Cardiac Depression Scale: Mokken scaling in heart failure patients

Background: There is a high prevalence of depression in patients with heart failure (HF) that is associated with worsening prognosis. The value of using a reliable and valid instrument to measure depression in this population is therefore essential. We validated the Cardiac Depression Scale (CDS) in heart failure patients using a model of ordinal unidimensional measurement known as Mokken scaling. Findings: We administered in face-to-face interviews the CDS to 603 patients with HF. Data were analysed using Mokken scale analysis. Items of the CDS formed a statistically significant unidimensional Mokken scale of low strength (H<0.40) and high reliability (Rho>0.8). Conclusions: The CDS has a hierarchy of items which can be interpreted in terms of the increasingly serious effects of depression occurring as a result of HF. Identifying an appropriate instrument to measure depression in patients with HF allows for early identification and better medical management. Keywords: Cardiac Depression Scale, Heart failure, Depression, Mokken scalin

Medical microbiology in dentistry

МИКРОБИОЛОГИЯСТОМАТОЛОГИЯСТОМАТОГНАТИЧЕСКИЕ БОЛЕЗНИУЧЕБНЫЕ ПОСОБИЯВключены разделы с информацией о наиболее распространенных стоматологических болезнях, ассоциированных с инфекциями, их патогенезе, лабораторной диагностике, профилактике и лечении

The Chinese version of the cardiac depression scale: Mokken scaling

<p>Abstract</p> <p>Background</p> <p>Myocardial infarction is a major cause of death and morbidity in many countries, including China. The aim of this study was to analyse a Mandarin Chinese translation of the Cardiac Depression Scale for a hierarchy of items according to the criteria of Mokken scaling.</p> <p>Findings</p> <p>Data from 438 Chinese participants who completed the Chinese translation of the Cardiac Depression Scale were analysed using the Mokken scaling procedure and the 'R' statistical programme using the diagnostics available in these programmes. Correlations between Mandarin Chinese items and Chinese translations of the Hospital Anxiety and Depression Scale and the Beck Depression Inventory were also analysed. Fifteen items from the Mandarin Chinese Cardiac Depression Scale were retained in a weak but reliable Mokken scale; invariant item ordering was evident but of low accuracy and the Mokken scaled items of the Chinese Cardiac Depression Scale correlated with the Hospital Anxiety and Depression Scale and the Beck Depression Inventory.</p> <p>Conclusions</p> <p>Items from the Mandarin Chinese Cardiac Depression Scale form a Mokken scale and this offers further insight into how the items of the Cardiac Depression Scale relate to the measurement of depression in people with a myocardial infarction.</p

Simvastatin impairs the induction of pulmonary fibrosis caused by a western style diet: A preliminary study

The role of an atherogenic diet in causing pulmonary fibrosis has received little attention and simvastatin has been shown to reduce pulmonary fibrosis in animal models. To determine if an atherogenic diet can induce pulmonary fibrosis and whether simvastatin treatment is beneficial by up-regulating heat shock protein 70 and 90. New Zealand white rabbits (n = 15) were divided: Group 1 (control); Group 2 (MC) received a normal rabbit diet with 1% methionine plus 0.5% cholesterol (atherogenic diet). Group 3 received the same diet as the MC group plus 5 mg/kg/day simvastatin orally (MCS). After 4 weeks, the lungs were collected and analysed. Picrosirus red staining of lung interstitial collagen content showed that the atherogenic diet increased fibrosis 2.9-fold (P < 0.05), bronchiole adventitial collagen was increased 2.3-fold (P < 0.05) and bronchiole epithelium was increased 34-fold (P < 0.05), and simvastatin treatment severely reduced this effect (P < 0.05). Western blot analysis showed that the atherogenic diet significantly reduced lung Hsp70 protein by 22% (P < 0.05) and Hsp90 protein by 18% (P < 0.05) and simvastatin treatment did not affect this result. However, aortic hyper-responsiveness to vasoconstrictors (angiotensin II and phenylephrine) were markedly reduced by simvastatin treatment. We report that an atherogenic diet stimulates pulmonary fibrosis and reduces lung Hsp70/Hsp90 protein concentration. Simvastatin impairs this by mechanisms unrelated to Hsp70/Hsp90, but possibly a reduction in angiotensin II receptor or alpha adrenergic receptor pathways. These results could have implications in idiopathic pulmonary fibrosis

A nurse-led up-titration clinic improves chronic heart failure optimization of beta-adrenergic receptor blocking therapy : a randomized controlled trial

BACKGROUND: Beta-adrenergic blockade has been shown to improve left ventricular function, reduce hospital admissions and improve survival in chronic heart failure with reduced ejection fraction (HFrEF), with mortality reduction starting early after beta-adrenergic receptor blocker initiation and being dose-related. The aim of this pilot study was to determine the effectiveness of a nurse-led titration clinic in improving the time required for patients to reach optimal doses of the beta-adrenergic receptor blocking agents. METHOD: We conducted a prospective pilot randomized controlled trial. Twenty eight patients with CHF were randomized to optimisation of beta-adrenergic receptor blocker therapy over six months by either a nurse-led titration (NLT) clinic, led by a nurse specialist with the support of a cardiologist in a CHF clinic, or by their primary care physician (usual care (UC)). The primary endpoint was time to maximal beta-adrenergic receptor blocker dose. The secondary end-point was the proportion of patients reaching the target dose of beta-adrenergic receptor blocker by six months. RESULTS: The patients were predominantly men (72%), age 67 ± 16 years; New York Heart Association (NYHA) functional class I (32%), II (44%) and III (20%); baseline left ventricular ejection fraction 33 ± 10%, and a low mean Charlson co-morbidity score of 2.5 ± 1.4. The time to maximum dose was shorter in the NLT group compared to the UC group (90 ± 14 vs 166 ± 8 days, p < 0.0005). At six months, in the NLT group there were nine patients (82%) on high dose and one patient (9%) on low dose beta-adrenergic receptor blocker compared to the UC group with five (42%) patients reaching maximum dose and five (42%) patients on low dose (p = 0.04). The patients allocated to the NLT group also had significantly less worsening of depression between baseline and six months (p = 0.006). CONCLUSION: A NLT clinic improves optimisation of beta-adrenergic receptor blocker therapy through increasing the proportion of patients reaching maximal dose and facilitating rapid up-titration of beta-adrenergic receptor blocker agents in patients with chronic HFrEF. TRIAL REGISTRATION: Australian Clinical Trials Registry (ACTRN012606000383561)

Clinical utility of exercise training in heart failure with reduced and preserved ejection fraction

Reduced exercise tolerance is an independent predictor of hospital readmission and mortality in patients with heart failure (HF). Exercise training for HF patients is well established as an adjunct therapy, and there is sufficient evidence to support the favorable role of exercise training programs for HF patients over and above the optimal medical therapy. Some of the documented benefits include improved functional capacity, quality of life (QoL), fatigue, and dyspnea. Major trials to assess exercise training in HF have, however, focused on heart failure with reduced ejection fraction (HFREF). At least half of the patients presenting with HF have heart failure with preserved ejection fraction (HFPEF) and experience similar symptoms of exercise intolerance, dyspnea, and early fatigue, and similar mortality risk and rehospitalization rates. The role of exercise training in the management of HFPEF remains less clear. This article provides a brief overview of pathophysiology of reduced exercise tolerance in HFREF and heart failure with preserved ejection fraction (HFPEF), and summarizes the evidence and mechanisms by which exercise training can improve symptoms and HF. Clinical and practical aspects of exercise training prescription are also discussed

Citizen science as a new tool in dog cognition research

The work of Á.M. was supported by the Hungarian Academy of Sciences (MTA 01 031).Family dogs and dog owners offer a potentially powerful way to conduct citizen science to answer questions about animal behavior that are difficult to answer with more conventional approaches. Here we evaluate the quality of the first data on dog cognition collected by citizen scientists using the Dognition. com website. We conducted analyses to understand if data generated by over 500 citizen scientists replicates internally and in comparison to previously published findings. Half of participants participated for free while the other half paid for access. The website provided each participant a temperament questionnaire and instructions on how to conduct a series of ten cognitive tests. Participation required internet access, a dog and some common household items. Participants could record their responses on any PC, tablet or smartphone from anywhere in the world and data were retained on servers. Results from citizen scientists and their dogs replicated a number of previously described phenomena from conventional lab-based research. There was little evidence that citizen scientists manipulated their results. To illustrate the potential uses of relatively large samples of citizen science data, we then used factor analysis to examine individual differences across the cognitive tasks. The data were best explained by multiple factors in support of the hypothesis that nonhumans, including dogs, can evolve multiple cognitive domains that vary independently. This analysis suggests that in the future, citizen scientists will generate useful datasets that test hypotheses and answer questions as a complement to conventional laboratory techniques used to study dog psychology.Publisher PDFPeer reviewe

Acute high-intensity interval exercise-induced redox signaling is associated with enhanced insulin sensitivity in obese middle-aged men

Background: Obesity and aging are associated with increased oxidative stress, activation of stress and mitogen activated protein kinases (SAPK), and the development of insulin resistance and metabolic disease. In contrast, acute exercise also increases oxidative stress and SAPK signaling, yet is reported to enhance insulin sensitivity and reduce the risk of metabolic disease. This study explored this paradox by investigating the effect of a single session of high-intensity interval-exercise (HIIE) on redox status, muscle SAPK and insulin protein signaling in eleven middle-aged obese men. Methods: Participants completed a 2 h hyperinsulinaemic-euglycaemic clamp at rest, and 60 min after HIIE (4 × 4 mins at 95% HRpeak; 2 min recovery periods), separated by 1–3 weeks. Results: Irrespective of exercise-induced changes to redox status, insulin stimulation both at rest and after HIIE similarly increased plasma superoxide dismutase activity, plasma catalase activity, and skeletal muscle 4-HNE; and significantly decreased plasma TBARS and hydrogen peroxide. The SAPK signaling pathways of p38 MAPK, NF-κB p65, and JNK, and the distal insulin signaling protein AS160Ser588, were activated with insulin stimulation at rest and to a greater extent with insulin stimulation after a prior bout of HIIE. Higher insulin sensitivity after HIIE was associated with higher insulin-stimulated SOD activity, JNK, p38 MAPK and NF-κB phosphorylation (r = 0.63, r = 0.71, r = 0.72, r = 0.71; p < 0.05, respectively). Conclusion: These findings support a role for redox homeostasis and SAPK signaling in insulin-stimulated glucose uptake which may contribute to the enhancement of insulin sensitivity in obese men 3 h after HIIE

Acute exercise alters skeletal muscle mitochondrial respiration and H2O2 emission in response to hyperinsulinemic-euglycemic clamp in middle-aged obese men

Obesity, sedentary lifestyle and aging are associated with mitochondrial dysfunction and impaired insulin sensitivity. Acute exercise increases insulin sensitivity in skeletal muscle; however, whether mitochondria are involved in these processes remains unclear. The aim of this study was to investigate the effects of insulin stimulation at rest and after acute exercise on skeletal muscle mitochondrial respiratory function (JO2) and hydrogen peroxide emission (JH2O2), and the associations with insulin sensitivity in obese, sedentary men. Nine men (means ± SD: 57 ± 6 years; BMI 33 ± 5 kg.m2) underwent hyperinsulinemic-euglycemic clamps in two separate trials 1–3 weeks apart: one under resting conditions, and another 1 hour after high-intensity exercise (4x4 min cycling at 95% HRpeak). Muscle biopsies were obtained at baseline, and pre/post clamp to measure JO2 with high-resolution respirometry and JH2O2 via Amplex UltraRed from permeabilized fibers. Post-exercise, both JO2 and JH2O2 during ADP stimulated state-3/OXPHOS respiration were lower compared to baseline (P<0.05), but not after subsequent insulin stimulation. JH2O2 was lower post-exercise and after subsequent insulin stimulation compared to insulin stimulation in the rest trial during succinate supported state-4/leak respiration (P<0.05). In contrast, JH2O2 increased during complex-I supported leak respiration with insulin after exercise compared with resting conditions (P<0.05). Resting insulin sensitivity and JH2O2 during complex-I leak respiration were positively correlated (r = 0.77, P<0.05). We conclude that in obese, older and sedentary men, acute exercise modifies skeletal muscle mitochondrial respiration and H2O2 emission responses to hyperinsulinemia in a respiratory state-specific manner, which may have implications for metabolic diseases involving insulin resistance

Comparing methods for prescribing exercise for individuals with chronic heart failure

This study examined the accuracy of current recommended guidelines for prescribing exercise intensity using the methods of percentage of heart rate reserve (%HRR), percentage of VO2 peak (%VO2peak) and percentage of VO2 reserve (%VO2R) in a clinical population of chronic heart failure (CHF) patients. The precision of prescription of exercise intensity for 45 patients with stable CHF (39:6 M:F, 65&plusmn;9 yrs (mean&plusmn;SD)) was investigated. VO2peak testing is relatively common among patients with cardiac disease, but the assessment of VO2rest is not common practice and the accepted standard value of 3.5 mL/kg/min is assumed in the application of %VO2R (%VO2R3.5). In this study, VO2rest was recorded for 3 min prior to the start of a symptom-limited exercise test on a cycle ergometer. Target exercise intensities were calculated using the VO2 corresponding to 50 or 80 %HRR, VO2peak and VO2R. The VO2 values were then converted into prescribed speeds on a treadmill in km/hr at 1 %grade using ACSM&rsquo;s metabolic equation for walking. Target intensities and prescribed treadmill speeds were also calculated with the %VO2R method using the mean VO2rest value of participants (3.9 mL/kg/min) (%VO2R3.9). This was then compared to the exercise intensities and prescribed treadmill speeds using patient&rsquo;s measured VO2rest. Error in prescription correlates the difference between %VO2R3.5 and %VO2R3.9 compared to %VO2R with measured VO2rest. Prescription of exercise intensity through the %HRR method is imprecise for patients on medications that blunt the HR response to exercise. %VO2R method offers a significant improvement in exercise prescription compared to %VO2peak. However, a disparity of 10 % still exists in the %VO2R method using the standard 3.5 mL/kg/min for VO2rest in the %VO2R equation. The mean measured VO2rest in the 45 CHF patients was 11 % higher (3.9&plusmn;0.8 mL/kg/min) than the standard value provided by ACSM. Applying the mean measured VO2rest value of 3.9 mL/kg/min rather than the standard assumed value of 3.5 mL/kg/min proved to be closer to the prescribed intensity determined by the actual measured resting VO2. These results suggest that the %HRR method should not be used to prescribe exercise intensity for CHF patients. Instead, VO2 should be used to prescribe exercise intensity and be expressed as %VO2R with measured variables (VO2rest and VO2peak).<br /