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Biomedical subjects

Robert M Carney

Publications and source records attributed to Robert M Carney.

At least 19 recordsLinked to original sources
PubMed2005

Mood disorders in the medically ill: scientific review and recommendations.

OBJECTIVE: The purpose of this review is to assess the relationship between mood disorders and development, course, and associated morbidity and mortality of selected medical illnesses, review evidence for treatment, and determine needs in clinical practice and research. DATA SOURCES: Data were culled from the 2002 Depression and Bipolar Support Alliance Conference proceedings and a literature review addressing prevalence, risk factors, diagnosis, and treatment. This review also considered the experience of primary and specialty care providers, policy analysts, and patient advocates. The review and recommendations reflect the expert opinion of the authors. STUDY SELECTION/DATA EXTRACTION: Reviews of epidemiology and mechanistic studies were included, as were open-label and randomized, controlled trials on treatment of depression in patients with medical comorbidities. Data on study design, population, and results were extracted for review of evidence that includes tables of prevalence and pharmacological treatment. The effect of depression and bipolar disorder on selected medical comorbidities was assessed, and recommendations for practice, research, and policy were developed. CONCLUSIONS: A growing body of evidence suggests that biological mechanisms underlie a bidirectional link between mood disorders and many medical illnesses. In addition, there is evidence to suggest that mood disorders affect the course of medical illnesses. Further prospective studies are warranted.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Low heart rate variability and the effect of depression on post-myocardial infarction mortality.

BACKGROUND: Depression is associated with an increased risk for mortality after acute myocardial infarction (MI). The purpose of this study was to determine whether low heart rate variability (HRV) mediates the effect of depression on mortality. METHODS: Twenty-four-hour ambulatory electrocardiograms were obtained from 311 depressed patients with a recent acute MI who were enrolled in the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial and from 367 nondepressed patients who met the ENRICHD medical inclusion criteria. Standard HRV indexes were extracted from the recordings. RESULTS: The log of very low-frequency (LnVLF) power, an index of HRV derived from power spectral analysis of the electrocardiogram signal (0.0033-0.04 Hz [in milliseconds squared]), was lower in the depressed than in the nondepressed patients (P<.001). There were 47 deaths (6.1%) during a 30-month follow-up. After adjusting for potential confounders, the depressed patients remained at higher risk for all-cause mortality compared with the nondepressed patients (hazard ratio, 2.8; 95% confidence interval [CI], 1.4-5.4; P<.003). When LnVLF power was entered into the model, the hazard ratio for depression dropped to 2.1 (95% CI, 1.1-4.2; P = .03). The proportion of the risk for depression attributable to LnVLF power was 0.27 (95% CI, 0.23-0.31; P<.001). CONCLUSIONS: Low HRV partially mediates the effect of depression on survival after acute MI. This finding helps to clarify the physiological mechanisms underlying depression's role as a risk factor for mortality in patients with coronary heart disease. It also raises the possibility that treatments that improve both depression and HRV might also improve survival in these patients.

Circadian Rhythm↗
PubMed2005

Relation of depressive symptoms to C-reactive protein and pathogen burden (cytomegalovirus, herpes simplex virus, Epstein-Barr virus) in patients with earlier acute coronary syndromes.

Despite mounting evidence that depressive symptoms increase the risk of morbidity and mortality in patients who have coronary artery disease, little is known about the biologic mechanisms that underlie this association. This study examined whether depressive symptoms are associated with markers of infection and inflammation that have been implicated in the pathogenesis of coronary artery disease. Sixty-five patients who were recovering from an acute coronary syndrome were enrolled (63% men; mean age 61 years, 90% white). Depressive symptoms were assessed through self-report and observer ratings; the inflammatory molecules C-reactive protein, interleukin-6, and tumor necrosis factor-alpha were measured in serum, as were antibody titers to 3 latent viruses associated with atherosclerosis. Patients who had more severe depressive symptoms exhibited higher levels of C-reactive protein (r = 0.27, p = 0.03) and higher rates of seropositivity to the latent viruses (r = 0.41, p = 0.001). These effects were large in magnitude: patients in the highest tertile of the depression distribution had C-reactive protein levels >50% higher than did patients in the middle and lowest tertiles; they also were 2 times as likely to show evidence of infection with all 3 latent viruses. Disparities in the extent, severity, or management of cardiac disease were not responsible for these associations. These findings provide evidence that depressive symptoms are associated with increases in C-reactive protein and pathogen burden in patients who have coronary artery disease. In doing so, they highlight a mechanism through which depressive symptoms might foster morbidity and mortality among patients who have cardiac disease.

Biomarkers↗
PubMed2005

Effects of antidepressant medication on morbidity and mortality in depressed patients after myocardial infarction.

BACKGROUND: Depression after myocardial infarction (MI) is associated with higher morbidity and mortality. Although antidepressants are effective in reducing depression, their use in patients with cardiovascular disease remains controversial. OBJECTIVE: To undertake a secondary analysis to determine the effects of using antidepressants on morbidity and mortality in post-MI patients who participated in the Enhancing Recovery in Coronary Heart Disease study. DESIGN: Observational secondary analysis. SETTING: Eight academic sites. PATIENTS: The Enhancing Recovery in Coronary Heart Disease clinical trial randomized 2481 depressed and/or socially isolated patients from October 1, 1996, to October 31, 1999. Depression was diagnosed using a structured clinical interview. This analysis was conducted on the 1834 patients enrolled with depression (849 women and 985 men). INTERVENTION: Use of antidepressant medication. MAIN OUTCOME MEASURES: Event-free survival was defined as the absence of death or recurrent MI. All-cause mortality was also examined. To relate exposure to antidepressants to subsequent morbidity and mortality, the data were analyzed using a time-dependent covariate model. RESULTS: During a mean follow-up of 29 months, 457 fatal and nonfatal cardiovascular events occurred. The risk of death or recurrent MI was significantly lower in patients taking selective serotonin reuptake inhibitors (adjusted hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.38-0.84), as were the risk of all-cause mortality (adjusted HR, 0.59; 95% CI, 0.37-0.96) and recurrent MI (adjusted HR, 0.53; 95% CI, 0.32-0.90), compared with patients who did not use selective serotonin reuptake inhibitors. For patients taking non-selective serotonin reuptake inhibitor antidepressants, the comparable HRs (95% CIs) were 0.72 (0.44-1.18), 0.64 (0.34-1.22), and 0.73 (0.38-1.38) for risk of death or recurrent MI, all-cause mortality, or recurrent MI, respectively, compared with nonusers. CONCLUSIONS: Use of selective serotonin reuptake inhibitors in depressed patients who experience an acute MI might reduce subsequent cardiovascular morbidity and mortality. A controlled trial is needed to examine this important issue.

Antidepressive Agents↗
PubMed2005

Depressive symptoms and the regulation of proinflammatory cytokine expression in patients with coronary heart disease.

OBJECTIVE: Depressive symptoms increase the risk of morbidity and mortality in patients with coronary heart disease (CHD). Mounting evidence indicates that inflammatory processes may underlie this association. This study examined whether depressive symptoms are associated with the dysregulation of inflammatory cytokine production in response to an in vitro infectious challenge. METHODS: Forty-one patients with CHD were enrolled 3 months or more after an acute myocardial infarction or revascularization procedure. Depressive symptoms were assessed through self-report and interviewer ratings. Cytokine production was measured after white blood cells were cultured in vitro with endotoxin in the presence of varying concentrations of dexamethasone. RESULTS: Depressive symptoms were not associated with the quantity of in vitro inflammatory cytokine production. However, to the extent that they reported symptoms of depression, patients showed greater sensitivity to the anti-inflammatory properties of glucocorticoids. This was manifested by increased suppression of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) production by dexamethasone. CONCLUSIONS: Increased sensitivity to glucocorticoid inhibition could render depressed patients vulnerable to latent infections and inflammatory processes that accelerate the progression of cardiac disease.

Adult↗
PubMed2005

Effects of anxiety and depression on heart disease attributions.

Cardiac patients' beliefs about the causes of their illness may influence their receptivity to psychosocial interventions. The purpose of this study was to determine whether depression or anxiety influence patients' attributions about the causes of their heart disease. The primary hypothesis was that depressed or anxious patients are more likely to endorse negative emotions as among the causes of their heart disease than are patients who are not depressed or anxious. Sixty-nine patients with documented ischemic heart disease recruited from an exercise stress testing laboratory completed the Beck Depression and Anxiety Inventories and a heart disease attribution checklist. Univariate analyses confirmed that patients who are depressed or anxious are more likely than other patients to endorse negative emotions as causes of their heart disease. Anxiety but not depression was retained as an independent predictor of negative emotion attributions in a logistic regression analysis. We conclude that mood state influences cardiac patients' beliefs about the causes of their heart disease.

Aged↗
PubMed2004

Exercise, depression, and mortality after myocardial infarction in the ENRICHD trial.

PURPOSE: The large and well-characterized population of acute myocardial infarction (AMI) patients studied in the recently completed Enhancing Recovery in Coronary Heart Disease (ENRICHD) multicenter clinical trial provides a unique opportunity to examine the importance of self-reported regular physical exercise in a large cohort of patients with a recent AMI who are depressed or report low levels of social support. METHODS: We prospectively examined the association between self-reported physical exercise and all-cause mortality and cardiovascular morbidity among 2078 men (N = 1175; 56.5%) and women (N = 903; 43.5%) with an AMI participating in the ENRICHD Trial. Six months after suffering an AMI, patients were surveyed about their exercise habits and were then followed for up to 4 yr. RESULTS: During an average 2 yr of follow-up, 187 fatal events occurred. Patients reporting regular exercise had less than half the events (5.7%) of those patients reporting they did not regularly exercise (12.0%). After adjustment for medical and demographic variables, the hazard ratio for fatal events was 0.62 (95% CI = 0.44-0.86, P = 0.004). The rate of nonfatal AMI among the exercisers was 6.5% compared with 10.5% who reported no regular exercise. After adjustment for covariates, the hazard ratio for nonfatal AMI was 0.72 (95% CI = 0.52-0.99, P = 0.044). CONCLUSIONS: The present findings demonstrate the potential value of exercise in reducing mortality and nonfatal reinfarction in AMI patients at increased risk for adverse events by virtue of their either being depressed or having low social support.

Cognitive Behavioral Therapy↗
PubMed2003

Depression as a risk factor for mortality after acute myocardial infarction.

The ENRICHD clinical trial, which compared an intervention for depression and social isolation to usual care, failed to decrease the rate of mortality and recurrent acute myocardial infarction (AMI) in post-AMI patients. One explanation for this is that depression was not associated with increased mortality in these patients. The purpose of this study was to determine if depression was associated with an increased risk of mortality in a subsample of the ENRICHD trial's depressed patients compared with a group of nondepressed patients recruited for an ancillary study. Three hundred fifty-eight depressed patients with an acute AMI from the ENRICHD clinical trial and 408 nondepressed patients who met the ENRICHD medical inclusion criteria were followed for up to 30 months. There were 47 deaths (6.1%) and 57 nonfatal AMIs (7.4%). After adjusting for other risk factors, depressed patients were at higher risk for all-cause mortality (hazard ratio 2.4, 95% confidence interval 1.2 to 4.7) but not for nonfatal recurrent infarction (hazard ratio 1.2, 95% confidence interval 0.7 to 2.0) compared with nondepressed patients. In conclusion, depression was an independent risk factor for death after AMI, but it did not have a significant effect on mortality until nearly 12 months after the acute event, nor did it predict nonfatal recurrent infarction.

Aged↗
PubMed2003

Depression, mortality, and medical morbidity in patients with coronary heart disease.

There is substantial evidence that depression is a risk factor for cardiac morbidity and mortality, both for patients without clinical evidence of coronary heart disease at index examination and for patients with established coronary disease. The relationship is most apparent for patients with a recent acute myocardial infarction. Many questions about the impact of depression on heart disease remain unresolved.

Comorbidity↗
PubMed2003

Effects of treating depression and low perceived social support on clinical events after myocardial infarction: the Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) Randomized Trial.

CONTEXT: Depression and low perceived social support (LPSS) after myocardial infarction (MI) are associated with higher morbidity and mortality, but little is known about whether this excess risk can be reduced through treatment. OBJECTIVE: To determine whether mortality and recurrent infarction are reduced by treatment of depression and LPSS with cognitive behavior therapy (CBT), supplemented with a selective serotonin reuptake inhibitor (SSRI) antidepressant when indicated, in patients enrolled within 28 days after MI. DESIGN, SETTING, AND PATIENTS: Randomized clinical trial conducted from October 1996 to April 2001 in 2481 MI patients (1084 women, 1397 men) enrolled from 8 clinical centers. Major or minor depression was diagnosed by modified Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria and severity by the 17-item Hamilton Rating Scale for Depression (HRSD); LPSS was determined by the Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) Social Support Instrument (ESSI). Random allocation was to usual medical care or CBT-based psychosocial intervention. INTERVENTION: Cognitive behavior therapy was initiated at a median of 17 days after the index MI for a median of 11 individual sessions throughout 6 months, plus group therapy when feasible, with SSRIs for patients scoring higher than 24 on the HRSD or having a less than 50% reduction in Beck Depression Inventory scores after 5 weeks. MAIN OUTCOME MEASURES: Composite primary end point of death or recurrent MI; secondary outcomes included change in HRSD (for depression) or ESSI scores (for LPSS) at 6 months. RESULTS: Improvement in psychosocial outcomes at 6 months favored treatment: mean (SD) change in HRSD score, -10.1 (7.8) in the depression and psychosocial intervention group vs -8.4 (7.7) in the depression and usual care group (P<.001); mean (SD) change in ESSI score, 5.1 (5.9) in the LPSS and psychosocial intervention group vs 3.4 (6.0) in the LPSS and usual care group (P<.001). After an average follow-up of 29 months, there was no significant difference in event-free survival between usual care (75.9%) and psychosocial intervention (75.8%). There were also no differences in survival between the psychosocial intervention and usual care arms in any of the 3 psychosocial risk groups (depression, LPSS, and depression and LPSS patients). CONCLUSIONS: The intervention did not increase event-free survival. The intervention improved depression and social isolation, although the relative improvement in the psychosocial intervention group compared with the usual care group was less than expected due to substantial improvement in usual care patients.

Adaptation, Psychological↗
PubMed2003

Pathways linking depression, adiposity, and inflammatory markers in healthy young adults.

Despite mounting evidence that depression increases risk for cardiovascular morbidity and mortality, little is known about the mechanisms responsible for this association. The current study examined the inter-relationships between depression, adiposity, and inflammatory molecules implicated in the pathogenesis of coronary heart disease. One hundred adults were enrolled. Half were clinically depressed; the others were matched controls with no history of psychiatric illness. All subjects were in excellent health, defined as having no acute infectious disease, chronic medical illness, or prescribed medication regimen. Structural equation modeling yielded support for a model in which depressive symptoms promote weight accumulation, which in turn activates an inflammatory response through two distinct pathways: expanded adipose tissue release of interleukin-6 and leptin-induced upregulation of interleukin-6 release by white blood cells (CFI =.99; NNFI =.99; RMSEA =.05). It did not support a sickness behavior model in which the inflammatory molecules arising from expanded adipose tissue promote depressive symptoms.

Adaptation, Physiological↗
PubMed2003

Cynical hostility, depressive symptoms, and the expression of inflammatory risk markers for coronary heart disease.

Although the prognostic significance of depression and hostility has been established, little is known about how they operate together to influence disease processes. This study explored the independent and interactive relationships between these constructs and the expression of inflammatory markers implicated in the pathogenesis of coronary heart disease. One hundred adults completed measures of cynical hostility and depressive symptoms, and had blood drawn to assess serum levels of interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha. Depression was directly related to inflammatory markers, but hostility was not. A significant interaction between hostility and depression emerged. Among participants scoring low in depressive symptoms, hostility was positively associated with interleukin-6 and tumor necrosis factor-alpha concentrations. Hostility's association with these inflammatory markers was much weaker among participants with moderate depressive symptoms, however, and virtually nil among participants with severe depressive symptoms. Neither depression nor hostility was associated with interleukin-1 beta concentrations. These findings highlight the importance of considering both the independent and interactive relationships among psychosocial characteristics involved in disease.

Adult↗
PubMed2003

A simple method to identify sleep apnea using Holter recordings.

INTRODUCTION: Despite its severe cardiovascular and other consequences, sleep apnea syndrome frequently is undiagnosed. Because apneas result in repeated autonomic arousals associated with cyclic variations in heart rate (CVHR), we hypothesized that sleep apnea syndrome could be identified from simple HR tachograms (graphs of HR vs time) derived from ECG monitoring. METHODS AND RESULTS: HR tachograms were generated from 57 digitized ECGs (46 clinical patients undergoing diagnostic studies and 11 research subjects) obtained during overnight polysomnography. Thirty-three had significant sleep apnea syndrome (apnea-hypopnea index > or = 15). Eight patients had simultaneous Holter recordings during sleep studies (3 with digitized ECGs and 5 with paper ECGs). Duration of CVHR on tachograms was determined. CVHR patterns were characterized as high amplitude (HR changes > or = 20 beats/min per cycle) versus lower amplitude (6-19 beats/min per cycle); or regular (in frequency, amplitude, and morphology) versus irregular. Tachograms were classified as having visible HR changes versus not visible (flat). Twenty-four studies proved to be split-night, so CVHR was quantified for the first 3 hours of each study only. When subjects were dichotomized into shorter (< 20%, < 36 min) and longer (> or = 20%) durations of CVHR, longer CVHR had a positive predictive accuracy of 86% for significant sleep apnea syndrome and 100% for abnormal sleep. When flat tachograms were excluded, negative predictive accuracy for shorter CVHR was 100%. All patients (N = 13) with > 36 min high-amplitude CVHR had significant obstructive sleep apnea. All predictions from Holter-only data were concordant with clinical diagnoses. CONCLUSION: HR tachogram patterns derived from ambulatory ECGs provide a simple method for identifying sleep apnea syndrome and other sleep disturbances in patients without major autonomic dysfunction.

Adult↗
PubMed2003

Psychiatric disorder and quality of life in patients awaiting lung transplantation.

STUDY OBJECTIVE: To examine the relationship between psychiatric comorbidity and quality of life in patients awaiting lung transplantation. SETTING: Duke University Medical Center/Lung Transplantation Program. PARTICIPANTS: One hundred patients with end-stage pulmonary disease listed for lung transplantation. MEASUREMENTS AND RESULTS: Twenty-five percent (n = 25) of the sample met diagnostic criteria for at least one current mood or anxiety disorder. Controlling for age, gender, ethnicity, percentage of predicted FEV, and lung disease diagnosis, patients with a current psychiatric diagnosis reported poorer general quality of life (p < 0.0001), poorer disease-specific quality of life (p < 0.0001), greater shortness of breath (p = 0.01), more symptoms of psychological distress (p < 0.0001), lower levels of social support (p < 0.0001), and fewer positive health habits (p < 0.04) than their counterparts without a psychiatric diagnosis. CONCLUSIONS: Psychiatric comorbidity affects a significant portion of patients awaiting lung transplantation and is associated with decreased health-related quality of life.

Anxiety Disorders↗
PubMed2002

Clinical depression and inflammatory risk markers for coronary heart disease.

Despite mounting evidence that psychiatric depression heightens risk for cardiac morbidity and mortality, little is known about the mechanisms responsible for this association. The present study examined the relation between depression and the expression of inflammatory risk markers implicated in the pathogenesis of coronary heart disease (CHD). One hundred adults were enrolled (68% women, 48% Caucasian, 48% African-American, mean age 30 +/- 2 years). Fifty subjects met the diagnostic criteria for clinical depression; the remaining 50 were demographically matched controls with no history of psychiatric illness. All subjects were in excellent health, defined as having no acute infectious disease, chronic medical illness, or regular medication regimen aside from oral contraceptives. The depressed subjects exhibited significantly higher levels of the inflammatory markers C-reactive protein (3.5 +/- 0.5 vs 2.5 +/- 5 mg/L, p = 0.04) and interleukin-6 (3.0 +/- 0.3 vs 1.9 +/- 0.2 pg/ml, p = 0.007) compared with control subjects. Mediational analyses aimed at identifying the pathways contributing to this association revealed that neither cigarette smoking nor subclinical infection with cytomegalovirus or Chlamydia pneumoniae had been responsible. However, depressed subjects exhibited greater body mass than control subjects, and analyses were consistent with adiposity accounting for a portion of the relation between clinical depression and increased expression of inflammatory markers. These findings indicate that in otherwise healthy adults, depression is associated with heightened expression of inflammatory markers implicated in the pathogenesis of CHD. Increased body mass appears to be partially, although not completely, responsible for this relation.

Adult↗