Underlying inflammation has no impact on the oxidative stress response to acute mental stress

Introduction: Mental stress is considered to be a trigger for acute myocardial infarction (MI), with inflammation thought to provide a mechanism. Inflammation is reciprocally linked to oxidative stress, which h as also been implicated in MI. The purpose of this study was to assess the effects of experimentally-induced inflammation on the oxidative stress response to mental stress in healthy participants. Methods: Healthy males undertook one of two inflammatory stimuli: typhoid vaccination (Vaccination paradigm, N= 17) or eccentric exercise (Eccentric exercise paradigm, N= 17). All participants completed a mental arithmetic stress task twice (within-subject design): 6. h after the inflammatory stimulus, and during a control non-inflammation condition. Blood samples were taken before, immediately and 30. min after the stress task. Plasma was assessed for interleukin-6 (IL-6), protein carbonyls (PC), lipid hydroperoxides (LOOH), total antioxidant capacity (TAC) and nitric oxide metabolites (NOx). Results: Vaccination paradigm: IL-6, PC and NOx were significantly higher in the vaccination condition, relative to the control condition (p < .05). PC, TAC, LOOH and NOx were unchanged in response to mental stress in both the vaccination and control conditions. Eccentric Exercise paradigm: IL-6 and TAC were significantly higher in the eccentric exercise condition (p < .05), relative to the control condition. PC, TAC and NOx were unchanged in response to mental stress in both the eccentric exercise and control conditions. Conclusions: Two different inflammatory paradigms were successful in increasing selective plasma markers of inflammation and oxidative stress prior to a mental stress task. However, experimentally induced transient inflammation had no impact on mental stress-induced changes in plasma LOOH, PC, TAC or NOx in young healthy participants

Impact of panic attacks on bronchoconstriction and subjective distress in asthma patients with and without panic disorder

© 2017 by the American Psychosomatic Society. Objective: Panic disorder (PD) is common among asthma patients and is associated with worse asthma outcomes. This may occur because of psychophysiological factors or cognitive/affective factors. This study evaluated the impact of panic attacks (PAs) on bronchoconstriction and subjective distress in people who have asthma with and without PD. Methods: A total of 25 asthma patients (15 with PD who had a PA [PD/PA], 10 without PD who did not have a PA [no PD/no PA] ) were recruited from an outpatient clinic. They underwent a panic challenge (one vital capacity inhalation of 35% carbon dioxide [CO 2 ]) and completed the Panic Symptom Scale, the Subjective Distress Visual Analogue Scale, and the Borg Scale before and after CO 2 . Forced expiratory volume in 1 second was assessed pre-and post-CO 2 ; respiratory (i.e., CO 2 production, minute ventilation, tidal volume) was continuously recorded, and physiological measures (i.e., systolic and diastolic blood pressure [SBP/DBP]) were recorded every 2 minutes. Results: Analyses adjusting for age, sex, and provocative concentration of methacholine revealed no significant differences between groups in forced expiratory volume in 1 second change after CO 2 inhalation (F(1, 23) < 0.01, p =.961). However, patients with PD/PA reported more panic (F(1, 22) = 18.10, p < .001), anxiety (F(1, 22) = 21.93, p < .001), worry (F(1, 22) = 26.31, p < .001), and dyspnea (F(1,22) = 4.68, p =.042) and exhibited higher levels of CO 2 production (F(1, 2843) = 5.89, p =.015), minute ventilation (F(1, 2844) = 4.48, p =.034), and tidal volume (F(1, 2844) = 4.62, p =.032) after the CO 2 challenge, compared with patients with no PD/no PA. Conclusions: Results, presented as hypothesis generating, suggest that asthma patients with PD/PA exhibit increased panic-like anxiety, breathlessness, and a respiratory pattern consistent with hyperventilation that was not linked to statistically significant drops in bronchoconstriction

Relationship between antidepressant therapy and risk for cardiovascular events in patients with and without cardiovascular disease

Objective: The American Heart Association has endorsed depression as a cardiac risk factor and recommends screening as part of routine practice. This has been met with controversy due to inconsistencies in the data linking depression treatment to better cardiovascular outcomes. Our objective was to prospectively assess the association between depression treatment (defined as being prescribed antidepressant medication) and major adverse cardiovascular events (MACE) in patients referred for exercise stress tests. Methods: 2385 consecutive patients presenting for myocardial perfusion exercise stress tests underwent a sociodemographic, medical, and psychiatric interview (PRIME-MD) and completed the Beck Depression Inventory (BDI). History of CVD and antidepressant use was self-reported and verified via chart review. Participants followed over an 8.8 year follow-up, and information regarding MACE incidence (including cardiac mortality, non-fatal myocardial infarction, revascularization procedures, cerebrovascular events) was obtained from provincial administrative databases. Results: 8% (n=190) of the sample were taking antidepressants at baseline, 41% (n=916) had a history of CVD, and 38.7% (n=921) had depression according to the PRIME-MD or BDI. Antidepressant treatment was associated with a 30% reduced risk of MACE (HR=0.697; 95%CI=0.504-0.964; p=.029). A 46% reduction in risk was associated with antidepressant treatment among those without CVD (HR=0.542; 95%CI=0.299-0.981; p=.043). In depressed patients, a 33% reduction in risk of MACE associated with antidepressant use was seen (adjusted HR=0.674; 95%CI=0.440-1.033; p=.07). Conclusions: Antidepressants may be cardio-protective among patients presenting for stress testing independent of risk factors including CVD and depression. Results support treating depression with antidepressants in this population to reduce risk of MACE

Reactive hyperemia is associated with adverse clinical outcomes in heart failure

© 2016 Elsevier Inc. All rights reserved. Introduction Impaired endothelial function, as assessed by brachial artery flow-mediated dilation (FMD), is an established risk factor for cardiovascular events. FMD is impaired in heart failure (HF) patients, but less is known about hyperemic brachial artery flow. We investigated the relationship between FMD and hyperemic flow with adverse clinical outcomes in HF patients. Methods Brachial artery FMD and hyperemic flow were assessed in 156 patients (70.5 % Male; 45.5% Caucasian; mean age (± SD) = 56.2 (±12.4) years) with HF and reduced left ventricular ejection fraction (LVEF). Cox proportional hazard models were used to assess the potential explanatory association of FMD and hyperemic flow with the composite outcome of death or cardiovascular hospitalization over a median 5-year follow-up period. Results Both FMD and hyperemic flow were negatively correlated with age, but unrelated to sex, race, body mass index, LVEF or N-terminal pro-B-Type natriuretic peptide (NT-ProBNP). Reduced hyperemic flow, but not FMD, was associated with an increased risk of death or cardiac hospitalization after controlling for traditional risk factors. Conclusion The association of reduced hyperemic flow with increased risk of adverse clinical outcomes suggests that micro-vascular function may be an important prognostic marker in patients with HF

Positive and negative affect is related to experiencing chest pain during exercise-induced myocardial ischemia

© 2017 by the American Psychosomatic Society. Objective: Silent myocardial ischemia is thought to be associated with worse cardiovascular outcomes due to a lack of perception of pain cues that initiate treatment seeking. Negative affect (NA) has been associated with increased pain reporting and positive affect (PA) with decreased pain reporting, but these psychological factors have not been examined within the context of myocardial ischemia. This study evaluated the associations between PA, NA, and chest pain reporting in patients with and without ischemia during exercise testing. Methods: A total of 246 patients referred for myocardial perfusion single-photon emission computed tomography exercise stress testing completed the positive and negative affect schedule-expanded version, a measure of PA and NA. Presence of chest pain and myocardial ischemia were evaluated using standardized protocols. Results: Logistic regression analyses revealed that for every 1-point increase in NA, there was a 13% higher chance for ischemic patients (odds ratio [OR] = 1.13; 95 % confidence interval [CI] = 1.02 to 1.26) and an 11% higher chance in nonischemic patients (OR = 1.11; 95% CI = 1.03 to 1.19) to report chest pain. A significant interaction of PA and NA on chest pain reporting (ß = 0.02; 95% CI = 0.002 to 0.031) was also observed; nonischemic patients with high NA and PA reported more chest pain (57%) versus patients with low NA and low PA (13%), with high NA and low PA (17%), and with high PA and low NA (7%). Conclusions: Patients who experience higher NA are more likely to report experiencing chest pain. In patients without ischemia, high NA and PA was also associated with a higher likelihood of reporting chest pain. Results suggest that high levels of PA as well as NA may increase the experience and/or reporting of chest pain

Blood pressure reactivity to psychological stress is associated with clinical outcomes in patients with heart failure

© 2017 Elsevier Inc. Introduction: Cardiovascular (CV) reactivity to psychological stress has been implicated in the development and exacerbation of cardiovascular disease (CVD). Although high CV reactivity traditionally is thought to convey greater risk of CVD, the relationship between reactivity and clinical outcomes is inconsistent and may depend on the patient population under investigation. The present study examined CV reactivity in patients with heart failure (HF) and its potential association with long-term clinical outcomes. Methods: One hundred ninety-nine outpatients diagnosed with HF, with ejection fraction ≤40%, underwent an evaluation of blood pressure (BP) and heart rate reactivity to a laboratory-based simulated public-speaking stressor. Cox proportional hazards regression models were used to examine the prospective association between BP and heart rate reactivity on a combined end point of death or CV hospitalization over a 5-year median follow-up period. Results: Both systolic blood pressure (SBP) and diastolic blood pressure (DBP) reactivity, quantified as continuous variables, were inversely related to risk of death or CV hospitalization (Ps < .01) after controlling for established risk factors, including HF disease severity and etiology. In similar models, heart rate reactivity was unrelated to outcome (P = .12). In models with tertiles of reactivity, high SBP reactivity, compared with intermediate SBP reactivity, was associated with lower risk (hazard ratio [HR] = .498, 95% CI .335-.742, P =.001), whereas low SBP reactivity did not differ from intermediate reactivity. For DBP, high reactivity was marginally associated with lower risk compared with intermediate DBP reactivity (HR = .767, 95% CI .515-1.14, P =.193), whereas low DBP reactivity was associated with greater risk (HR = 1.49, 95% CI 1.027-2.155, P =.0359). No relationship of heart rate reactivity to outcome was identified. Conclusions: For HF patients with reduced ejection fraction, a robust increase in BP evoked by a laboratory-based psychological challenge was associated with lower risk for adverse CVD events and may be a novel and unique marker of left ventricular systolic reserve that is accompanied by a more favorable long-term prognosis

Supplementary information files for Sedentary behaviour, physical activity and psychobiological stress reactivity: a systematic review

Supplementary files for article Sedentary behaviour, physical activity and psychobiological stress reactivity: a systematic review. Background Sedentary behaviour, physical activity, and psychobiological reactivity to acute psychological stress are independent risk factors for cardiovascular disease. Sedentary behaviour and physical activity influence autonomic, haemodynamic, and inflammatory pathways under resting conditions, and these pathways become activated under acute psychological stress. However, it is unclear whether sedentary behaviour and physical activity relate to psychobiological responses to stress. Thus, the aim of this study is to systematically review sedentary behaviour and physical activity in the context of psychobiological reactivity to acute psychological stress. Methods Sedentary behaviour, physical activity and psychobiological stress reactivity search terms were combined, and several databases were searched in duplicate. Eligibility criteria included: (1) a validated measure of sedentary behaviour/physical activity; (2) cardiovascular, inflammatory, neuroendocrine, or respiratory markers measured at rest and in response to laboratory-induced acute psychological stress. Results 6084 articles were screened, with 11 included in a narrative synthesis. No studies measured postural components of sedentary behaviour, but 2/4 studies found that markers of sedentary behaviour (e.g., physical inactivity) were associated with elevated heart rate, dysregulated heart rate variability, or lowered cortisol responses to stress. Higher volumes of physical activity were linked to lower HR, cortisol, or immune responses to stress in 4/7 studies. Conclusions Extensive methodological variability precludes conclusions from being drawn. This review should be used to guide a more homogeneous and gold-standard literature, which accounts for postural components of sedentary behaviour using inclinometery, and the whole physical activity intensity spectrum using universal and reproducible approaches.</p

Supplementary information files for Sedentary behaviour, but not moderate-to-vigorous physical activity, is associated with respiratory responses to acute psychological stress

Supplementary files for article Sedentary behaviour, but not moderate-to-vigorous physical activity, is associated with respiratory responses to acute psychological stress Background Acute psychological stress induces respiratory responses, and stress-induced respiratory changes can be used to non-invasively reflect metabolic regulation. Respiratory and cardiovascular responses to stress are both driven by sympathetic mechanisms. Higher volumes of sedentary behaviour and lower volumes of physical activity are associated with elevated sympathetic tone and larger cardiovascular responses to stress. The aim of this study was to test whether these associations translate to measures of respiratory stress reactivity. Methods Daily hours of sedentary behaviour (thigh-mounted activPAL) and moderate-to-vigorous physical activity (MVPA; wrist-mounted ActiGraph) were assessed across seven days. Breath-by-breath respiratory (e.g., breathing frequency [BF], end-tidal carbon dioxide partial pressure [PetCO2], carbon dioxide output [V̇CO2] and respiratory exchange ratio [RER]) responses to an 8-min Paced Auditory Serial Addition Test were then measured using a Cortex MetaLyzer3B. Results Healthy participants (N = 61, mean age ± SD = 25.7 ± 8.9 years) recorded high volumes of sedentary behaviour (9.96 ± 1.48 hours/day) and MVPA (1.70 ± 0.71 hours/day). In adjusted models (with the inclusion of sedentary behaviour, MVPA, and other a priori selected covariates) hours of daily sedentary behaviour were associated with baseline to stress changes in BF (Β = 0.695, 95% CI = 0.281 — 1.109, p =.014), VT (Β = -0.042, 95% CI = -0.058 — -0.026, p =.014), PetCO2 (Β = -0.537, 95% CI = -0.829 — -0.245, p =.014), V̇CO2 (Β = -0.008, 95% CI = -0.014 — -0.003, p =.030), and RER (Β = -0.013, 95% CI = -0.021 — -0.005, p =.022). Daily hours of MVPA were not linked with respiratory responses to stress. Discussion Sedentary behaviour, but not MVPA, is associated with respiratory stress reactivity. Future work should untangle the underlying mechanisms of these findings and explore the consequences for cardiometabolic disease.</p

Frequently interrupting prolonged sitting with light body-weighted resistance activity alters psychobiological responses to acute psychological stress: A randomized crossover trial

Background: Uninterrupted prolonged sitting and exaggerated psychobiological reactivity to acute psychological stress are associated with increased risk of cardiovascular disease (CVD). Breaking up prolonged sitting with frequent, short bouts of light intensity physical activity acutely lowers CVD risk markers under resting conditions. Purpose: To examine whether frequent interruptions to prolonged sitting with body-weighted resistance activity can acutely lower SBP (primary outcome) and other cardiovascular, inflammatory and cortisol (secondary outcomes) responses to acute psychological stress. Methods: This randomised crossover trial included 17 sedentary participants (9 men; mean ± SD age; 24.0 ± 0.5 years) who completed two conditions: (1) interrupting 4h of sitting with 4-min of light body-weighted resistance activity every 30-min (BREAK), and (2) 4h of uninterrupted sitting (SIT). Following the BREAK and SIT intervention windows, cardiovascular, inflammatory and cortisol markers were measured at rest, during stress tasks (8-min Paced Auditory Serial Addition Test [PASAT] and 3-min Cold Pressor [CP]) and during 45-min recovery periods. Results: There were main effects of time for cardiovascular parameters (SBP, DBP, HR, cardiac output, and total peripheral resistance [all p Conclusions: Interrupting prolonged sitting with frequent bouts of light intensity bodyweighted resistance activity alters psychobiological responses to acute psychological stress. Further research should explore the longer-term implications for CVD risk. </p

Cardiovascular reactivity to acute psychological stress is associated with generalised self-efficacy and self-efficacy outcomes during adventure challenges

Outdoor adventure challenges are commonly used to enhance self-efficacy, but the physiological mechanisms involved remain unexplored. Additionally, while studies have documented the influence of self-efficacy on stress management, general self-efficacy has yet to be fully understood in the context of cardiovascular stress reactivity (CVR). This study investigated the influence of self-efficacy beliefs on CVR during acute psychological stress tasks. Additionally, it explored whether CVR serves as a novel mechanism underlying the outcomes of outdoor adventure challenges. As part of a wider randomised controlled trial, participants (n = 55) were invited to complete a laboratory session to assess CVR to an active (Paced Auditory Serial Addition Test (PASAT)) and a passive (cold pressor test (CPT)) stress task. Randomised participants (n = 33) to the experimental condition also engaged in a high ropes challenge course after the laboratory session. It was found that greater baseline self-efficacy was associated with larger CVR during the CPT and positively associated with perceived engagement and performance during the PASAT. Secondly, participants reporting positive change in self-efficacy post-intervention were associated with greater CVR and greater CVR was associated with higher ratings of intervention engagement and perceived challenge. This study provides preliminary evidence suggesting that self-efficacy may heighten CVR to passive acute psychological stressors. Habitual stress reactivity may represent a novel mechanism involved in outdoor and adventure-based interventions. Future research should continue to explore the impact of psychological variables on stress physiology and examine CVR as a potential mechanism in adventure experiences.</p