与年龄和僵硬指数呈正相关。多元回归分析显示，调整风险参数后，T是唯一能预测动脉僵硬指数的激素。颈动脉研究前5至10年的T值也是僵硬指数的预测因子。通径分析表明，随着年龄的增长，T的减小直接或间接地通过脉压的增加增加了刚度指标。DHEAS似乎没有直接导致动脉僵硬。目前的工作是检查动脉硬度和壁厚对报告的愤怒状态的反应。愤怒和动脉硬化之间的正相关关系随着年龄的变化而变化。此外，我们正在研究代谢综合征对动脉特性的影响。

The project studies the carotid artery and intracerebral blood flow velocity using doppler ultrasonography in Baltimore Longitudinal Study of Aging participants. The goal is to determine how arterial anatomic and physiologic properties are associated with cerebrovascular diseases and aging. We are currently examining the relationship between several carotid arterial measurements and alcohol usage in the BLSA. We find that mild to moderate alcohol usage is associated with greater arterial elasticity and decreased stiffness in the common carotid artery. A less impressive association was observed with arterial wall thickness and diameter. The changes were independent of blood pressure and age. The response of the artery to alcohol usage may represent one mechanism for its protective effect against cardiovascular disease. In previous work we had shown that the use of estrogen replacement in postmenopausal women was associated with lower arterial stiffness. Male sex hormones are known to decline with increasing age, and have been associated with atherosclerotic disease and with risk factors for atherosclerosis. We have examined the relationship between androgenic hormones and arterial stiffness (beta stiffness index). Both testosterone and free testosterone (assessed by the free testosterone index) were negatively correlated with age, pulse pressure and stiffness index, while SHBG was positively correlated with age and stiffness index. Multiple regression analysis revealed that T was the only hormone that predicted the arterial stiffness index after adjustment for risk parameters. T values 5 to 10 years prior to the carotid study were also a predictor of the stiffness index. A path analysis revealed that decreasing T with advancing age increased stiffness index directly and indirectly through increasing pulse pressure. DHEAS did not appear to directly contribute to arterial stiffness. Current work is examining the response of arterial stiffness and wall thickness to the state of reported anger. A positive relationship is being seen between anger and arterial stiffness that varies across age. In addition, we are examining the impact of the Metabolic Syndrome to arterial properties.