BIOBEHAVIORAL BASES OF CHD RISK AND MANAGEMENT

该计划项目的延续将包括一个综合的， 冠心病生物行为学基础的多学科研究 冠心病（CHD）的风险和管理。 我们的工作假设是：（1） 一个积极的反馈回路，包括增加交感神经系统 (SNS)活动，胰岛素抵抗（IR）和高胰岛素血症，增加CHD 通过促进一系列变量（向心性肥胖， 高血糖、高血压、血脂异常）称为代谢综合征; （2）情绪压力源、吸烟、不良饮食和缺乏体育锻炼 运动会影响循环，增加冠心病风险。 方案项目 （1）评估行为风险促进之间的关系 变量（社会心理压力、吸烟、不良饮食、缺乏运动）， 假定的中介变量（SNS活动和胰岛素代谢）和CHD 风险因素;（2）确定行为干预是否可以减少 SNS张力和胰岛素抵抗（IR），从而降低CHD风险。 Thr 计划项目由4个项目组成，每个项目都有核心设施支持 技术/生物医学项目（例如，生物化学测定、工程学） 统计支持。 一个项目将比较青少年与高 vs.在空腹胰岛素、口服葡萄糖方面血压（BP）正常 耐受性，肥胖，有氧健身，饮食，心脏质量，自主神经 反应性、心理社会特征和家族病史。 （一） BP状态通知，条件。 另一个项目将研究IR和 接受以下治疗的MI后患者的CHD危险因素：（1）标准 药物治疗;或（2）标准药物治疗加 行为治疗，包括压力管理、饮食监督和 自我指导的练习。 将对受试者进行评估（超声心动图， 肱动脉超声，正常血糖-高胰岛素钳夹，社会心理和 生活质量评估）治疗前和治疗后。 因为以前的 研究表明，BP对冷加压试验的反应性预示着未来 高血压 另一个项目将探讨IR与 总外周阻力（TPR）作为高反应性的基础， 确定高反应性是否与代谢综合征有关。 项目 4将为理解反应性提供神经生物学框架， 使用兔模型描绘中枢传出通路介导 心血管防御成分（心输出量）和警惕性 (TPR)反应.

This Program Project continuation will consist of an integrated, multidisciplinary inquiry into biobehavioral bases of coronary heart disease (CHD) risk and management. Our working hypotheses are that: (1) a positive feedback loop, involving increases in sympathetic nervous system (SNS) activity, insulin resistance (IR) and hyperinsulinemia, increases CHD risk by promoting a constellation of variables (central obesity, hyperglycemia, hypertension, dyslipidemia) called the metabolic syndrome; and (2) emotional stressors, smoking, poor diet and lack of physical exercise influence th loop and exacerbate CHD risk. The Program Project would; (1) assess relationships among the behavioral risk promoting variables (psychosocial stress, smoking, poor diet, physical inactivity), presumed mediating variables (SNS activity and insulin metabolism) and CHD risk factors; and (2) determine if behavioral interventions can decrease SNS tone and insulin resistance (IR), thereby reducing CHD risk. Thr Program Project consists of 4 Projects with Core facilities supporting each project with technical/biomedical (e.g., biochemical assays, engineering) and statistical support. One project will compare adolescents with high vs. normal blood pressure (BP) in terms of fasting insulin, oral glucose tolerance, adiposity, aerobic fitness, diet, cardiac mass, autonomic reactivity, psychosocial characteristics and family medical history. (1) BP status notification, conditions. Another project will examine IR and CHD risk factors in post-MI patients receiving; (1) standard pharmacological treatment; or (2) standard pharmacological treatment plus behavioral treatment including stress management, dietary supervision and self-directed exercise. Subjects will be assessed (echocardiography, brachial ultrasound, euglycemic-hyperinsulinemic clamp, psychosocial and quality of life assessment) pre- and post-treatment. Because previous studies indicate the BP reactivity to the cold pressor test predicts future hypertension. Another project will explore possible links between IR and total peripheral resistance (TPR) as the basis for hyperreactivity and determine if hyperreactivity is related to the metabolic syndrome. Project 4 will provide a neurobiological framework for understanding reactivity by using a rabbit model to delineate the central efferent pathways mediating cardiovascular components of the defense (cardiac output) and vigilance (TPR) reactions.