Publications by authors named "Laura S Redwine"

24 Publications

  • Page 1 of 1

Systemic Inflammation and Cognitive Decrements in Patients with Stage B Heart Failure.

Psychosom Med 2021 Oct 12. Epub 2021 Oct 12.

College of Behavioral and Community Sciences, University of South Florida, Tampa, FL, USA Department of Psychiatry, University of California School of Medicine, San Diego, CA, USA Department of Family Medicine and Public Health, University of California School of Medicine, San Diego, CA, USA Division of Cardiology, University of Miami Miller School of Medicine, Miami, FL, USA Behavioral Medicine Research Center, University of Miami, Miami, Florida, USA; Department of Psychology, University of Miami, Coral Gables, Florida, USA; Division of Endocrinology, Diabetes and Metabolism, Miller School of Medicine, University of Miami, Miami, Florida, USA Department of Medicine, University of California School of Medicine, San Diego, CA, USA Department of Public Health Sciences, University of Miami Miller School of Medicine, Miami, FL, USA.

Objective: To investigate the role of systemic inflammation in reduced cognitive functioning in patients with early-stage heart failure (HF), while taking associations with other cardiovascular risk factors into account.

Methods: Patients with stage B HF (n = 270; mean age 66.1 ± 10.1) were examined cross-sectionally for relationships among cardiovascular disease (CVD) and psychological risk factors, c-reactive protein (CRP) and Montreal Cognitive Assessment (MoCA) scores. A subsample (n = 83), at high-risk for stage C HF (B-type natriuretic peptide (BNP) levels >65 pg/mL) were followed for 12-months for relationships between CRP levels and cognitive function.

Results: Baseline smoking (c2 = 6.33), unmarried (c2 = 12.0), hypertension (c2 = 5.72), greater body mass index (d = .45), and physical fatigue (d = .25) were related to higher CRP levels (p's < .05). Cross-sectionally, CRP levels were negatively related to MoCA scores, beyond CVD (DR2 = .022, b = -.170, p < .010) and psychological risk factors (DR2 = .016, b = .145, p < .027) and related to MCI criteria (odds ratio = 1.35, 95% CI 1.00 - 1.81, p = .046). Across 12-months, BNP high-risk patients with CRP levels ≥3 mg/L had lower MoCA scores (23.6; 95% CI 22.4 - 24.8) than patients with CRP levels <3 mg/L (25.4; 95% CI 24.4 - 26.5) (p = .024).

Conclusion: Patients with stage B HF and heightened CRP levels had greater cognitive impairment at baseline and follow-up, independent of CVD and potentially psychological risk factors. Low-grade systemic inflammation may be one mechanism involved in cognitive dysfunction at early stages of HF.
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http://dx.doi.org/10.1097/PSY.0000000000001033DOI Listing
October 2021

Effects of Caloric Intake and Aerobic Activity in Individuals with Prehypertension and Hypertension on Levels of Inflammatory, Adhesion and Prothrombotic Biomarkers-Secondary Analysis of a Randomized Controlled Trial.

J Clin Med 2020 Feb 28;9(3). Epub 2020 Feb 28.

Department of Psychiatry, University of California, San Diego, CA 92093, USA.

Background: Cardiopulmonary fitness and low calorie diets have been shown to reduce inflammation but few studies have been conducted in individuals with elevated blood pressure (BP) in a randomized intervention setting. Thereby, adhesion biomarkers, e.g., soluble intercellular adhesion molecule (sICAM)-3, have not been examined so far.

Methods: Sixty-eight sedentary prehypertensive and mildly hypertensive individuals (mean age ± SEM: 45 ± 1 years; mean BP: 141/84 ± 1/1 mmHg) were randomized to one of three 12-week intervention groups: cardio training and caloric reduction, cardio training alone, or wait-list control group. Plasma levels of inflammatory, adhesion and prothrombotic biomarkers were assessed. In a second step, intervention groups were combined to one sample and multivariate regression analyses were applied in order to account for exercise and diet behavior changes.

Results: There were no significant differences among the intervention groups. In the combined sample, greater caloric reduction was associated with a larger increase of sICAM-3 ( = 0.026) and decrease of C-reactive protein ( = 0.018) as a result of the interventions. More cardio training was associated with increases of sICAM-3 ( = 0.046) as well as interleukin-6 ( = 0.004) and a decrease of tumor necrosis factor- ( = 0.017) levels. Higher BP predicted higher plasminogen activator inhibitor (PAI)-1 ( = 0.001), and greater fitness predicted lower PAI-1 levels ( = 0.006) after the intervention.

Conclusions: In prehypertensive and hypertensive patients, plasma levels of the adhesion molecule sICAM-3 and inflammatory biomarkers have different response patterns to cardio training with and without caloric reduction. Such anti-inflammatory and anti-thrombotic effects may have implications for the prevention of atherothrombotic cardiovascular disease among individuals at increased risk.
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http://dx.doi.org/10.3390/jcm9030655DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7141349PMC
February 2020

An exploratory randomized sub-study of light-to-moderate intensity exercise on cognitive function, depression symptoms and inflammation in older adults with heart failure.

J Psychosom Res 2020 01 26;128:109883. Epub 2019 Nov 26.

Psychology Department, University of Miami, USA.

Objective: Almost half of patients with heart failure (HF) have cognitive impairment. While exercise relates to better cognitive health, a hallmark of HF is exercise intolerance. The study objective was to explore whether light-to-moderate exercise improves cognitive function in patients with HF.

Methods: This was an exploratory parallel design study of 69 patients with symptomatic HF (mean age = 65, SD = 10), recruited from VA and University of California, San Diego Healthcare Systems. Participants were randomized to Tai Chi (TC) (n = 24), resistance band (RB) exercise (n = 22) or treatment as usual (TAU) (n = 23). The primary outcome was change in Montreal Cognitive Assessment (MoCA) scores. We further explored if changes in Beck Depression Inventory - IA (BDI-IA) scores or inflammation biomarkers, CRP, TNFα and IL-6 related to altered cognitive function.

Results: There was a fixed effect of group for MoCA scores changes (F = 8.07, p = .001). TC and RB groups had greater MoCA score increases versus TAU, but no differences were found between TC and RB. Depression symptom changes predicted altered MoCA scores (ΔR = 0.15, Β = -0.413, p = .001). However, group did not interact with depression symptom levels for MoCA alterations (p = .392). Changes in CRP levels predicted MoCA scores (ΔR = 0.078, Β = -0.283, p = .01), but group did not interact with CRP levels for MoCA alterations (p = .689).

Conclusions: Light-to-moderate exercises, TC and RB may improve cognitive function. However, the mechanisms remain unclear. ClinicalTrials.gov: NCT01625819.
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http://dx.doi.org/10.1016/j.jpsychores.2019.109883DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7571258PMC
January 2020

Self-reported sleep disturbances are associated with poorer cognitive performance in older adults with hypertension: a multi-parameter risk factor investigation.

Int Psychogeriatr 2020 07;32(7):815-825

Department of Psychiatry, University of California, San Diego, USA.

Objectives: Given the evidence of multi-parameter risk factors in shaping cognitive outcomes in aging, including sleep, inflammation, cardiometabolism, and mood disorders, multidimensional investigations of their impact on cognition are warranted. We sought to determine the extent to which self-reported sleep disturbances, metabolic syndrome (MetS) factors, cellular inflammation, depressive symptomatology, and diminished physical mobility were associated with cognitive impairment and poorer cognitive performance.

Design: This is a cross-sectional study.

Setting: Participants with elevated, well-controlled blood pressure were recruited from the local community for a Tai Chi and healthy-aging intervention study.

Participants: One hundred forty-five older adults (72.7 ± 7.9 years old; 66% female), 54 (37%) with evidence of cognitive impairment (CI) based on Montreal Cognitive Assessment (MoCA) score ≤24, underwent medical, psychological, and mood assessments.

Measurements: CI and cognitive domain performance were assessed using the MoCA. Univariate correlations were computed to determine relationships between risk factors and cognitive outcomes. Bootstrapped logistic regression was used to determine significant predictors of CI risk and linear regression to explore cognitive domains affected by risk factors.

Results: The CI group were slower on the mobility task, satisfied more MetS criteria, and reported poorer sleep than normocognitive individuals (all p < 0.05). Multivariate logistic regression indicated that sleep disturbances, but no other risk factors, predicted increased risk of evidence of CI (OR = 2.00, 95% CI: 1.26-4.87, 99% CI: 1.08-7.48). Further examination of MoCA cognitive subdomains revealed that sleep disturbances predicted poorer executive function (β = -0.26, 95% CI: -0.51 to -0.06, 99% CI: -0.61 to -0.02), with lesser effects on visuospatial performance (β = -0.20, 95% CI: -0.35 to -0.02, 99% CI: -0.39 to 0.03), and memory (β = -0.29, 95% CI: -0.66 to -0.01, 99% CI: -0.76 to 0.08).

Conclusions: Our results indicate that the deleterious impact of self-reported sleep disturbances on cognitive performance was prominent over other risk factors and illustrate the importance of clinician evaluation of sleep in patients with or at risk of diminished cognitive performance. Future, longitudinal studies implementing a comprehensive neuropsychological battery and objective sleep measurement are warranted to further explore these associations.
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http://dx.doi.org/10.1017/S1041610219001492DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8011648PMC
July 2020

A Randomized Study Examining the Effects of Mild-to-Moderate Group Exercises on Cardiovascular, Physical, and Psychological Well-being in Patients With Heart Failure.

J Cardiopulm Rehabil Prev 2019 11;39(6):403-408

Departments of Psychiatry (Drs Redwine, Rutledge, and Mills and Ms Chinh) and Family Medicine and Public Health (Ms Wilson and Drs Pung and Mills), University of California, San Diego; and College of Nursing, University of South Florida, Tampa (Drs Redwine and Smith).

Purpose: To compare 2 mild-to-moderate group exercises and treatment as usual (TAU) for improvements in physical function and depressive symptoms.

Methods: Patients with heart failure (n = 70, mean age = 66 yr, range = 45-89 yr) were randomized to 16 wk of tai chi (TC), resistance band (RB) exercise, or TAU.

Results: Physical function differed by group from baseline to follow-up, measured by distance walked in the 6-min walk test (F = 3.19, P = .03). Tai chi participants demonstrated a nonsignificant decrease of 162 ft (95% confidence interval [CI], 21 to -345, P = .08) while distance walked by RB participants remained stable with a nonsignificant increase of 70 ft (95% CI, 267 to -127, P = .48). Treatment as usual group significantly decreased by 205 ft (95% CI, -35 to -374, P = .02) and no group differences occurred over time in end-systolic volume (P = .43) and left ventricular function (LVEF) (P = .67). However, groups differed over time in the Beck Depression Inventory (F = 9.2, P < .01). Both TC and RB groups improved (decreased) by 3.5 points (95% CI, 2-5, P < .01). Treatment as usual group decreased insignificantly 1 point (95% CI, -1 to 3, P = .27).

Conclusions: Tai chi and RB participants avoided a decrease in physical function decrements as seen with TAU. No groups changed in cardiac function. Both TC and RB groups saw reduced depression symptoms compared with TAU. Thus, both TC and RB groups avoided a decrease in physical function and improved their psychological function when compared with TAU.
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http://dx.doi.org/10.1097/HCR.0000000000000430DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6832782PMC
November 2019

Differential Peripheral Inflammatory Factors Associated with Cognitive Function in Patients with Heart Failure.

Neuroimmunomodulation 2018 23;25(3):146-152. Epub 2018 Oct 23.

College of Nursing, University of South Florida, Tampa, Florida, USA.

Objective: Cognitive deficits are common in patients with heart failure (HF), and can negatively affect self-care, predict rehospitalizations, and increase mortality rates 5-fold. Inflammation can produce vascular pathology, reducing cerebral blood flow to brain regions necessary for optimal cognitive function. The purpose of the investigation was to identify a pattern of peripheral blood inflammation-related biomarkers associated with cognitive impairment in patients with HF.

Methods: Forty-five outpatients (median age = 67 years, SD = 9.9) were recruited from University of California, San Diego (UCSD) and Veterans Affairs San Diego Healthcare Systems (VASDHS), diagnosed with New York Heart Association Stages I-III HF. Participants were administered the Montreal Cognitive Assessment (MoCA) as a measure of global cognitive impairment, and blood was analyzed for plasma biomarkers, interferon-γ, tumor necrosis factor-α (TNFα), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), brain-derived neurotrophic factor (BDNF), interleukin-8 (IL-8), matrix metallopeptidase-9 (MMP-9), IL-6, C-reactive protein (CRP), and serum amyloid-A (SAA).

Results: Almost half the patients scored below the threshold on the MoCA, indicating at least mild cognitive impairment. A factor analysis produced three biomarker factors: vascular inflammatory factor-1: TNFα, sICAM1, sVCAM1; neuroinflammatory factor-2: BDNF, MMP-9, IL-8; peripheral inflammatory factor-3: IL-6, CRP, SAA. Only vascular inflammatory factor-1 was significantly associated with cognitive function (MoCA) (ΔR2 = 0.214, beta = -0.468, p = 0.008).

Conclusions: In this cohort with HF, vascular inflammation appears related to poorer cognitive function. This could indicate targets for treatment to reduce cognitive deficits in HF. However, this is a preliminary study, and further research is needed.
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http://dx.doi.org/10.1159/000493142DOI Listing
January 2019

Pilot Randomized Study of a Gratitude Journaling Intervention on Heart Rate Variability and Inflammatory Biomarkers in Patients With Stage B Heart Failure.

Psychosom Med 2016 Jul-Aug;78(6):667-76

From the Departments of Psychiatry (Redwine, Henry, Chinh, Jain, Rutledge), Family Medicine and Public Health (Pung, Wilson, Mills), and Medicine (Knight, Greenberg, Maisel), University of California, San Diego, California.

Objective: Stage B, asymptomatic heart failure (HF) presents a therapeutic window for attenuating disease progression and development of HF symptoms, and improving quality of life. Gratitude, the practice of appreciating positive life features, is highly related to quality of life, leading to development of promising clinical interventions. However, few gratitude studies have investigated objective measures of physical health; most relied on self-report measures. We conducted a pilot study in Stage B HF patients to examine whether gratitude journaling improved biomarkers related to HF prognosis.

Methods: Patients (n = 70; mean [standard deviation] age = 66.2 [7.6] years) were randomized to an 8-week gratitude journaling intervention or treatment as usual. Baseline (T1) assessments included the six-item Gratitude Questionnaire, resting heart rate variability (HRV), and an inflammatory biomarker index. At T2 (midintervention), the six-item Gratitude Questionnaire was measured. At T3 (postintervention), T1 measures were repeated but also included a gratitude journaling task.

Results: The gratitude intervention was associated with improved trait gratitude scores (F = 6.0, p = .017, η = 0.10), reduced inflammatory biomarker index score over time (F = 9.7, p = .004, η = 0.21), and increased parasympathetic HRV responses during the gratitude journaling task (F = 4.2, p = .036, η = 0.15), compared with treatment as usual. However, there were no resting preintervention to postintervention group differences in HRV (p values > .10).

Conclusions: Gratitude journaling may improve biomarkers related to HF morbidity, such as reduced inflammation; large-scale studies with active control conditions are needed to confirm these findings.

Trial Registration: Clinicaltrials.govidentifier:NCT01615094.
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http://dx.doi.org/10.1097/PSY.0000000000000316DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4927423PMC
July 2017

Progenitor cells are mobilized by acute psychological stress but not beta-adrenergic receptor agonist infusion.

Brain Behav Immun 2015 Oct 6;49:49-53. Epub 2015 Mar 6.

Department of Clinical Psychology, University of Amsterdam, Amsterdam, The Netherlands. Electronic address:

Objectives: Stimuli that activate the sympathetic nervous system, such as acute psychological stress, rapidly invoke a robust mobilization of lymphocytes into the circulation. Experimental animal studies suggest that bone marrow-derived progenitor cells (PCs) also mobilize in response to sympathetic stimulation. Here we tested the effects of acute psychological stress and brief pharmacological β-adrenergic (βAR) stimulation on peripheral PC numbers in humans.

Methods: In two studies, we investigated PC mobilization in response to an acute speech task (n=26) and βAR-agonist (isoproterenol) infusion (n=20). A subset of 8 participants also underwent the infusion protocol with concomitant administration of the βAR-antagonist propranolol. Flow cytometry was used to enumerate lymphocyte subsets, total progenitor cells, total haematopoietic stem cells (HSC), early HSC (multi-lineage potential), late HSC (lineage committed), and endothelial PCs (EPCs).

Results: Both psychological stress and βAR-agonist infusion caused the expected mobilization of total monocytes and lymphocytes and CD8(+) T lymphocytes. Psychological stress also induced a modest, but significant, increase in total PCs, HSCs, and EPC numbers in peripheral blood. However, infusion of a βAR-agonist did not result in a significant change in circulating PCs.

Conclusion: PCs are rapidly mobilized by psychological stress via mechanisms independent of βAR-stimulation, although the findings do not exclude βAR-stimulation as a possible cofactor. Considering the clinical and physiological relevance, further research into the mechanisms involved in stress-induced PC mobilization seems warranted.
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http://dx.doi.org/10.1016/j.bbi.2015.02.028DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4561221PMC
October 2015

Leukocyte ß-adrenergic receptor sensitivity and depression severity in patients with heart failure.

Psychosom Med 2014 Nov-Dec;76(9):726-31

From the Departments of Psychiatry (L.S.R., S.H., T.R., B.W., M.P., P.J.M.), and Department of Medicine (M.G.Z., A.M., B.G.), University of California, San Diego, La Jolla, California; and Research Services (L.S.R., T.R., A.M.), VA San Diego Healthcare System, La Jolla, California.

Objectives: Clinical outcomes are worse for patients with heart failure (HF) and elevated depression symptoms. Depression-related sympathoimmune dysregulation may be one mechanism leading to poorer HF prognosis. Sympathetically mediated adrenergic activity is known to regulate immune activity via β-adrenergic receptors (β-ARs). However, studies show conflicting relationships between leukocyte β-AR sensitivity and depression symptoms. The aim of this study was to determine in patients with HF the relationship of leukocyte β-AR sensitivity with two diverse measures of depression, self-report questionnaire versus clinical diagnostic interview.

Methods: Patients with HF (N = 73, mean [standard deviation] age = 56.3 [13.0]) completed the Beck Depression Inventory-1A and a modified Structured Clinical Interview for the DSM-IV. Leukocyte β-AR sensitivity was determined from isoproterenol-stimulated cyclic adenosine monophosphate levels; plasma norepinephrine and epinephrine were also assessed.

Results: Patients with major depression determined by Structured Clinical Interview for the DSM-IV had significantly higher β-AR sensitivity than did nondepressed patients (F(6,72) = 9.27, p = .003, η = 0.12). The Beck Depression Inventory-1A revealed a more complex relationship. Minimal, mild, and moderate-to-severe depression symptom groups had significant differences in β-AR sensitivity (F(7,72) = 7.03, p = .002, η = 0.18); mild symptoms were associated with reduced β-AR sensitivity and moderate-to-severe symptoms with higher β-AR sensitivity compared with patients with minimal depressive symptoms.

Conclusions: Clinical depression was associated with elevated β-AR sensitivity in patients with HF. By deconstructing depression measurements, a greater depth of information may be garnered to potentially reveal subtypes of depression symptoms and their relation to β-AR sensitivity.
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http://dx.doi.org/10.1097/PSY.0000000000000119DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4744799PMC
July 2015

A meta-analysis of mental health treatments and cardiac rehabilitation for improving clinical outcomes and depression among patients with coronary heart disease.

Psychosom Med 2013 May 29;75(4):335-49. Epub 2013 Apr 29.

Psychology Service (116B), VA San Diego Healthcare System, 3350 La Jolla Village Drive, San Diego, CA 92161, USA.

Objective: To quantify the efficacy of mental health (antidepressants & psychotherapies) and cardiac rehabilitation treatments for improving secondary event risk and depression among patients with coronary heart disease (CHD).

Methods: Using meta-analytic methods, we evaluated mental health and cardiac rehabilitation therapies for a) reducing secondary events and 2) improving depression severity in patients with CHD. Key word searches of PubMed and Psychlit databases and previous reviews identified relevant trials.

Results: Eighteen mental health trials evaluated secondary events and 22 trials evaluated depression reduction. Cardiac rehabilitation trials for the same categories numbered 17 and 13, respectively. Mental health treatments did not reduce total mortality (absolute risk reduction [ARR] = -0.001, confidence interval [95% CI] = -0.016 to 0.015; number needed to treat [NNT] = ∞), showed moderate efficacy for reducing CHD events (ARR = 0.029, 95% CI = 0.007 to 0.051; NNT = 34), and a medium effect size for improving depression (Cohen d = 0.297). Cardiac rehabilitation showed similar efficacy for treating depression (d = 0.23) and reducing CHD events (ARR = 0.017, 95% CI = 0.007 to 0.026; NNT = 59) and reduced total mortality (ARR = 0.016, 95% CI = 0.005 to 0.027; NNT = 63).

Conclusions: Among patients with CHD, mental health treatments and cardiac rehabilitation may each reduce depression and CHD events, whereas cardiac rehabilitation is superior for reducing total mortality risk. The results support a continued role for mental health treatments and a larger role for mental health professionals in cardiac rehabilitation.
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http://dx.doi.org/10.1097/PSY.0b013e318291d798DOI Listing
May 2013

Relationships between clinical characteristics and nocturnal cardiac autonomic activity in Parkinson's disease.

Auton Neurosci 2012 Nov 8;171(1-2):85-8. Epub 2012 Nov 8.

Department of General Psychology, University of Padova, Italy.

Background: The aim of the present study was to explore the association between Parkinson's disease (PD) clinical characteristics and cardiac autonomic control across sleep stages.

Methods: Frequency-domain heart rate variability (HRV) measures were estimated in 18 PD patients undergoing a night of polysomnography.

Results: Significant relationships were found between PD severity and nocturnal HRV indices. The associations were restricted to rapid eye movement (R) sleep.

Conclusions: The progressive nocturnal cardiac autonomic impairment occurring with more severe PD can be subclinical emerging only during conditions requiring active modulation of physiological functions such as R-sleep.
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http://dx.doi.org/10.1016/j.autneu.2012.10.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3501606PMC
November 2012

A pilot study exploring the effects of a 12-week t'ai chi intervention on somatic symptoms of depression in patients with heart failure.

J Altern Complement Med 2012 Aug 30;18(8):744-8. Epub 2012 Jul 30.

Department of Psychiatry, University of California, San Diego, CA 92093, USA.

Background: Patients with chronic heart failure (HF) and with elevated depression symptoms are at greater risk of morbidity and mortality. Somatic symptoms of depression are particularly prevalent in HF and are related to worse disease prognosis. T'ai chi practice is related to increased emotional well-being in various clinical populations; however, relatively little is known about t'ai chi's effects on somatic versus cognitive symptom dimensions of depression in HF.

Purpose: The objective of the study was to measure whether a t'ai chi intervention effectively reduces somatic and/or cognitive symptoms of depression in patients with HF.

Methods: Patients with HF were assigned to either t'ai chi training (n=16) or a usual-care group (n=12). At baseline and after the 12-week intervention period, participants were evaluated for changes in depressive symptoms using Beck Depression Inventory (BDI) total scores (BDI-t) and subcategorized scores of BDI-somatic (BDI-s) and BDI-cognitive (BDI-c), and for symptoms of fatigue using the Multidimensional Fatigue Symptom Inventory-Short Form.

Results: Patients with HF in the t'ai chi group compared to the usual-care group had reduced BDI-s (p≤0.017), but not BDI-c (p=0.50) scores from pre- to postintervention. Although t'ai chi did not significantly reduce fatigue, changes in physical fatigue (p≤0.05) were independently associated with changes in BDI-t scores.

Conclusions: T'ai chi practice reduced somatic symptoms of depression, which have been linked to worse prognosis in HF. Reductions in fatigue appear to explain some but not all of the reductions in somatic symptoms of depression.
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http://dx.doi.org/10.1089/acm.2011.0314DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3419850PMC
August 2012

Post-traumatic stress disorder: a fast track to premature cardiovascular disease?

Cardiol Rev 2013 Jan-Feb;21(1):16-22

Department of Psychiatry and Behavioral Medicine, University of California, San Diego, CA, USA.

An increasing body of evidence reported in the literature indicates a possible role for post-traumatic stress disorder (PTSD) as a cause for cardiovascular disease (CVD). However, mechanistic evidence on the progression of adverse cardiac outcomes in PTSD is lacking. In this review, we examine the potential paths by which CVD could occur in those with PTSD. Dysregulation of the hypothalamic-pituitary-adrenal axis and autonomic nervous dysfunction are commonly observed in PTSD, which in turn leads to a variety of physiological changes potentially damaging to the heart. Increased inflammation, dysfunction of the vascular endothelium, hypercoagulability, and cardiac hyperreactivity all have been noted in patients with PTSD. Altered neurochemistry, most notably increased arginine vasopressin, as well as an increased prevalence of the metabolic syndrome, may also contribute to adverse cardiac outcomes. Although the association between PTSD and physical disease is often complicated by health risk behaviors or comorbid psychiatric conditions, the evidence for a link between PTSD and CVD is substantial. In our examination, we attempt to identify potential cardiac biomarkers that may be useful in detecting increased cardiac risk in patients with PTSD. As research in this area is exceedingly limited, we hope to inspire further research, as there is great potential value in identifying prognostically useful cardiac biomarkers so as to predict and prevent the onset of CVD in patients with PTSD.
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http://dx.doi.org/10.1097/CRD.0b013e318265343bDOI Listing
May 2013

Depression as a potential modulator of Beta-adrenergic-associated leukocyte mobilization in heart failure patients.

J Am Coll Cardiol 2010 Nov;56(21):1720-7

Department of Psychiatry, University of California, San Diego, La Jolla, California 92161, USA.

Objectives: the aim of this study was to determine whether depressive symptoms are related to alterations in the sensitivity of peripheral blood mononuclear cells to β-adrenergic agonists in patients with heart failure (HF) by measuring in vitro chemotaxis (CTX) to isoproterenol at rest and after acute exercise in patients with HF and controls.

Background: clinical outcomes are worse for patients with HF presenting with symptoms of depression. Sympathetically modulated immune dysregulation associated with depression may be one mechanism leading to worse prognosis.

Methods: seventy-seven patients with HF and 44 controls (mean age 56.4 ± 1.3 years) completed the Beck Depression Inventory and a 15-min mild-graded exercise task on a stationary bicycle. Exercise intensity was kept relative to fitness levels for all participants by gradually increasing resistance to reach a Borg scale subjective rating of 12 to 13, "somewhat hard." Plasma norepinephrine and epinephrine levels were measured before and after exercise. Chemotaxis to isoproterenol was determined by measuring in vitro peripheral blood mononuclear cell migration through a modified Boyden chamber.

Results: In patients with HF, depressive symptom severity was associated with greater CTX after exercise (p = 0.001). Higher resting norepinephrine in patients with HF was also associated with increased CTX to exercise (p = 0.03).

Conclusions: patients with HF with higher depressive symptoms and norepinephrine exhibited increased peripheral blood mononuclear cell CTX to isoproterenol to mild exercise, suggesting greater β-adrenergic sensitivity. Increased immune migration in patients with HF who have elevated depressive symptoms could be associated with cardiac remodeling and HF disease progression.
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http://dx.doi.org/10.1016/j.jacc.2010.04.064DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2999627PMC
November 2010

Increases in B-type natriuretic peptide after acute mental stress in heart failure patients are associated with alcohol consumption.

J Stud Alcohol Drugs 2010 Sep;71(5):786-94

Department of Psychiatry, University of California, San Diego, La Jolla, California, USA.

Objective: The aim of this study was to investigate in heart failure (HF) patients whether acute mental stress induces increases in the HF-severity biomarker B-type natriuretic peptide (BNP) and if alcohol consumption is associated with such stress-induced increases.

Method: Twenty-one male HF patients and 19 male non-HF controls (M = 56 years, SEM = 2) underwent a 15-minute acute mental stress test combining public speaking and mental arithmetic. Plasma levels of BNP were determined immediately before as well as 2 hours after the stress test. Alcohol consumption was assessed by self-reported number of drinks per month and history of use.

Results: HF patients had higher BNP levels before and after stress, F(1, 38) = 23.42, p < .001, and showed greater stress-induced increases in BNP levels, F(1, 38) = 4.52, p = .04, compared with controls. HF status (beta = .32, p = .015, deltaR(2) = .10) and higher alcohol consumption ((beta = .61, p< .001, deltaR(2) = .37) were independently associated with higher BNP stress increases. Moreover, higher alcohol consumption moderated the greater BNP stress increases in HF patients but not in controls (p = .49, p < .001, delta(2) = .20), although alcohol consumption did not differ between groups.

Conclusions: For individuals with HF, particularly those who drink moderate to more substantial amounts of alcohol, exposure to acute psychological stress leads to increases in circulating levels of BNP, a biomarker which is associated with increased morbidity and mortality in HF.
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http://dx.doi.org/10.15288/jsad.2010.71.786DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2930511PMC
September 2010

Commentary on hostility and physiological responses to laboratory stress in acute coronary syndrome patients.

J Psychosom Res 2010 Feb;68(2):117-9

Department of Clinical Psychology and Psychotherapy, University of Zürich, Binzmühlestrasse 14/Box 26, Zurich, Switzerland.

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http://dx.doi.org/10.1016/j.jpsychores.2009.11.005DOI Listing
February 2010

A potential shift from adaptive immune activity to nonspecific inflammatory activation associated with higher depression symptoms in chronic heart failure patients.

J Card Fail 2009 Sep 14;15(7):607-15. Epub 2009 Mar 14.

Department of Psychiatry, University of California, San Diego, La Jolla, CA 92161, USA.

Background: Chronic heart failure (CHF) patients with elevated depression symptoms are at greater risk of morbidity and mortality. The mechanisms linking symptoms of depression with disease progression in CHF are unclear. However, research studies have found evidence of alterations in immune activity associated with depression symptoms that may influence heart function. The present study sought to determine the relationship between depression symptoms and chemotaxis of peripheral blood mononuclear cells (PBMCs) in CHF patients, both at rest and in response to moderate exercise.

Methods And Results: Sixty-five patients diagnosed with CHF (mean age, 59.8 +/- 14.5 years) and 45 non-CHF control subjects (mean age, 52.1 +/- 11.6) completed the Beck Depression Inventory (BDI) before undergoing a moderate 20-minute bicycle exercise task. Chemotaxis of PBMCs was examined in vitro to a bacterial peptide f-met leu phe (fMLP) and a physiologic chemokine, stromal cell derived factor-1 (SDF-1) immediately before and after exercise. CHF patients had reduced chemotaxis to SDF-1 (P = .025) compared with non-CHF subjects. Higher BDI scores were associated with reduced baseline chemotaxis to SDF-1 in both CHF and non-CHF subjects (P = .027). In contrast, higher BDI scores were associated with increased chemotaxis to fMLP (P = .049) and SDF-1 (P = .018) in response to exercise in the CHF patients.

Conclusion: The present study suggests a shift in immune cell mobility in CHF patients with greater depression symptom severity, with reduced chemotaxis to a physiologically specific chemokine at rest but increased chemotaxis to both nonspecific and specific chemical attractants in response to physical activity. This could have implications for cardiac repair and remodeling in CHF patients and therefore may affect disease progression.
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http://dx.doi.org/10.1016/j.cardfail.2009.01.011DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348482PMC
September 2009

Circulating levels of soluble intercellular adhesion molecule-1 (sICAM-1) independently predict depressive symptom severity after 12 months in heart failure patients.

Brain Behav Immun 2010 Mar 13;24(3):366-9. Epub 2009 Feb 13.

Department of Clinical Psychology and Psychotherapy, Psychological Institute, University of Zurich, Switzerland; Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA.

Objective: To determine whether inflammatory markers prospectively predict depressive symptom severity 12 months later in heart failure (HF) patients.

Methods: In 30 HF patients we assessed depressive symptom severity by the Beck depression inventory (BDI) at baseline as well as 12 months later. We measured circulating levels of the soluble intercellular adhesion molecule (sICAM)-1, the cytokine interleukin (IL)-6 and the acute phase protein C-reactive protein (CRP) at baseline assessment.

Results: sICAM-1 (r=.38, p=.045) but not CRP or IL-6 correlated with BDI scores 12 months later. Hierarchical linear regression analysis revealed that independent of baseline BDI assessment, cardiovascular risk factors, indicators of HF disease severity, and medication intake, sICAM-1 significantly predicted BDI scores 12 months later. sICAM-1 independently explained between 7% (beta=.26, p=.040) and 10% (beta=.35, p=.045) of the total variance in BDI scores 12 months later.

Conclusion: The findings from this exploratory analysis suggest that the adhesion molecule sICAM-1 is an independent predictor of depressive symptoms 12 months later in HF patients. Our prospective findings support the suggested role for inflammation in increasing future depressive symptom severity and extend this linkage for the first time to HF.
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http://dx.doi.org/10.1016/j.bbi.2009.02.004DOI Listing
March 2010

Independent association between lower level of social support and higher coagulation activity before and after acute psychosocial stress.

Psychosom Med 2009 Jan 5;71(1):30-7. Epub 2009 Jan 5.

Department of Clinical Psychology and Psychotherapy, University of Zurich, Zurich, Switzerland.

Objective: To investigate the relationship between social support and coagulation parameter reactivity to mental stress in men and to determine if norepinephrine is involved. Lower social support is associated with higher basal coagulation activity and greater norepinephrine stress reactivity, which in turn, is linked with hypercoagulability. However, it is not known if low social support interacts with stress to further increase coagulation reactivity or if norepinephrine affects this association. These findings may be important for determining if low social support influences thrombosis and possible acute coronary events in response to acute stress. We investigated the relationship between social support and coagulation parameter reactivity to mental stress in men and determined if norepinephrine is involved.

Methods: We measured perceived social support in 63 medication-free nonsmoking men (age (mean +/- standard error of the mean) = 36.7 +/- 1.7 years) who underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. We measured plasma D-dimer, fibrinogen, clotting Factor VII activity (FVII:C), and plasma norepinephrine at rest as well as immediately after stress and 20 minutes after stress.

Results: Independent of body mass index, mean arterial pressure, and age, lower social support was associated with higher D-dimer and fibrinogen levels at baseline (p < .012) and with greater increases in fibrinogen (beta = -0.36, p = .001; DeltaR(2) = .12), and D-dimer (beta = -0.21, p = .017; DeltaR(2) = .04), but not in FVII:C (p = .83) from baseline to 20 minutes after stress. General linear models revealed significant main effects of social support and stress on fibrinogen, D-dimer, and norepinephrine (p < .035). Controlling for norepinephrine did not change the significance of the reported associations between social support and the coagulation measures D-dimer and fibrinogen.

Conclusions: Our results suggest that lower social support is associated with greater coagulation activity before and after acute stress, which was unrelated to norepinephrine reactivity.
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http://dx.doi.org/10.1097/PSY.0b013e31818f6868DOI Listing
January 2009

Depressive symptoms are associated with soluble P-selectin reactivity to acute exercise in heart failure.

Biol Psychiatry 2009 May 31;65(9):801-7. Epub 2008 Dec 31.

Department of Clinical Psychology and Psychotherapy, Psychological Institute, University of Zurich, Zurich, Switzerland.

Background: To determine the effects of depressive symptom severity on the circulating soluble adhesion molecule response to an acute exercise challenge in patients with heart failure (HF) compared with control subjects.

Methods: Thirty-eight male HF patients and 19 male control subjects (mean age +/- SEM: 55.5 +/- 1.9) completed the Beck Depression Inventory (BDI) before undergoing a moderate 20-minute bicycle exercise at approximately 65% to 70% VO(2peak). Plasma levels of the soluble adhesion molecules P-selectin (sP-selectin) (sCD62P) and soluble intercellular adhesion molecule-1 (sICAM-1) were determined immediately before and after and 10 minutes after exercise.

Results: Higher BDI scores moderated greater increases in sP-selectin levels in response to exercise over time in HF patients as compared with control subjects [F(1.8/84.5) = 3.25, p = .05]. Post hoc testing revealed that in HF patients, but not in control subjects, higher BDI scores were significantly associated with greater increases in sP-selectin levels over time in response to exercise [BDI by exercise interaction: F(1.6/49.6) = 5.67, p = .010]. Also, in HF patients, but not in control subjects, higher BDI scores were associated with higher sP-selectin levels at pre-exercise and postexercise time points [main effect BDI: F(1/31) = 4.86, p = .035].

Conclusions: Our findings suggest that in male HF patients with increasing depressive symptom severity, levels of the adhesion molecule sP-selectin are higher before and after exercise and have greater increases in response to exercise. This could have implications for acute coronary syndromes associated with exercise and thereby may impact mortality.
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http://dx.doi.org/10.1016/j.biopsych.2008.11.013DOI Listing
May 2009

Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response.

Metabolism 2009 Jan;58(1):30-7

Department of Clinical Psychology and Psychotherapy, Psychological Institute, University of Zurich, Binzmühlestrasse 14/Box 26, CH-8050 Zurich, Switzerland.

Hypertension is a known risk factor for cardiovascular disease. Hypertensive individuals show exaggerated norepinephrine (NE) reactivity to stress. Norepinephrine is a known lipolytic factor. It is unclear if, in hypertensive individuals, stress-induced increases in NE are linked with the elevations in stress-induced circulating lipid levels. Such a mechanism could have implications for atherosclerotic plaque formation. In a cross-sectional, quasi-experimentally controlled study, 22 hypertensive and 23 normotensive men (mean +/- SEM, 45 +/- 3 years) underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. We measured plasma NE and the plasma lipid profile (total cholesterol [TC], low-density-lipoprotein cholesterol [LDL-C], high-density-lipoprotein cholesterol, and triglycerides) immediately before and after stress and at 20 and 60 minutes of recovery. All lipid levels were corrected for stress hemoconcentration. Compared with normotensives, hypertensives had greater TC (P = .030) and LDL-C (P = .037) stress responses. Independent of each other, mean arterial pressure (MAP) upon screening and immediate increase in NE predicted immediate stress change in TC (MAP: beta = .41, P = .003; NE: beta = .35, P = .010) and LDL-C (MAP: beta = .32, P = .024; NE: beta = .38, P = .008). Mean arterial pressure alone predicted triglycerides stress change (beta = .32, P = .043) independent of NE stress change, age, and BMI. The MAP-by-NE interaction independently predicted immediate stress change of high-density-lipoprotein cholesterol (beta = -.58, P < .001) and of LDL-C (beta = -.25, P < .08). We conclude that MAP and NE stress reactivity may elicit proatherogenic changes of plasma lipids in response to acute psychosocial stress, providing one mechanism by which stress might increase cardiovascular risk in hypertension.
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http://dx.doi.org/10.1016/j.metabol.2008.08.003DOI Listing
January 2009

Coagulation activity before and after acute psychosocial stress increases with age.

Psychosom Med 2008 May;70(4):476-81

Department of Clinical Psychology and Psychotherapy, University of Zurich, Binzmühlestrasse 14, Box 26, CH-8050 Zurich, Switzerland.

Objective: To assess whether stress further increases hypercoagulation in older individuals. We investigated whether acute stress-induced changes in coagulation parameters differ with age. It is known that hypercoagulation occurs in response to acute stress and that a shift in hemostasis toward a hypercoagulability state occurs with age. However, it is not yet known whether acute stress further increases hypercoagulation in older individuals, and thus may increase their risk for cardiovascular disease (CVD).

Methods: A total of 63 medication-free nonsmoking men, aged between 20 and 65 years (mean +/- standard error of the mean = 36.7 +/- 1.7 years), underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. We measured plasma clotting factor VII activity (FVII:C), fibrinogen, and D-dimer at rest, immediately, and 20 minutes after stress.

Results: Increased age predicted greater increases in fibrinogen (beta = 0.26, p = 0.041; DeltaR(2) = 0.05), FVII:C (beta = 0.40, p = .006; DeltaR(2) = 0.11), and D-dimer (beta = 0.51, p < .001; DeltaR(2) = 0.18) from rest to 20 minutes after stress independent of body mass index and mean arterial blood pressure. General linear models revealed significant effects of age and stress on fibrinogen, FVII:C, and D-dimer (main effects: p < .04), and greater D-dimer stress reactivity with older age (interaction age-by-stress: F(1.5/90.4) = 4.36, p = .024; f = 0.33).

Conclusions: Our results suggest that acute stress might increase vulnerability in the elderly for hypercoagulability and subsequent hemostasis-associated diseases like CVD.
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http://dx.doi.org/10.1097/PSY.0b013e31816e03a5DOI Listing
May 2008

Complementary and alternative treatments for late-life depression, anxiety, and sleep disturbance: a review of randomized controlled trials.

J Clin Psychiatry 2007 Oct;68(10):1461-71

Division of Geriatric Psychiatry, Department of Psychiatry, University of California, San Diego, USA.

Objective: We reviewed randomized controlled trials of complementary and alternative medicine (CAM) treatments for depression, anxiety, and sleep disturbance in nondemented older adults.

Data Sources: We searched PubMed (1966-September 2006) and PsycINFO (1984-September 2006) databases using combinations of terms including depression, anxiety, and sleep; older adult/elderly; randomized controlled trial; and a list of 56 terms related to CAM.

Study Selection: Of the 855 studies identified by database searches, 29 met our inclusion criteria: sample size >or= 30, treatment duration >or= 2 weeks, and publication in English. Four additional articles from manual bibliography searches met inclusion criteria, totaling 33 studies.

Data Extraction: We reviewed identified articles for methodological quality using a modified Scale for Assessing Scientific Quality of Investigations (SASQI). We categorized a study as positive if the CAM therapy proved significantly more effective than an inactive control (or as effective as active control) on at least 1 primary psychological outcome. Positive and negative studies were compared on the following characteristics: CAM treatment category, symptom(s) assessed, country where the study was conducted, sample size, treatment duration, and mean sample age.

Data Synthesis: 67% of the 33 studies reviewed were positive. Positive studies had lower SASQI scores for methodology than negative studies. Mind-body and body-based therapies had somewhat higher rates of positive results than energy- or biologically-based therapies.

Conclusions: Most studies had substantial methodological limitations. A few well-conducted studies suggested therapeutic potential for certain CAM interventions in older adults (e.g., mind-body interventions for sleep disturbances and acupressure for sleep and anxiety). More rigorous research is needed, and suggestions for future research are summarized.
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http://dx.doi.org/10.4088/jcp.v68n1001DOI Listing
October 2007

Cardiac-related hospitalization and/or death associated with immune dysregulation and symptoms of depression in heart failure patients.

Psychosom Med 2007 Jan;69(1):23-9

Department of Medicine, University of California, San Diego, CA, USA.

Objective: Congestive heart failure (CHF) patients with depressive symptoms have a greater risk of morbidity and mortality. Immune activity such as inflammation is increasingly implicated as underlying this relationship. However, it is unknown whether there is a broader spectrum of immune dysregulation beyond inflammatory activity. This study examined in CHF patients the relationship of depressive symptoms with cellular immune activity measured by Th1/Th2 ratios and cardiac rehospitalization and/or death.

Method: Eighteen patients with CHF (mean age = 62, NYHA classes II-IV) were enrolled and depressive symptoms were measured with interviewer ratings using the Hamilton Rating Scale-Depression. For the determination of Th1/Th2 ratios, intracellular cytokine expression of interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) CD4+ T cells were measured by flow cytometry. Plasma interleukin-6 levels were measured to ascertain circulating inflammatory cytokine activity. Patient records were examined for cardiac related rehospitalization or cardiac related death over a two-year period after baseline depression and immune measures were taken.

Results: Higher depression scores were associated with a prospective increase in incidence of cardiac related hospitalizations and/or death (p = .037). Lesser IFN-gamma/IL-10 expressing CD4+ T cell ratios were related to higher depressive symptom scores at baseline (p = .005) and a prospective increased incidence of cardiac related hospitalization or death over a two-year period (p = .05).

Conclusions: A shift in the Th1/Th2 ratio may play a role in the association between depressive symptoms and morbidity and mortality in CHF patients, suggesting broader immune dysregulation than previously considered.
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http://dx.doi.org/10.1097/PSY.0b013e31802e2f35DOI Listing
January 2007
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