Traumatic stress and cardiopulmonary disease burden among low-income, urban heart failure patients.

BACKGROUND: Traumatic events and posttraumatic stress disorder (PTSD) are associated with increased risk for cardiopulmonary disease (CPD) in veterans, men, and primarily White populations. Less is known about trauma, PTSD, and CPD burden among low-income, racial minority residents who are at elevated risk for trauma and PTSD. It was hypothesized that traumatic events and PTSD would be significantly associated with CPD burden among low-income, racial minority residents. METHODS: We evaluated cross-sectional relationships between traumatic events, PTSD, depression, and CPD burden in 251 low-income, urban, primarily Black adults diagnosed with heart failure. Data were analyzed using bivariate analyses, logistic and linear regression. RESULTS: Forty-three percent endorsed at least one traumatic event. Twenty-one percent endorsed two or more traumatic events. In logistic regression analyses, traumatic events were associated with increased prevalence of coronary artery disease (adjusted odds=1.33, p<.05), hypertension (adjusted odds=1.28, p<.05), chronic obstructive pulmonary disease (adjusted odds=1.52, p<.01), and cardiac arrest (adjusted odds=1.27, p<.05). PTSD was also related to increased risk for chronic obstructive pulmonary disease (adjusted odds=1.22, p<.05) and was associated with earlier onset of heart failure (ß=-.13, p<.05). LIMITATIONS: The study utilizes cross-sectional, self-report data. CONCLUSIONS: Findings support the link between traumatic events, PTSD, and CPD burden in low-income, primarily Black patients with heart failure. Depression appears to be less closely linked to CPD burden, despite receiving significant attention in the literature. The accumulation of traumatic events may exacerbate CPD burden among urban, low-income, racial minority residents with heart failure; findings highlight the importance of PTSD screening.

Posttraumatic stress and depression: potential pathways to disease burden among heart failure patients.

BACKGROUND AND OBJECTIVES: Posttraumatic stress disorder (PTSD) and Major Depressive Disorder (MDD) are associated with high disease burden. Pathways by which PTSD and MDD contribute to disease burden are not understood. DESIGN: Path analysis was used to examine pathways between PTSD symptoms, MDD symptoms, and disease burden among 251 low-income heart failure patients. METHODS: In Model 1, we explored the independent relationship between PTSD and MDD symptoms on disease burden. In Model 2, we examined the association of PTSD symptoms and disease burden on MDD symptoms. We also examined indirect associations of PTSD symptoms on MDD symptoms, mediated by disease burden, and of PTSD symptoms on disease burden mediated by MDD symptoms. RESULTS: Disease burden correlated with PTSD symptoms (r = .41; p < .001) and MDD symptoms (r = .43; p < .001) symptoms. Both models fit the data well and displayed comparable fit. MDD symptoms did not mediate the association of PTSD symptoms with disease burden. Disease burden did mediate the relationship between PTSD symptoms and MDD symptoms. CONCLUSIONS: Results support the importance of detection of PTSD in individuals with disease. Results also provide preliminary models for testing longitudinal data in future studies.

Respiratory sinus arrhythmia reactivity in current and remitted major depressive disorder.

OBJECTIVE: Low resting respiratory sinus arrhythmia (RSA) levels and blunted RSA reactivity are thought to index impaired emotion regulation capacity. Major depressive disorder (MDD) has been associated with aberrant RSA reactivity and recovery to a speech stressor task relative to healthy controls. Whether impaired RSA functioning reflects aspects of the depressed mood state or a stable vulnerability marker for depression is unknown. METHODS: We compared resting RSA and RSA reactivity between adults with MDD (n = 49), remitted depression (RMD, n = 24), and healthy controls (n = 45). Electrocardiogram data were collected during a resting baseline, a paced-breathing baseline, and two reactivity tasks (speech stressor, cold exposure). RESULTS: A group by time quadratic effect emerged (F(2,109) = 4.36, p = .015) for RSA across phases of the speech stressor (baseline, instruction, preparation, speech, recovery). Follow-up analyses revealed that those with MDD uniquely exhibited blunted RSA reactivity, whereas RMD and controls both exhibited the anticipated task-related vagal withdrawal and posttask recovery. The group by time interaction remained after covariation for age, sex, waist circumference, physical activity, and respiration, but not sleep quality. CONCLUSIONS: These results provide new evidence that aberrant RSA reactivity marks features that track the depressed state, such as poor sleep, rather than a stable trait evident among asymptomatic persons.

Emotional reactivity to daily events in major and minor depression.

Although emotional dysfunction is an important aspect of major depressive disorder (MDD), it has rarely been studied in daily life. Peeters, Nicolson, Berkhof, Delespaul, and deVries (2003) observed a surprising mood-brightening effect when individuals with MDD reported greater reactivity to positive events. To better understand this phenomenon, we conducted a multimethod assessment of emotional reactivity to daily life events, obtaining detailed reports of appraisals and event characteristics using the experience-sampling method and the Day Reconstruction Method (Kahneman, Krueger, Schkade, Schwarz, & Stone, 2004) in 35 individuals currently experiencing a major depressive episode, 26 in a minor depressive (mD) episode, and 38 never-depressed healthy controls. Relative to healthy controls, both mood-disordered groups reported greater daily negative affect and lower positive affect and reported events as less pleasant, more unpleasant, and more stressful. Importantly, MDD and mD individuals reported greater reductions in negative affect following positive events, an effect that converged across assessment methods and was not explained by differences in prevailing affect, event appraisals, or medications. Implications of this curious mood-brightening effect are discussed.

Major depressive disorder is associated with attenuated cardiovascular reactivity and impaired recovery among those free of cardiovascular disease.

OBJECTIVE: To examine cardiovascular reactivity and recovery to laboratory stress among a naturalistic sample of individuals diagnosed with major depressive disorder (MDD) and healthy control participants. Prospective evidence suggests that MDD confers risk for cardiovascular disease equal to or greater than the risk associated with depressed mood. Enhanced cardiovascular reactivity has been proposed as a mechanism explaining increased risk, but data are inconsistent as to whether depressed individuals exhibit enhanced or attenuated reactivity. Further, few studies have examined appraisal and recovery differences. DESIGN: Participants diagnosed with MDD (N = 25) and healthy control participants (N = 25) engaged in a cardiovascular reactivity protocol including 2 tasks, each followed by a brief recovery period. MAIN OUTCOME MEASURES: Blood pressure, heart rate, pre-ejection period, cardiac output and total peripheral resistance were assessed. Appraisals of tasks were assessed prior to each task. RESULTS: Depressed participants exhibited significantly less systolic blood pressure, heart rate, and cardiac output reactivity during speech, less heart rate reactivity during mirror tracing, and less heart rate recovery after speech and mirror tracing than controls. Depressed participants appraised the tasks as more demanding, threatening, and stressful and reported being less able to cope than controls. Appraisals were related to heart rate reactivity, but appraisals did not mediate the relationship between depression group and reactivity. CONCLUSION: Impaired recovery rather than exaggerated cardiovascular reactivity may partially explain the increased prospective cardiovascular disease risk in depressed individuals.

RSA fluctuation in major depressive disorder.

Cardiac vagal control, as measured by indices of respiratory sinus arrhythmia (RSA), has been investigated as a marker of impaired self-regulation in mental disorders, including depression. Past work in depressed samples has focused on deficits in resting RSA levels, with mixed results. This study tested the hypothesis that depression involves abnormal RSA fluctuation. RSA was measured in depressed and healthy control participants during rest and during two reactivity tasks, each followed by a recovery period. Relative to controls, depressed persons exhibited lower resting RSA levels as well as less RSA fluctuation, primarily evidenced by a lack of task-related vagal suppression. Group differences in RSA fluctuation were not accounted for by differences in physical health or respiration, whereas group differences in resting RSA level did not survive covariate analyses. Depression may involve multiple deficits in cardiac vagal control.