A review of neuroimaging studies of stressor-evoked blood pressure reactivity: Emerging evidence for a brain-body pathway to coronary heart disease risk

Gianaros, Peter J.; Sheu, Lei K.

doi:10.1016/j.neuroimage.2009.04.073

Cited by 155 publications

(143 citation statements)

References 228 publications

(340 reference statements)

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“…The findings of the present systematic review and other studies on HRV and functional brain imaging are consistent with research on the brain areas implicated in stressorevoked blood pressure reactivity [25]. Those studies indicated that the insula, cingulate cortex, and amygdala are the core components implicated in the blood pressure responses to stress.…”

Section: Systematic Reviewsupporting

confidence: 89%

“…Those studies indicated that the insula, cingulate cortex, and amygdala are the core components implicated in the blood pressure responses to stress. Blood pressure responses were also related to altered rCBF or BOLD signal changes in the medial, lateral, and dorsal prefrontal cortices, the parietal cortex, occipital cortex, somatosensory cortex, cuneus, lentiform area, caudate, thalamus, and cerebellum [25]. Interpretation and generalisation of the results of the present systematic review and other summary articles in this area are complicated by methodological differences, the potential of statistical type I error related to the analysis of multiple brain structures, and the relatively small number of studies that simultaneously assessed cardiovascular measures and brain responses to psychological distress.…”

Section: Systematic Reviewmentioning

confidence: 99%

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Central nervous system involvement in the autonomic responses to psychological distress

et al. 2012

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Psychological distress can trigger acute coronary syndromes and sudden cardiac death in vulnerable patients. The primary pathophysiological mechanism that plays a role in stress-induced cardiac events involves the autonomic nervous system, particularly disproportional sympathetic activation and parasympathetic withdrawal. This article describes the relation between psychological distress and autonomic nervous system function, with a focus on subsequent adverse cardiovascular outcomes. The role of the central nervous system in these associations is addressed, and a systematic review is presented of studies examining the association between stress-induced central nervous system responses measured by neuroimaging techniques and autonomic nervous system activation. Results of the systematic review indicate that the primary brain areas involved in the autonomic component of the brain-heart association are the insula, medial prefrontal cortex, and cerebellum (based on 121 participants across three studies that fitted the inclusion criteria). Other areas involved in stress-induced autonomic modulation are the (anterior) cingulate cortex, parietal cortex, somatomotor cortex/precentral gyrus, and temporal cortex. The interaction between central and autonomic nervous system responses may have implications for further investigations of the brain-heart associations and mechanisms by which acute and chronic psychological distress increase the risk of myocardial infarction, cardiac arrhythmias, and sudden cardiac death.

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Section: Systematic Reviewsupporting

confidence: 89%

Section: Systematic Reviewmentioning

confidence: 99%

Central nervous system involvement in the autonomic responses to psychological distress

et al. 2012

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“…Among the brain areas most consistently related in previous work to stressor‐evoked cardiovascular reactivity—as well as some markers of autonomic cardiovascular control, inflammation, and arterial markers of preclinical vascular disease—are areas within the medial prefrontal cortex, anterior cingulate cortex, insula, extended amygdala, hippocampus, and hindbrain and brainstem cell groups 1, 13, 16. It has been proposed that signaling patterns between these areas may serve to calibrate the magnitude of physiological (eg, cardiovascular) reactions to anticipated self‐relevant demands (eg, stressors) to support contextually adaptive behavioral coping processes 13, 46, 47. Moreover, an individual's propensity to exhibit “ mis ‐calibrations” between brain and physiological activity may reflect a dimension of individual difference that underlies the expression of “exaggerated” (metabolically excessive or pathophysiological) autonomic, inflammatory, and cardiovascular reactions, including stressor‐evoked BP reactions that have been linked to preclinical CVD 46, 47, 48.…”

Section: Discussionmentioning

confidence: 99%

A Brain Phenotype for Stressor‐Evoked Blood Pressure Reactivity

Gianaros

Sheu

Uyar

et al. 2017

JAHA

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BackgroundIndividuals who exhibit large‐magnitude blood pressure (BP) reactions to acute psychological stressors are at risk for hypertension and premature death by cardiovascular disease. This study tested whether a multivariate pattern of stressor‐evoked brain activity could reliably predict individual differences in BP reactivity, providing novel evidence for a candidate neurophysiological source of stress‐related cardiovascular risk.Methods and ResultsCommunity‐dwelling adults (N=310; 30–51 years; 153 women) underwent functional magnetic resonance imaging with concurrent BP monitoring while completing a standardized battery of stressor tasks. Across individuals, the battery evoked an increase systolic and diastolic BP relative to a nonstressor baseline period (M ∆systolic BP/∆diastolic BP=4.3/1.9 mm Hg [95% confidence interval=3.7–5.0/1.4–2.3 mm Hg]). Using cross‐validation and machine learning approaches, including dimensionality reduction and linear shrinkage models, a multivariate pattern of stressor‐evoked functional magnetic resonance imaging activity was identified in a training subsample (N=206). This multivariate pattern reliably predicted both systolic BP (r=0.32; P<0.005) and diastolic BP (r=0.25; P<0.01) reactivity in an independent subsample used for testing and replication (N=104). Brain areas encompassed by the pattern that were strongly predictive included those implicated in psychological stressor processing and cardiovascular responding through autonomic pathways, including the medial prefrontal cortex, anterior cingulate cortex, and insula.ConclusionsA novel multivariate pattern of stressor‐evoked brain activity may comprise a phenotype that partly accounts for individual differences in BP reactivity, a stress‐related cardiovascular risk factor.

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“…Combined with behavioral research showing that lower-status individuals tend to be more engaged during social interactions (Kraus and Keltner, 2009) and are better at reading the emotions of others (Kraus et al, 2010), these patterns suggest that DMPFCrelated attention to others' thoughts and feelings may also track with lower perceived social status. The DMPFC has strong connections with the amygdala and other brainstem regions whose activity can drive stress-related changes in the cardiovascular system and the hypothalamic-pituitary-adrenal axis (Gianaros and Sheu, 2009;Eisenberger and Cole, 2012;Muscatell and Eisenberger, 2012), and as such, it is possible that the DMPFC may also play a key role in linking social status and inflammation. To date, however, no known research has tested this possibility.…”

Section: Introductionmentioning

confidence: 99%

Neural mechanisms linking social status and inflammatory responses to social stress

Muscatell

Dedovic

Slavich

et al. 2016

Social Cognitive and Affective Neuroscience

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Social stratification has important implications for health and well-being, with individuals lower in standing in a hierarchy experiencing worse outcomes than those higher up the social ladder. Separate lines of past research suggest that alterations in inflammatory processes and neural responses to threat may link lower social status with poorer outcomes. This study was designed to bridge these literatures to investigate the neurocognitive mechanisms linking subjective social status and inflammation. Thirty-one participants reported their subjective social status, and underwent a functional magnetic resonance imaging scan while they were socially evaluated. Participants also provided blood samples before and after the stressor, which were analysed for changes in inflammation. Results showed that lower subjective social status was associated with greater increases in inflammation. Neuroimaging data revealed lower subjective social status was associated with greater neural activity in the dorsomedial prefrontal cortex (DMPFC) in response to negative feedback. Finally, results indicated that activation in the DMPFC in response to negative feedback mediated the relation between social status and increases in inflammatory activity. This study provides the first evidence of a neurocognitive pathway linking subjective social status and inflammation, thus furthering our understanding of how social hierarchies shape neural and physiological responses to social interactions.

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A review of neuroimaging studies of stressor-evoked blood pressure reactivity: Emerging evidence for a brain-body pathway to coronary heart disease risk

Cited by 155 publications

References 228 publications

Central nervous system involvement in the autonomic responses to psychological distress

Central nervous system involvement in the autonomic responses to psychological distress

A Brain Phenotype for Stressor‐Evoked Blood Pressure Reactivity

Neural mechanisms linking social status and inflammatory responses to social stress

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