Polydisperse spray flames in vortex flows

[EN] A new mathematical analysis of the dynamics of laminar spray diffusion flames in the vicinity of a vortex flow field is presented. The governing equations for a spray evaporating in an unsteady vortex are studied. New similarity solutions are found for the dynamics of the spray and the flame it supports. Analytical solutions for the spray flames are derived using Schvab-Zeldovich parameters, through which the radial evolution of the flames is found. The results based on the solution reveal the significant influence the droplets size has on the diffusion flame dynamics in the vicinity of vortical flows.Dagan, Y.; Katoshevski, D.; Greenberg, BJ. (2017). Polydisperse spray flames in vortex flows. En Ilass Europe. 28th european conference on Liquid Atomization and Spray Systems. Editorial Universitat Politècnica de València. 702-708. https://doi.org/10.4995/ILASS2017.2017.4716OCS70270

Depressive symptoms in asymptomatic stage B heart failure with Type II diabetic mellitus.

BackgroundThe presence of concomitant Type II diabetic mellitus (T2DM) and depressive symptoms adversely affects individuals with symptomatic heart failure (HF).HypothesisIn presymptomatic stage B HF, this study hypothesized the presence of greater inflammation and depressive symptoms in T2DM as compared to non-T2DM Stage B patients.MethodsThis cross-sectional study examined clinical parameters, inflammatory biomarkers, and depressive symptoms in 349 T2DM and non-T2DM men with asymptomatic stage B HF (mean age 66.4 years ±10.1; range 30-91).ResultsFewer diabetic HF patients had left ventricular (LV) systolic dysfunction (P < .05) although more had LV diastolic dysfunction (P < .001). A higher percentage of T2DM HF patients were taking ACE-inhibitors, beta-blockers, calcium channel blockers, statins, and diuretics (P values < .05). T2DM HF patients had higher circulating levels of interleukin-6 (IL-6) (P < .01), tumor necrosis factor-alpha (P < .01), and soluble ST2 (sST2) (P < .01) and reported more somatic/affective depressive symptoms (Beck Depression Inventory II) (P < .05) but not cognitive/affective depressive symptoms (P = .20). Among all patients, in a multiple regression analysis predicting presence of somatic/affective depressive symptoms, sST2 (P = .026), IL-6 (P = .010), B-type natriuretic peptide (P = .016), and sleep (Pittsburgh Sleep Quality Index [P < .001]) were significant predictors (overall model F = 15.39, P < .001, adjusted R2 = .207).ConclusionsSomatic/affective but not cognitive/affective depressive symptoms are elevated in asymptomatic HF patients with T2DM patients. Linkages with elevated inflammatory and cardiac relevant biomarkers suggest shared pathophysiological mechanisms among T2DM HF patients with somatic depression, and these conditions are responsive to routine interventions, including behavioral. Copyright © 2019 John Wiley & Sons, Ltd

Brief report: Characteristics of antidepressant use in patients with heart failure

Paul J Mills1, Joel E Dimsdale1, Suzi Hong1, Geoffrey Van Den Brande2, Laura Redwine2, Barry H Greenberg2, Thomas Rutledge11Department of Psychiatry; 2Department of Medicine, University of California San Diego, La Jolla, CA, USABackground: Depression is common in heart failure (HF), but there is little data on the characteristics of antidepressant use in patients with HF.Objective: To survey basic information on antidepressant prescription characteristics, use, effectiveness, and follow-up.Methods: Observational study in two outpatient cardiology clinics of 37 NYHA class I–IV HF patients taking antidepressant medication.Results: Thirty-one percent of prescriptions for antidepressants were obtained from psychiatrists, 58% from primary care physicians, and 8% from cardiologists. The majority of patients (87%) reported regularly taking their antidepressant medication as prescribed, however 48% reported never having had the dosage of their antidepressant medication adjusted. Only 53% of the patients reported that the medication had helped their mood “almost entirely” or “mostly” back to normal since starting their antidepressants, while the remaining patients reported that their mood was only “halfway” or “somewhat” back to normal or that the medication had not helped their depression at all. Among a subset of 10 patients who completed the Beck Depression (BDI) inventory, 6 still had depressed mood (BDI ≥ 10).Conclusion: The findings from this survey study provide insight into the characteristics of antidepressant use in patients with HF and argue for better follow up of HF patients who are prescribed antidepressants.Keywords: heart failure, antidepressant medication, adherence, effectivenes

Occult purulent pericarditis detected by indium-111 leukocyte imaging.

Leukocyte imaging with indium-111 is a relatively new technique which, to this point in time, has been discussed almost exclusively in the radiologic literature. Although this procedure has been used mainly to detect intra-abdominal infection, the thorax is routinely imaged along with the abdomen, and therefore detection of cardiac disease may be feasible. This case report is of a young woman after liver transplantation who developed occult purulent pericarditis initially detected by a leukocyte scan with indium-111. This case demonstrates that striking pericardial uptake on a whole-body indium-111 leukocyte scan can occur with purulent pericarditis, and it reemphasizes how insidiously purulent pericarditis may present in an immunosuppressed patient

New-onset atrial fibrillation in patients with worsening heart failure and coronary artery disease:an analysis from the COMMANDER-HF trial

Background: Atrial fibrillation (AF) in the presence of heart failure (HF) is associated with poor outcomes including a high-risk of stroke and other thromboembolic events. Identifying patients without AF who are at high-risk of developing this arrhythmia has important clinical implications. Aims: To develop a risk score to identify HF patients at high risk of developing AF. Methods: The COMMANDER-HF trial enrolled 5022 patients with HF and a LVEF ≤ 40%, history of coronary artery disease, and absence of AF at baseline (confirmed with an electrocardiogram). Patients were randomized to either rivaroxaban (2.5 mg bid) or placebo. New-onset AF was confirmed by the investigator at study visits. Results 241 (4.8%) patients developed AF during the follow-up (median 21 months). Older age (≥ 65 years), LVEF < 35%, history of PCI or CABG, White race, SBP < 110 mmHg, and higher BMI (≥ 25 kg/m2) were independently associated with risk of new-onset AF, whereas the use of DAPT was associated with a lower risk of new-onset AF. We then built a risk score from these variables (with good accuracy C-index = 0.71) and calibration across observed and predicted tertiles of risk. New-onset AF events rates increased steeply by increasing tertiles of the risk-score. Compared to tertile 1, the risk of new-onset AF was 2.5-fold higher in tertile 2, and 6.3-fold higher in tertile 3. Rivaroxaban had no effect in reducing new-onset AF. In time-updated models, new-onset AF was associated with a higher risk of subsequent all-cause death: HR (95%CI) 1.38 (1.11–1.73). Conclusions: A well-calibrated risk-score identified patients at risk of new-onset AF in the COMMANDER-HF trial. Patients who developed AF had a higher risk of subsequent death

A novel approach to modeling tissue-level activity of cortisol levels according to the theory of Endobiogeny, applied to chronic heart failure

Background: Chronic heart failure (CHF) is an inflammatory disorder in which cortisol plays an important role. Despite this, cortisol is not routinely quantitatively measured for a number of reasons. It is considered non-specific. Accuracy and validity remain in question. It is not considered convenient or cost effective. Finally, tissue level effects of cortisol do not correlate linearly to quantitative levels. If the functional, tissue level effectiveness of cortisol could be modeled, its evaluation in CHF patient may become relevant. Endobiogeny is a global systems theory that claims to be able to model complex physiology through biomarkers, offering context-rich interpretations of data for meaningful clinical applicability. Cortisol is known to alter circulating levels of elements from a complete blood count (CBC). By relating these biomarkers in a qualitative fashion, the theory of Endobiogeny posits that these elements can be contextualized to reflect the tissue level activity of cortisol, referred to as the cortisol index (CI). The algorithm derived from the theory is called the Biology of Functions (BoF). Aim: The aim of this study was to determine if the cortisol index is accurate in reflecting a greater expression of cortisol activity in ambulatory CHF patients versus controls subjects. Methods: A retrospective observational case control study was performed in 93 patients with New York Heart Association class II-III heart failure patients and 104 individuals with no cardiovascular pathology as a control group. Results from a CBC were entered into BOF modeling software, from which the cortisol index is derived. Results: The Cortisol index (3-7) was significantly elevated in CHF vs. control patients (12.8±0.91 vs. 8.48±0.74, p< 001), as were individual CBC elements used to form the index. Conclusions: The cortisol index, derived from the theory of Endobiogeny showed results consistent with CHF pathophysiology. The cortisol index was able to model the effective tissue level activity of cortisol in CHF patients using only a CBC, without measuring serum cortisol. Future studies should compare the cortisol index to standard inflammatory markers in CHF patients to further correlate the validity of the index to other known effects of cortisol

The roles of inflammation and immune mechanisms in Alzheimer's disease

AbstractThe Alzheimer's Association's Research roundtable met in April 2015 to explore the role of neuroinflammatory mechanisms in the progression of Alzheimer's disease (AD). The ability of innate immune cells, particularly microglia and astrocytes, to mediate neuroinflammation in AD has been implicated as a significant contributor to disease pathogenesis. Adaptive immunity, which plays an important role in responding to injury and some diseases of the central nervous system, may contribute to neuroinflammation in AD as well. Communication between the central and peripheral immune systems may also be important in AD. An increased understanding of the physiology of the innate immune system may aid the identification of new therapeutic targets or mechanisms. The development of predictive animal models and translatable neuroinflammation biomarkers for AD would also facilitate the advancement of novel treatments for innate immunity. Important challenges impeding the advancement of new therapeutic agents and strategies to overcome them were discussed

Rivaroxaban in patients with heart failure, sinus rhythm, and coronary disease

Background: Heart failure is associated with activation of thrombin-related pathways, which predicts a poor prognosis. We hypothesized that treatment with rivaroxaban, a factor Xa inhibitor, could reduce thrombin generation and improve outcomes for patients with worsening chronic heart failure and underlying coronary artery disease. Methods: In this double-blind, randomized trial, 5022 patients who had chronic heart failure, a left ventricular ejection fraction of 40% or less, coronary artery disease, and elevated plasma concentrations of natriuretic peptides and who did not have atrial fibrillation were randomly assigned to receive rivaroxaban at a dose of 2.5 mg twice daily or placebo in addition to standard care after treatment for an episode of worsening heart failure. The primary efficacy outcome was the composite of death from any cause, myocardial infarction, or stroke. The principal safety outcome was fatal bleeding or bleeding into a critical space with a potential for causing permanent disability. Results: Over a median follow-up period of 21.1 months, the primary end point occurred in 626 (25.0%) of 2507 patients assigned to rivaroxaban and in 658 (26.2%) of 2515 patients assigned to placebo (hazard ratio, 0.94; 95% confidence interval [CI], 0.84 to 1.05; P=0.27). No significant difference in all-cause mortality was noted between the rivaroxaban group and the placebo group (21.8% and 22.1%, respectively; hazard ratio, 0.98; 95% CI, 0.87 to 1.10). The principal safety outcome occurred in 18 patients who took rivaroxaban and in 23 who took placebo (hazard ratio, 0.80; 95% CI, 0.43 to 1.49; P=0.48). Conclusions: Rivaroxaban at a dose of 2.5 mg twice daily was not associated with a significantly lower rate of death, myocardial infarction, or stroke than placebo among patients with worsening chronic heart failure, reduced left ventricular ejection fraction, coronary artery disease, and no atrial fibrillation. (Funded by Janssen Research and Development; COMMANDER HF ClinicalTrials.gov number, NCT01877915.

Cause of Death in Patients With Acute Heart Failure: Insights From RELAX-AHF-2

OBJECTIVES: This study sought to better understand the discrepant results of 2 trials of serelaxin on acute heart failure (AHF) and short-term mortality after AHF by analyzing causes of death of patients in the RELAX-AHF-2 (Efficacy, Safety and Tolerability of Serelaxin When Added to Standard Therapy in AHF-2) trial. BACKGROUND: Patients with AHF continue to suffer significant short-term mortality, but limited systematic analyses of causes of death in this patient population are available. METHODS: Adjudicated cause of death of patients in RELAX-AHF-2, a randomized, double-blind, placebo-controlled trial of serelaxin in patients with AHF across the spectrum of ejection fraction (EF), was analyzed. RESULTS: By 180 days of follow-up, 11.5% of patients in RELAX-AHF-2 died, primarily due to heart failure (HF) (38% of all deaths). Unlike RELAX-AHF, there was no apparent effect of treatment with serelaxin on any category of cause of death. Older patients (≥75 years) had higher rates of mortality (14.2% vs. 8.8%) and noncardiovascular (CV) death (27% vs. 19%) compared to younger patients. Patients with preserved EF (≥50%) had lower rates of HF-related mortality (30% vs. 40%) but higher non-CV mortality (36% vs. 20%) compared to patients with reduced EF. CONCLUSIONS: Despite previous data suggesting benefit of serelaxin in AHF, treatment with serelaxin was not found to improve overall mortality or have an effect on any category of cause of death in RELAX-AHF-2. Careful adjudication of events in the serelaxin trials showed that older patients and those with preserved EF had fewer deaths from HF or sudden death and more deaths from other CV causes and from noncardiac causes. (Efficacy, Safety and Tolerability of Serelaxin When Added to Standard Therapy in AHF [RELAX-AHF-2]; NCT01870778)