hypertension; coronary heart disease; psychoneurobiological mechanisms; emotion processing; biological CHD risk factors; prospective CHD risk; acute mental stress; physiological hyperreactivity; oxytocin; imaging; essential hypertension; stress reactivity
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The present proposal aims to elucidate psychoneurobiological mechanisms in essential hypertension and CHD. It combines assessment of psychological parameters and intermediate biological risk factors for CHD, both in prospective CHD assessment as well as in cross-sectional mechanistic neuroimaging and psychopharmacological intervention studies in hypertensive subjects, in patients with overt CHD, and in normotensive healthy controls. Specific scientific aims are: (A) To investigate emotion processing in essential hypertension and coronary heart disease (CHD).(B) To determine the prospective association between psychological factors including emotion processing, intermediate biological CHD risk factors, and future CHD in patients, essential hypertensives, and healthy controls.(C) To evaluate the effect of social support and oxytocin administration on reducing physiological hyperreactivity to stress in essential hypertension.(D) To identify the neural basis of physiological hyperreactivity to stress in essential hypertension and its association with emotion processing.Coronary heart disease (CHD) is a leading cause of premature death in industrialized countries and arterial hypertension is a major risk factor for CHD. 90% of hypertensive patients are diagnosed as “essential hypertensives” as the cause for their chronically elevated arterial blood pressure is unknown. The psychoneurobiological mechanisms underlying essential hypertension, its association with increased incidence of CHD, and heightened morbidity and mortality among CHD patients are still poorly understood. Interdisciplinary research suggests a role for associations between emotion processing and future CHD risk. We previously found first evidence for poor emotion regulation in essential hypertensives compared to normotensive controls but emotion processing remains to be further elucidated, particularly in CHD. Project A is therefore intended to measure emotion processing in hypertension and CHD by assessing emotion recognition of facial affect in a representative sample size of hypertensive and normotensive individuals including women, and CHD patients. Moreover, although recent meta-analyses document associations between anger and hostility with future CHD, both in healthy controls and CHD patients, the prospective association between emotion processing and future CHD has not yet been investigated. Project B therefore aims to determine the prospective association between emotion processing and other psychosocial risk factors with future CHD in a longitudinal study over a 3-year follow-up period in a sizable number of CHD patients, essential hypertensives, and healthy controls. In addition to the psychosocial factors (i.e. vital exhaustion, depressive symptom severity, overcommitment, hostility, anger, low social support, Type D personality) and emotion processing, intermediate biological CHD risk factors (i.e. inflammation markers, lipids, coagulation), as well as continuous CHD indicators (i.e. intima media thickness, six-minute walk test) will be assessed at baseline and after 18 and 36 months. This will allow complex assessment of the individual contribution of each psychological risk factor to future CHD indicators, while studying potential underlying biological pathways. The testing of physiological reactivity to controlled challenges such mental stress, which is considered as a window into complex psychological and physiological processes involved in the development of cardiovascular disease, demonstrated prospective associations between greater physiological stress reactivity and poor cardiovascular risk status. The physiological hyperreactivity to stress in terms of sympathetic nervous system and hypothalamus-pituitary-adrenal axis activity, blood lipids, and coagulation activity that we and others observed in essential hypertension, has therefore been suggested to play a mechanistic role in the association between hypertension and heightened CHD risk. Moreover, we found lower perceived social support in hypertensives (which may suggest a potential deficit in social interaction abilities) as compared to normotensives with highest physiological stress responses in hypertensives with low perceived social support. Given that oxytocin and social support have been shown interact in reducing psychophysiological responses to stress in normotensive individuals and that oxytocin exerts positive social interaction in healthy humans, exogenous oxytocin administration may enable hypertensives to effectively take advantage of provided social support. Thereby, oxytocin may enhance the effect of social support on reducing the previously observed physiological hyperreactivity to stress in essential hypertensives. Project C therefore aims to evaluate a psychopharmacological intervention strategy intended to elucidate neuroendocrine pathways underlying the observed association between lower social support and heightened physiological stress reactivity in hypertensives: In a placebo-controlled, double-blind study design, hypertensive and normotensive men (subgroups of project B) will randomly be assigned to receive intranasal oxytocin (24 IU) or placebo 50 min before stress, and either social support from their best friend during the preparation period of the stress protocol or no social support. All participants will be exposed to a standardized social laboratory stressor (Trier Social Stress Test) and neuroendocrine reactivity will be measured repeatedly. As our recent findings suggests strong associations between social support and heightened coagulation activity in healthy subjects before and after social stress and as we found higher lipid and coagulation reactivity to social stress in hypertensives, biological risk factors for CHD will be assessed as well. Finally, whereas attempts have been done to identify neural correlates of physiological stress reactivity in healthy persons, the neural mechanisms underlying the physiological hyperreactivity to stress in hypertension have been subject to speculation but are still unknown. Project D is therefore intended to study the neural basis of physiological hyperreactivity to acute stress in hypertension. Physiological reactivity will be assessed by repeated measurement of neuroendocrine reactivity as well as of reactivity of intermediate biological risk factors for CHD to psychosocial stress during functional magnetic resonance imaging in a subsample of hypertensive and normotensive men of project B. Psychosocial stress will be induced by the Montreal Imaging Stress Task (MIST) a standardized psychosocial stress paradigm developed for functional imaging studies. The project aims to investigate potential differences between hypertensive and normotensive men in their neural reactivity to the MIST and at finding associations between neural reactivity and peripheral reactivity of neuroendocrine parameters and intermediate biological risk factors. Given the observed association between poor emotion regulation and physiological hyperreactivity in our hypertensives, a potential modulation of neurophysiological stress reactivity by emotion processing (project A) will be additionally studied.Taken together, the innovative and integrative approach of the proposal allows for a better understanding of psychoneurobiological mechanisms underlying the heightened stress reactivity and CHD risk in essential hypertension as well as the adverse disease outcomes in CHD patients. The implications of the proposed studies may provide important new information for the development of interdisciplinary intervention strategies for essential hypertension and CHD.