Cardiovascular and autonomic reactivity to psychological stress: Neurophysiological substrates and links to cardiovascular disease

Abstract

Psychologically stressful experiences evoke changes in cardiovascular physiology that may influence risk for cardiovascular disease (CVD). But what are the neural circuits and intermediate physiological pathways that link stressful experiences to cardiovascular changes that might in turn confer disease risk? This question is important because it has broader implications for our understanding of the neurophysiological pathways that link stressful and other psychological experiences to physical health. This review highlights selected findings from brain imaging studies of stressor-evoked cardiovascular reactivity and CVD risk. Converging evidence across these studies complements animal models and patient lesion studies to suggest that a network of cortical, limbic, and brainstem areas for central autonomic and physiological control are important for generating and regulating stressor-evoked cardiovascular reactivity via visceromotor and viscerosensory mechanisms. Emerging evidence further suggests that these brain areas may play a role in stress-related CVD risk, specifically by their involvement in mediating metabolically-dysregulated or extreme stressor-evoked cardiovascular reactions. Contextually, the research reviewed here offers an example of how brain imaging and health neuroscience methods can be integrated to address open and mechanistic questions about the neurophysiological pathways linking psychological stress and physical health.

Keywords: Cardiovascular disease; Central autonomic network; Functional connectivity; Stressor-evoked cardiovascular reactivity; Visceral prediction errors.

Figure 1

Conceptual illustration of brain-body pathways linking psychological stress to stressor-evoked cardiovascular reactions linked to cardiovascular disease risk. A network of forebrain areas appraise psychological stimuli as threats that tax or exceed coping capacities. These appraisals lead to visceromotor commands or ‘predictions’ for anticipated metabolic support for motivated behaviors. These commands are relayed via subcortical and brainstem cell groups to influence autonomic and neuroendocrine outflow to the heart and vasculature. Chronically exaggerated or metabolically disproportionate stressor-evoked cardiovascular (e.g., BP) reactions may exert shear or tensile stress on blood vessel walls over time, and they may accelerate atherosclerosis or influence risk for later cardiovascular disease endpoints. Vagal and other viscerosensory channels relay feedback signals from visceral organs and systems in the periphery, enabling the afferent representation of peripheral stressor-evoked physiological reactions by forebrain areas. Afferent feedback may influence the magnitude, duration, or general patterning of stressor-evoked reactions and may also affect appraisal-related neural activity.