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BackgroundInsomnia may be a risk factor for cardiovascular disease in HIV (HIV-CVD); however, mechanisms have yet to be elucidated.MethodsWe examined cross-sectional associations of insomnia symptoms with biological mechanisms of HIV-CVD (immune activation, systemic inflammation, and coagulation) among 1,542 people with HIV from the Veterans Aging Cohort Study (VACS) Biomarker Cohort. Past-month insomnia symptoms were assessed by the item, "Difficulty falling or staying asleep?," with the following response options: "I do not have this symptom" or "I have this symptom and…" "it doesn't bother me," "it bothers me a little," "it bothers me," "it bothers me a lot." Circulating levels of the monocyte activation marker soluble CD14 (sCD14), inflammatory marker interleukin-6 (IL-6), and coagulation marker D-dimer were determined from blood specimens. Demographic- and fully-adjusted (CVD risk factors, potential confounders, HIV-related factors) regression models were constructed, with log-transformed biomarker variables as the outcomes. We present the exponentiated regression coefficient (exp[b]) and its 95% confidence interval (CI).ResultsWe observed no significant associations between insomnia symptoms and sCD14 or IL-6. For D-dimer, veterans in the "Bothers a Lot" group had, on average, 17% higher D-dimer than veterans in the "No Difficulty Falling or Staying Asleep" group in the demographic-adjusted model (exp[b] = 1.17, 95%CI = 1.01-1.37, p = .04). This association was nonsignificant in the fully-adjusted model (exp[b] = 1.09, 95%CI = 0.94-1.26, p = .27).ConclusionWe observed little evidence of relationships between insomnia symptoms and markers of biological mechanisms of HIV-CVD. Other mechanisms may be responsible for the insomnia-CVD relationship in HIV; however, future studies with comprehensive assessments of insomnia symptoms are warranted.

BackgroundHeart failure (HF) is a major source of morbidity and mortality. Fluid retention and shortness of breath are its cardinal manifestations for which loop diuretics are used. Although their usefulness is well accepted, less is known about their role in improving clinical outcomes.ObjectivesThe purpose of this study was to determine the relationship between loop diuretics and clinical outcomes in patients with HF.MethodsOf the 25,345 older patients hospitalized for HF in the Medicare-linked OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure) registry, 9,866 (39%) received no pre-admission diuretics. The study excluded 1,083 patients receiving dialysis and 847 discharged on thiazide diuretics. Of the remaining 7,936 patients, 5,568 (70%) were prescribed loop diuretics at discharge. Using propensity scores for receipt of loop diuretics estimated for each of the 7,936 patients, a matched cohort of 2,191 pairs of patients was assembled balanced on 74 baseline characteristics. Hazard ratios (HRs) and 95% confidence intervals (CIs) for outcomes were estimated in the matched cohort.ResultsMatched patients (n = 4,382) had a mean age of 78 years, 54% were women, and 11% were African American. The 30-day all-cause mortality occurred in 4.9% (107 of 2,191) and 6.6% (144 of 2,191) of patients in the loop diuretic and no loop diuretic groups, respectively (HR when the use of loop diuretics was compared with nonuse: 0.73; 95% CI: 0.57 to 0.94; p = 0.016). Patients in the loop diuretic group had a significantly lower risk of 30-day HF readmission (HR: 0.79; 95% CI: 0.63 to 0.99; p = 0.037) but not of 30-day all-cause readmission (HR: 0.89; 95% CI: 0.79 to 1.01; p = 0.081). None of the associations was statistically significant during 60 days of follow-up.ConclusionsHospitalized older patients not taking diuretics prior to hospitalization for HF decompensation who received a discharge prescription for loop diuretics had significantly better 30-day clinical outcomes than those not discharged on loop diuretics. These findings provide new information about short-term clinical benefits associated with loop diuretic use in HF.

More than 1 million heart failure hospitalizations occur annually, and congestion is the predominant cause. Rehospitalizations for recurrent congestion portend poor outcomes independently of age and renal function. Persistent congestion trumps serum creatinine increases in predicting adverse heart failure outcomes. No decongestive pharmacological therapy has reduced these harmful consequences. Simplified ultrafiltration devices permit fluid removal in lower-acuity hospital settings, but with conflicting results regarding safety and efficacy. Ultrafiltration performed at fixed rates after onset of therapy-induced increased serum creatinine was not superior to standard care and resulted in more complications. In contrast, compared with diuretic agents, some data suggest that adjustment of ultrafiltration rates to patients' vital signs and renal function may be associated with more effective decongestion and fewer heart failure events. Essential aspects of ultrafiltration remain poorly defined. Further research is urgently needed, given the burden of congestion and data suggesting sustained benefits of early and adjustable ultrafiltration.

BackgroundBoth HIV and depression are associated with increased heart failure (HF) risk. Depression, a common comorbidity, may further increase the risk of HF among adults with HIV infection (HIV+). We assessed the association between HIV, depression, and incident HF.Methods and resultsVeterans Aging Cohort Study (VACS) participants free from cardiovascular disease at baseline (n=81 427: 26 908 HIV+, 54 519 without HIV [HIV-]) were categorized into 4 groups: HIV- without major depressive disorder (MDD) [reference], HIV- with MDD, HIV+ without MDD, and HIV+ with MDD. International Classification of Diseases, Ninth Revision codes from medical records were used to determine MDD and the primary outcome, HF. After 5.8 years of follow-up, HF rates per 1000 person-years were highest among HIV+ participants with MDD (9.32; 95% confidence interval [CI], 8.20-10.6). In Cox proportional hazards models, HIV+ participants with MDD had a significantly higher risk of HF (adjusted hazard ratio, 1.68; 95% CI, 1.45-1.95) compared with HIV- participants without MDD. MDD was associated with HF in separate fully adjusted models for HIV- and HIV+ participants (adjusted hazard ratio, 1.21; 95% CI, 1.06-1.37; and adjusted hazard ratio, 1.29; 95% CI, 1.11-1.51, respectively). Among those with MDD, baseline antidepressant use was associated with lower risk of incident HF events (adjusted hazard ratio, 0.76; 95% CI, 0.58-0.99).ConclusionsOur study is the first to suggest that MDD is an independent risk factor for HF in HIV+ adults. These results reinforce the importance of identifying and managing MDD among HIV+ patients. Future studies must clarify mechanisms linking HIV, MDD, antidepressants, and HF and identify interventions to reduce HF morbidity and mortality in those with both HIV and MDD.

The purpose of this study was to explore the relationship of serum osmolality to HF-related fatigue, controlling for select physiologic covariates. Fatigue is a common symptom of heart failure (HF) associated with deleterious outcomes including increased morbidity and mortality. Underlying physiologic mechanisms of HF-related fatigue are not well understood. Hypervolemia and hypovolemia have been suggested as potential mechanisms of HF-related fatigue. Serum osmolality has been used as a physiologic measure to assess changes in volume status with therapeutic treatments to manage fluid imbalances. Low serum osmolality is associated with increased risk of mortality and hospital readmission in persons with HF. However, the relationship of serum osmolality and HF-related fatigue has not been well described. We analyzed cross-sectional data from two waves of the National Health and Nutrition Examination Survey (2015-2016 and 2017-2018). Adults who self-reported having HF without co-morbid conditions known to contribute to fatigue were included in the study (unweighted n = 126). Data were weighted to provide US national estimates, and complex sample design used for analyses. Independent t tests and chi-square tests were used to explore differences between fatigued and nonfatigued adults with HF. Logistic regression analyses were used to calculate the odds of having fatigue. Bivariate logistic regression models were performed to assess the individual contributions of select physiologic covariates: age, sex, hemoglobin, body mass index (BMI) and presence of shortness of breath. Covariates with a significance of p≤.10 were included in the final model. Multivariate logistic regression was performed on the presence of fatigue as the outcome with physiologic predictors selected from the bivariate analysis: BMI and serum osmolality. Being female was associated with higher odds of experiencing fatigue when controlling for serum osmolality and body mass index (OR=4.91, p<.001, CI 2.200 – 10.954). Serum osmolality was lower in those that experienced fatigue compared to those without fatigue (t=-2.37, p=.032) Higher serum osmolality was associated with 7.6% lower odds of experiencing fatigue when controlling for sex and BMI (OR=.924, p=.014, CI.870 -.982). Despite the deleterious outcomes associated with HF-related fatigue, physiologic mechanisms remain poorly understood. Serum osmolality may be associated with the experience of fatigue in persons with HF. Serum osmolality reflects the concentration of serum sodium, urea, and glucose. The differences in serum osmolality noted may be explained by dietary sodium, serum blood glucose, fluid restrictions or use of diuretics. Yet, serum osmolality is associated with mortality in persons with HF, suggesting changes in serum osmolality may inform disease severity and may influence the presentation of symptoms. Our findings also suggest HF-related fatigue may follow a sexually dimorphic pattern. Differences in symptom presentation may be related to physiologic differences. Women compared to men, have smaller ventricular mass, increased myocardial contractility, lower cellular turnover, lower blood pressures, less catecholamine-mediated vasoconstriction, and less total body water. These physiologic differences may contribute to fatigue presentation and severity of fatigue. Sex-based interventions may therefore be useful in managing the symptom. [ABSTRACT FROM AUTHOR]