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Early childhood trauma alters neurological responses to mental stress in patients with coronary artery disease.

ABSTRACT: BACKGROUND:Early childhood trauma is known to independently increase adverse outcome risk in coronary artery disease (CAD) patients, although the neurological correlates are not well understood. The purpose of this study was to examine whether early childhood trauma alters neural responses to acute mental stress in CAD patients. METHODS:Participants (n?=?152) with CAD underwent brain imaging with High Resolution Positron Emission Tomography and radiolabeled water during control (verbal counting, neutral speaking) and mental stress (mental arithmetic, public speaking). Traumatic events in childhood were assessed with the Early Trauma Inventory (ETI-SR-SF) and participants were separated by presence (ETI+) or absence (ETI-) of early childhood trauma. Brain activity during mental stress was compared between ETI+ and ETI-. RESULTS:Compared to ETI-, ETI+ experienced greater (p < 0.005) activations during mental stress within the left anterior cingulate, bilateral frontal lobe and deactivations (p < 0.005) within the left insula, left parahippocampal gyrus, right dorsal anterior cingulate, bilateral cerebellum, bilateral fusiform gyrus, left inferior temporal gyrus, and right parietal lobe. Significant (p < 0.005) positive correlations between brain activation and ETI-SR-SF scores were observed within the left hippocampus, bilateral frontal lobe, left occipital cuneus, and bilateral temporal lobe. LIMITATIONS:Results in non-CAD samples may differ and ETI may be subject to recall bias. CONCLUSION:Early childhood trauma exacerbated activations in stress-responsive limbic and cognitive brain areas with direct and indirect connections to the heart, potentially contributing to adverse outcomes in CAD patients.

SUBMITTER: Wittbrodt MT

PROVIDER: S-EPMC6592739 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Early childhood trauma alters neurological responses to mental stress in patients with coronary artery disease.

Wittbrodt Matthew T MT Moazzami Kasra K Lima Bruno B BB Alam Zuhayr S ZS Corry Daniel D Hammadah Muhammad M Campanella Carolina C Ward Laura L Quyyumi Arshed A AA Shah Amit J AJ Vaccarino Viola V Nye Jonathon A JA Douglas Bremner J J

Journal of affective disorders 20190511

<h4>Background</h4>Early childhood trauma is known to independently increase adverse outcome risk in coronary artery disease (CAD) patients, although the neurological correlates are not well understood. The purpose of this study was to examine whether early childhood trauma alters neural responses to acute mental stress in CAD patients.<h4>Methods</h4>Participants (n = 152) with CAD underwent brain imaging with High Resolution Positron Emission Tomography and radiolabeled water during control (v ...[more]

PMID: 31103906

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Project description:BACKGROUND:Coronary microvascular dysfunction may contribute to myocardial ischemia during mental stress (MS). However, the role of coronary epicardial and microvascular function in regulating coronary blood flow (CBF) responses during MS remains understudied. We hypothesized that coronary vasomotion during MS is dependent on the coronary microvascular endothelial function and will be reflected in the peripheral microvascular circulation. METHODS AND RESULTS:In 38 patients aged 59±8 years undergoing coronary angiography, endothelium-dependent and endothelium-independent coronary epicardial and microvascular responses were measured using intracoronary acetylcholine and nitroprusside, respectively, and after MS induced by mental arithmetic testing. Peripheral microvascular tone during MS was measured using peripheral arterial tonometry (Itamar Inc, Caesarea, Israel) as the ratio of digital pulse wave amplitude compared to rest (peripheral arterial tonometry ratio). MS increased the rate-pressure product by 22% (±23%) and constricted epicardial coronary arteries by -5.9% (-10.5%, -2.6%) (median [interquartile range]), P=0.001, without changing CBF. Acetylcholine increased CBF by 38.5% (8.1%, 91.3%), P=0.001, without epicardial coronary diameter change (0.1% [-10.9%, 8.2%], P=not significant). The MS-induced CBF response correlated with endothelium-dependent CBF changes with acetylcholine (r=0.38, P=0.03) but not with the response to nitroprusside. The peripheral arterial tonometry ratio also correlated with the demand-adjusted change in CBF during MS (r=-0.60, P=0.004), indicating similarity between the microcirculatory responses to MS in the coronary and peripheral microcirculation. CONCLUSIONS:The coronary microvascular response to MS is determined by endothelium-dependent, but not endothelium-independent, coronary microvascular function. Moreover, the coronary microvascular responses to MS are reflected in the peripheral microvascular circulation.

Project description:ImportanceThe clinical significance of hemodynamic reactivity to mental stress in the population with coronary artery disease (CAD) is unclear.ObjectiveTo investigate the association between hemodynamic reactivity to mental stress and the risk of adverse cardiovascular events in patients with stable CAD.Design, setting, and participantsThis cohort study included individuals with stable CAD from 2 prospective studies from a university-based hospital network: the Mental Stress Ischemia Prognosis Study (MIPS) and the Myocardial Infarction and Mental Stress Study 2 (MIMS2). Participants were enrolled between June 2011 and March 2016 and followed up for a median of 6.0 (IQR, 5.6-6.0) years in MIPS and 4.6 (IQR, 3.8-5.3) years in MIMS2. Data were analyzed from December 1, 2022, to February 15, 2023.ExposuresThe rate-pressure product (RPP) was calculated as the mean systolic blood pressure times the mean heart rate at rest. Rate-pressure product reactivity was calculated as the maximum RPP during a standardized mental stress test minus the RPP at rest.Main outcomes and measuresThe primary outcome was a composite of cardiovascular death or nonfatal myocardial infarction. The secondary end point additionally included hospitalizations for heart failure.ResultsFrom the total of 938 individuals from the pooled cohort (mean [SD] age, 60.2 [10.1] years; 611 [65.1%] men), 631 participated in MIPS and 307 in MIMS2. A total of 373 individuals (39.8%) were Black, 519 (55.3%) were White, and 46 (4.9%) were of unknown race or ethnicity. The RPP increased by a mean (SD) of 77.1% (23.1%) during mental stress (mean [SD] absolute change, 5651 [2878]). For every SD decrease in RPP reactivity with mental stress, the adjusted hazard ratios for the primary and secondary end points were 1.30 (95% CI, 1.04-1.72) and 1.30 (95% CI, 1.06-1.56), respectively, in MIPS and 1.41 (95% CI, 1.06-1.97) and 1.21 (95% CI, 1.02-1.60), respectively, in MIMS2. In the pooled sample, when RPP reactivity to mental stress was added to a model including traditional clinical risk characteristics, model discrimination for adverse events improved (increase in C statistic of 5% for the primary end point; P = .009).Conclusions and relevanceIn this cohort study of individuals with stable CAD, a blunted cardiovascular reactivity to mental stress was associated with adverse outcomes. Future studies are needed to assess the clinical utility of mental stress reactivity testing in this population.

Project description:A greater understanding of why some people are more at risk of developing PTSD is required. We examine the relationship between temperament traits in early childhood and subsequent trauma exposure and risk of PTSD. We used data on 2017 participants from the Avon Longitudinal Study of Parents and Children (ALSPAC). Temperament was measured using the Carey Infant Temperament Scale (average score from ages 6 and 24 months). This provided data on 9 individuals traits, and Easy, Medium, and Difficult temperament clusters. Trauma exposure was measured from 0 to 17 years, and PTSD at age 23 years using the PTSD Checklist for DSM-V (PCL-5). Regression models were used to estimate associations between temperament and both trauma and PTSD, and to examine mediation (of temperament to PTSD pathway) and interaction (temperament X trauma on PTSD) effects. 1178 (58.4%) individuals were exposed to a trauma in childhood and 112 (5.5%) had PTSD. Higher levels of Intensity were associated with a small increase in trauma exposure (ORadjusted 1.23, 95% CI 1.12, 1.34; p < 0.001) and PTSD (ORadjusted 1.27, 95% CI 1.05, 1.54; p = 0.012). Higher levels of Activity, Adaptability, Mood and Threshold temperament traits were also associated with trauma exposure. Medium (ORadjusted 1.49, 95% CI 1.21, 1.84; p < 0.001) and Difficult (ORadjusted 1.47, 95% CI 1.18, 1.84; p = 0.001) temperament clusters were associated with increased trauma exposure compared to an Easy cluster, but were not associated with PTSD. The relationship between trait Intensity and adult PTSD was partially mediated by childhood/adolescent trauma (Indirect ORadjusted 1.08, 95% CI 1.01, 1.16, p = 0.024, proportion mediated 26.2%). There was some evidence that trait Intensity modified the relationship between trauma and PTSD (ORadjusted 1.66, 95% CI 1.07, 2.55, p = 0.023). PTSD in early adulthood is more common in those with intense stimuli responsiveness in childhood. Temperament traits might be useful predictors of trauma exposure and mental health outcomes and offer potential targets for supportive interventions.

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Early childhood trauma alters neurological responses to mental stress in patients with coronary artery disease.

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Early childhood trauma alters neurological responses to mental stress in patients with coronary artery disease.

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