ABSTRACT
Many clinic investigations support the relation between coronary heart disease (CAD) and psychosocial factors (PFs) and how these two entities influence each other. On one hand, FPs like depression, anxiety, social isolation, stress and some types of personality, contribute significantly to the pathogenesis and expression of CAD. Pathophysiological mechanisms underly in this interrelation, can be divided between FPs conditions that contribute to a higher frequency of adverse health behaviors (eg. smoking) or directly increasing the platelets and neuroendocrine activity. In this review there is information relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. Recent data also indicate that the foregoing effects are in part a result of the endothelial dysfunction and injury induced by acute stress. The complex interactions among vascular endothelium, platelets, serotonin and blood components are one of the most exciting research areas today. The importance of maximizing the efficacy of psychological and psychopharmacology interventions is in part because of the knowledge that psychosocial stresses tend to cluster together and when this takes place, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia. Thus, to know about these mechanisms, helps to widen the view and use therapeutic strategies that go beyond symptomatic effects and commit us to an interdisciplinary work.
Subject(s)
Anxiety/epidemiology , Anxiety/therapy , Coronary Disease/epidemiology , Coronary Disease/therapy , Patient Care Team , Stress, Psychological/epidemiology , Stress, Psychological/therapy , HumansABSTRACT
Many clinic investigations support the relation between coronary heart disease (CAD) and psychosocial factors (PFs) and how these two entities influence each other. On one hand, FPs like depression, anxiety, social isolation, stress and some types of personality, contribute significantly to the pathogenesis and expression of CAD. Pathophysiological mechanisms underly in this interrelation, can be divided between FPs conditions that contribute to a higher frequency of adverse health behaviors (eg. smoking) or directly increasing the platelets and neuroendocrine activity. In this review there is information relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. Recent data also indicate that the foregoing effects are in part a result of the endothelial dysfunction and injury induced by acute stress. The complex interactions among vascular endothelium, platelets, serotonin and blood components are one of the most exciting research areas today. The importance of maximizing the efficacy of psychological and psychopharmacology interventions is in part because of the knowledge that psychosocial stresses tend to cluster together and when this takes place, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia. Thus, to know about these mechanisms, helps to widen the view and use therapeutic strategies that go beyond symptomatic effects and commit us to an interdisciplinary work.
ABSTRACT
Many clinic investigations support the relation between coronary heart disease (CAD) and psychosocial factors (PFs) and how these two entities influence each other. On one hand, FPs like depression, anxiety, social isolation, stress and some types of personality, contribute significantly to the pathogenesis and expression of CAD. Pathophysiological mechanisms underly in this interrelation, can be divided between FPs conditions that contribute to a higher frequency of adverse health behaviors (eg. smoking) or directly increasing the platelets and neuroendocrine activity. In this review there is information relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. Recent data also indicate that the foregoing effects are in part a result of the endothelial dysfunction and injury induced by acute stress. The complex interactions among vascular endothelium, platelets, serotonin and blood components are one of the most exciting research areas today. The importance of maximizing the efficacy of psychological and psychopharmacology interventions is in part because of the knowledge that psychosocial stresses tend to cluster together and when this takes place, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia. Thus, to know about these mechanisms, helps to widen the view and use therapeutic strategies that go beyond symptomatic effects and commit us to an interdisciplinary work.
