Depression, Healthcare Utilization, and Death in Heart Failure: A Community Study.

Depression, Healthcare Utilization, and Death in Heart Failure: A Community Study.

Circ Heart Fail. 2013 Mar 19;
Moraska AR, Chamberlain AM, Shah ND, Vickers KS, Rummans TA, Dunlay SM, Spertus JA, Weston SA, McNallan SM, Redfield MM, Roger VL

BACKGROUND: -The increasing prevalence of heart failure (HF) and high associated costs have spurred investigation of factors leading to adverse outcomes in HF patients. Studies to date report inconsistent evidence regarding the link between depression and outcomes with only limited data on emergency department (ED) and outpatient visits. METHODS AND RESULTS: -Olmsted, Dodge, and Fillmore county, MN residents with HF were prospectively recruited between October 2007 and December 2010, and completed a one-time 9-item Patient Health Questionnaire (PHQ-9) for depression categorized as: none-minimal (PHQ-9 score 0-4), mild (5-9), or moderate-severe (?10). Andersen-Gill models were used to determine if depression predicted hospitalizations and ED visits while negative binomial regression models explored the association of depression with outpatient visits. Cox proportional hazards regression characterized the relationship between depression and all-cause mortality. Among 402 HF patients (mean age 73±13, 58% male), 15% had moderate-severe depression, 26% mild, and 59% none-minimal. Over a mean follow-up of 1.6 years, 781 hospitalizations, 1000 ED visits, 15,515 outpatient visits, and 74 deaths occurred. After adjustment, moderate-severe depression was associated with nearly a 2-fold increased risk of hospitalization (HR 1.79, 95% CI 1.30-2.47) and ED visits (HR 1.83, 95% CI 1.34-2.50), a modest increase in outpatient visits (RR 1.20, 95% CI 1.00-1.45), and a 4-fold increase in all-cause mortality (HR 4.06, 95% CI 2.35-7.01). CONCLUSIONS: -In this prospective cohort study, depression independently predicted an increase in the use of healthcare resources and mortality. Greater recognition and management of depression in HF may optimize clinical outcomes and resource utilization. HubMed – depression


Clinical and Molecular Genetics of Psychotic Depression.

Schizophr Bull. 2013 Mar 19;
Domschke K

This review provides a comprehensive overview of clinical and molecular genetic as well as pharmacogenetic studies regarding the clinical phenotype of “psychotic depression.” Results are discussed with regard to the long-standing debate on categorical vs dimensional disease models of affective and psychotic disorders on a continuum from unipolar depression over bipolar disorder and schizoaffective disorder to schizophrenia. Clinical genetic studies suggest a familial aggregation and a considerable heritability (39%) of psychotic depression partly shared with schizoaffective disorder, schizophrenia, and affective disorders. Molecular genetic studies point to potential risk loci of psychotic depression shared with schizoaffective disorder (1q42, 22q11, 19p13), depression, bipolar disorder, and schizophrenia (6p, 8p22, 10p13-12, 10p14, 13q13-14, 13q32, 18p, 22q11-13) and several vulnerability genes possibly contributing to an increased risk of psychotic symptoms in depression (eg, BDNF, DBH, DTNBP1, DRD2, DRD4, GSK-3beta, MAO-A). Pharmacogenetic studies implicate 5-HTT, TPH1, and DTNBP1 gene variation in the mediation of antidepressant treatment response in psychotic depression. Genetic factors are suggested to contribute to the disease risk of psychotic depression in partial overlap with disorders along the affective-psychotic spectrum. Thus, genetic research focusing on psychotic depression might inspire a more dimensional, neurobiologically and symptom-oriented taxonomy of affective and psychotic disorders challenging the dichotomous Kraepelinian view. Additionally, pharmacogenetic studies might aid in the development of a more personalized treatment of psychotic depression with an individually tailored antidepressive/antipsychotic pharmacotherapy according to genotype. HubMed – depression


Validation of the Pittsburgh Sleep Quality Index Addendum for Posttraumatic Stress Disorder (PSQI-A) in U.S. Male Military Veterans.

J Trauma Stress. 2013 Mar 19;
Insana SP, Hall M, Buysse DJ, Germain A

Sleep disturbances are core symptoms of posttraumatic-stress disorder (PTSD), yet they bear less stigma than other PTSD symptoms. Given the growing number of returning military veterans, brief, valid assessments that identify PTSD in a minimally stigmatizing way may be useful in research and clinical practice. The study purpose was to evaluate the psychometric properties of the Pittsburgh Sleep Quality Index Addendum for PTSD (PSQI-A), and to examine its ability to identify PTSD cases among U.S. male military veterans. Male military veterans (N = 119) completed the PSQI-A, as well as measures of sleep quality, combat exposure, posttraumatic stress, depression, and anxiety. Veterans with PTSD had higher PSQI-A identified disruptive nocturnal behaviors than veterans without PTSD. The PSQI-A had good internal consistency and convergent validity with sleep quality, combat exposure, PTSD symptoms, depression, and anxiety. A cutoff score ? 4 provided an area under the curve = .81, with 71% sensitivity, 82% specificity, and 60% positive and 83% negative predictive value for a clinical diagnosis of PTSD; correct classification was 74%. The PSQI-A is a valid measure to possibly detect PTSD among male military veterans. Assessment of disruptive nocturnal behaviors may provide a cost-effective, nonstigmatizing approach to PTSD screening without directly probing for trauma exposure(s). HubMed – depression


An Open-Label Investigation of the Pharmacokinetic Profiles of Lisdexamfetamine Dimesylate and Venlafaxine Extended-Release, Administered Alone and in Combination, in Healthy Adults.

Clin Drug Investig. 2013 Mar 20;
Ermer J, Haffey MB, Richards C, Lasseter K, Roesch B, Purkayastha J, Corcoran M, Harlin B, Martin P

BACKGROUND: Lisdexamfetamine dimesylate (LDX), a prodrug consisting of d-amphetamine and l-lysine, is being studied in clinical trials of major depressive disorder. Additional drug-drug interaction studies were warranted. OBJECTIVE: This study aimed to describe the pharmacokinetics and safety of LDX and venlafaxine extended-release (VXR), alone or combined. STUDY DESIGN: The study was an open-label, two-arm, single-sequence crossover investigation with randomization to treatment sequence. SETTING AND PARTICIPANTS: The study was conducted at two clinical study centres and included healthy adult males and females (18-45 years of age). INTERVENTION: The study included two single-sequence crossover designs: LDX alone followed by LDX + VXR (Treatment Arm A); and VXR alone followed by VXR + LDX (Treatment Arm B). Drug treatment was initiated on day 1 with once-daily LDX or VXR alone with 15 days’ titration to final dose (LDX 30, 50 and 70 mg for 5 days each; VXR 75, 150 and 225 mg for 5 days each). On days 16-30, VXR, titrated to a final dose of 225 mg, or LDX, titrated to a final dose of 70 mg, was coadministered for participants in Treatment Arm A or B, respectively. On days 31-38, VXR doses were tapered. MAIN OUTCOME MEASURES: On days 1-2, 15-16 and 30-31, safety evaluations and blood samples were obtained pre-dose through 24 h post-dose for analysis of LDX, d-amphetamine, venlafaxine (VEN), and O-desmethylvenlafaxine (ODV). Combination treatment was considered bioequivalent to single treatment if 90 % confidence intervals (CIs) for geometric mean ratios (GMRs) of analytes fell within the interval 0.80-1.25 based on maximum plasma concentration (Cmax) and area under the plasma concentration-time curve (AUC) from time zero to time of last measurable concentration (AUC?). Safety assessments included treatment-emergent adverse events (TEAEs), pulse rate and blood pressure (BP), clinical laboratory assessments, and 12-lead electrocardiograms (ECG). RESULTS: Among 80 enrolled subjects, 77 were included in pharmacokinetic and safety analyses. Combination LDX + VXR was bioequivalent to LDX alone, based on exposure to d-amphetamine (GMR [95 % CI], Cmax (ng/mL): 0.97 [0.82, 1.14], AUC?: 0.95 [0.81, 1.12]). Exposure to VEN with LDX + VXR (vs. VXR alone) was increased (Cmax: 1.10 [0.88, 1.38], AUC?: 1.13 [0.88, 1.45]) and ODV decreased (Cmax: 0.91 [0.77, 1.06], AUC?: 0.83 [0.71, 0.96]), whereas composite VEN + ODV was bioequivalent to VXR alone (Cmax: 0.96 [0.84, 1.09], AUC?: 0.98 [0.85, 1.13]). TEAEs with LDX or LDX + VXR were similar. Maximum mean increases from baseline were: pulse rate, +8.73 to 12.76 beats/min with either treatment alone and +17.67 to 20.85 beats/min with LDX + VXR; systolic BP, +4.32 to 6.56 mmHg with either treatment alone and +12.96 to 13.78 mmHg with LDX + VXR; diastolic BP, +5.39 to 5.74 mmHg with either treatment alone and +12.09 to 12.46 mmHg with LDX + VXR. One participant was withdrawn due to a serious TEAE (presyncope). No unexpected, clinically meaningful trends or changes from baseline in mean laboratory or ECG parameters were observed during the trial. CONCLUSION: In healthy adults, combination LDX + VXR (vs. LDX alone) did not alter exposure to d-amphetamine. Although small changes in exposure to VEN (increased) and ODV (decreased) were seen with combination treatment, total VEN + ODV exposure showed no change (vs. VEN alone). LDX + VXR led to increases in BP and pulse rate, supporting existing recommendations for vital sign monitoring when using these medications. HubMed – depression



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