BIOBEHAVIORAL BASES OF CHD RISK AND MANAGEMENT

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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.