Combined aerobic and resistance exercise program improves task performance in patients with heart failure

OBJECTIVES: To assess the effects of a home-based aerobic and resistance training program on the physical function of adults with New York Heart Association (NYHA) class II and III patients and systolic heart failure (HF). DESIGN: Randomized controlled trial. SETTING: Home based. PARTICIPANTS: Stable patients (N=24; mean age, 60±10y; left ventricular ejection fraction, 25%±9%; 50% white; 50% women) with New York Heart Association (NYHA) classes II and III (NYHA class III, 58%) systolic heart failure (HF). INTERVENTION: A 12-week progressive home-based program of moderate-intensity aerobic and resistance exercise. Attention control wait list participants performed light stretching and flexibility exercises. MAIN OUTCOME MEASURES: A 10-item performance-based physical function measure, the Continuous Scale Physical Functional Performance test (CS-PFP10), was the major outcome variable and included specific physical activities measured in time to complete a task, weight carried during a task, and distance walked. Other measures included muscle strength, HRQOL (Minnesota Living With Heart Failure Questionnaire, Epworth Sleepiness Scale), functional capacity (Duke Activity Status Index), and disease severity (brain natriuretic peptide) levels. RESULTS: After the exercise intervention, 9 of 10 specific task activities were performed more rapidly, with increased weight carried by exercise participants compared with the attention control wait list group. Exercise participants also showed significant improvements in CS-PFP10 total score (P<.025), upper and lower muscle strength, and HRQOL (P<.001) compared with the attention control wait list group. Adherence rates were 83% and 99% for the aerobic and resistance training, respectively. CONCLUSIONS: Patients with stable HF who participate in a moderate-intensity combined aerobic and resistance exercise program may improve performance of routine physical activities of daily living by using a home-based exercise approach. Performance-based measures such as the CS-PFP10 may provide additional insights into physical function in patients with HF that more commonly used exercise tests may not identify. Early detection of subtle changes that may signal declining physical function that are amenable to intervention potentially may slow further loss of function in this patient population

Turning Over Patient Turnover: An Ethnographic Study of Admissions, Discharges, and Transfers: PATIENT TURNOVER

The impact on nursing work of patient turnover (admissions, discharges, and transfers) became evident in an ethnographic study of turbulence. The patient turnover data were generated from extensive observations, 21 formal interviews, and a year of admission and discharge records on one medical and one surgical unit. Timing of turnover events on the two units differed, but on both units admissions typically interrupted workflow more than did discharges, clustered admissions were more disruptive than staggered admissions, and patient turnover during change of shift was more disruptive than during medication administration. Understanding the complexity of patient turnover will elucidate the work involved and improve the evidence base for nurse staffing, a key determinant of quality and safety of care

Dietary energy density: a mediator of depressive symptoms and abdominal obesity or independent predictor of abdominal obesity?

BACKGROUND: In the U.S., Europe, and throughout the world, abdominal obesity prevalence is increasing. Depressive symptoms may contribute to abdominal obesity through the consumption of diets high in energy density. PURPOSE: To test dietary energy density ([DED]; kilocalories/gram of food and beverages consumed) for an independent relationship with abdominal obesity or as a mediator between depressive symptoms and abdominal obesity. METHODS: This cross-sectional study included 87 mid-life, overweight adults; 73.6% women; 50.6% African-American. Variables and measures: Beck Depression Inventory-II (BDI-II) to measure depressive symptoms; 3-day weighed food records to calculate DED; waist circumference, an indicator of abdominal obesity. Hierarchical regression tested if DED explained waist circumference variance while controlling for depressive symptoms and consumed food and beverage weight. Three approaches tested DED as a mediator. RESULTS: Nearly three-quarters of participants had abdominal obesity, and the mean waist circumference was 103.2 (SD 14.3) cm. Mean values: BDI-II was 8.67 (SD 8.34) which indicates most participants experienced minimal depressive symptoms, and 21.8% reported mild to severe depressive symptoms (BDI-II ≥ 14); DED was 0.75 (SD 0.22) kilocalories/gram. Hierarchical regression showed an independent association between DED and waist circumference with DED explaining 7.0% of variance above that accounted for by BDI-II and food and beverage weight. DED did not mediate between depressive symptoms and abdominal obesity. CONCLUSIONS: Depressive symptoms and DED were associated with elevated waist circumference, thus a comprehensive intervention aimed at improving depressive symptoms and decreasing DED to reduce waist circumference is warranted

Development, psychometric testing, and revision of the atlanta heart failure knowledge test

BACKGROUND AND RESEARCH OBJECTIVE: Several heart failure (HF) knowledge tools have been developed and tested over the past decade; however, they vary in content, format, psychometric properties, and availability. This article details the development, psychometric testing, and revision of the Atlanta Heart Failure Knowledge Test (A-HFKT) as a standardized instrument for both the research and clinical settings. PARTICIPANTS AND METHODS: Development and psychometric testing of the A-HFKT were undertaken with 116 New York Heart Association (NYHA) class II and III community-dwelling HF patients and their family members (FMs) participating in a family intervention study. Internal consistency, reliability, and content validity were examined. Construct validity was assessed by correlating education level, literacy, dietary sodium ingestion, medication adherence, and healthcare utilization with knowledge. RESULTS: Content validity ratings on relevance and clarity ranged from 0.55 to 1.0, with 81% of the items rated from 0.88 to 1.0. Cronbach α values were .84 for patients, .75 for FMs, and .73 for combined results. Construct validity testing revealed a small but significant correlation between higher patient and FM knowledge on sodium restriction questions and lower ingested sodium, r = −0.17, P = .05 and r = −0.19, P = .04, respectively, and between patient knowledge and number of days that medications were taken correctly (diuretics: r = 0.173, P < .05, and angiotensin-converting enzyme: r = 0.223, P = .01). Finally, patients seeking emergency care or requiring hospitalization in the 4 months before study entry were found to have significantly lower FM knowledge using both t test and logistic regression modeling. CONCLUSIONS: The A-HFKT was revised using the content and construct validity data and is available for use with HF patients and FMs. The construct validity testing indicates that patient knowledge has a significant relationship to aspects of self-care. Furthermore, family knowledge may influence patient adherence with sodium restriction and healthcare utilization behavior

Different Reactive Oxygen Species Lead to Distinct Changes of Cellular Metal Ions in the Eukaryotic Model Organism Saccharomyces cerevisiae

Elemental uptake and export of the cell are tightly regulated thereby maintaining the ionomic homeostasis. This equilibrium can be disrupted upon exposure to exogenous reactive oxygen species (ROS), leading to reduction or elevation of the intracellular metal ions. In this study, the ionomic composition in the eukaryotic model organism Saccharomyces cerevisiae was profiled using the inductively-coupled plasma optical emission spectrometer (ICP-OES) following the treatment with individual ROS, including hydrogen peroxide, cumen hydroperoxide, linoleic acid hydroperoxide (LAH), the superoxide-generating agent menadione, the thiol-oxidising agent diamide [diazine-dicarboxylic acid-bis(dimethylamide)], dimedone and peroxynitrite. The findings demonstrated that different ROS resulted in distinct changes in cellular metal ions. Aluminium (Al3+) level rose up to 50-fold after the diamide treatment. Cellular potassium (K+) in LAH-treated cells was 26-fold less compared to the non-treated controls. The diamide-induced Al3+ accumulation was further validated by the enhanced Al3+ uptake along the time course and diamide doses. Pre-incubation of yeast with individual elements including iron, copper, manganese and magnesium failed to block diamide-induced Al3+ uptake, suggesting Al3+-specific transporters could be involved in Al3+ uptake. Furthermore, LAH-induced potassium depletion was validated by a rescue experiment in which addition of potassium increased yeast growth in LAH-containing media by 26% compared to LAH alone. Taken together, the data, for the first time, demonstrated the linkage between ionomic profiles and individual oxidative conditions

The Mitochondria-Targeted Methylglyoxal Sequestering Compound, MitoGamide, Is Cardioprotective in the Diabetic Heart

Abstract: Purpose: Methylglyoxal, a by-product of glycolysis and a precursor in the formation of advanced glycation end-products, is significantly elevated in the diabetic myocardium. Therefore, we sought to investigate the mitochondria-targeted methylglyoxal scavenger, MitoGamide, in an experimental model of spontaneous diabetic cardiomyopathy. Methods: Male 6-week-old Akita or wild type mice received daily oral gavage of MitoGamide or vehicle for 10 weeks. Several morphological and systemic parameters were assessed, as well as cardiac function by echocardiography. Results: Akita mice were smaller in size than wild type counterparts in terms of body weight and tibial length. Akita mice exhibited elevated blood glucose and glycated haemoglobin. Total heart and individual ventricles were all smaller in Akita mice. None of the aforementioned parameters was impacted by MitoGamide treatment. Echocardiographic analysis confirmed that cardiac dimensions were smaller in Akita hearts. Diastolic dysfunction was evident in Akita mice, and notably, MitoGamide treatment preferentially improved several of these markers, including e′/a′ ratio and E/e′ ratio. Conclusions: Our findings suggest that MitoGamide, a novel mitochondria-targeted approach, offers cardioprotection in experimental diabetes and therefore may offer therapeutic potential for the treatment of cardiomyopathy in patients with diabetes

Mapping Time-course Mitochondrial Adaptations in the Kidney in Experimental Diabetes

Abstract Oxidative phosphorylation drives ATP production by mitochondria, which are dynamic organelles, constantly fusing and dividing to maintain kidney homeostasis. In diabetic kidney disease, mitochondria appear dysfunctional, but the temporal development of diabetes-induced adaptations in mitochondrial structure and bioenergetics, have not been previously documented. Here, we map the changes in mitochondrial dynamics and function in rat kidney mitochondria at 4, 8, 16 and 32 weeks of diabetes. Our data reveal that changes in mitochondrial bioenergetics and dynamics precede the development of albuminuria and renal histological changes. Specifically, in early diabetes (4 weeks) a decrease in ATP content and mitochondrial fragmentation within proximal tubule epithelial cells of diabetic kidneys were clearly apparent, but no change urinary albumin excretion or glomerular morphology were evident at this time. By 8 weeks of diabetes, there was increased capacity for mitochondrial permeability transition (mPT) by pore opening, which persisted over time and correlated with mitochondrial hydrogen peroxide generation and glomerular damage. Late in diabetes, by week 16, tubular damage was evident with increased urinary Kidney injury molecule (Kim)-1 excretion, where an increase in Complex I-linked oxygen consumption rate, in the context of a decrease in kidney ATP, indicated mitochondrial uncoupling. Taken together, these data show that changes in mitochondrial bioenergetics and dynamics may precede the development of the renal lesion in diabetes, and this supports the hypothesis that mitochondrial dysfunction is a primary cause of diabetic kidney disease. Summary statement We identified that dysfunction of cellular power stations, mitochondria, may precede the development of kidney disease in diabetes. This suggests that mitochondrial dysfunction is a primary cause of diabetic nephropathy, which could be targeted to improve the burden of this disease. Short title: Mitochondrial adaptations in diabetic nephropath

Mapping time-course mitochondrial adaptations in the kidney in experimental diabetes

Abstract Oxidative phosphorylation (OXPHOS) drives ATP production by mitochondria, which are dynamic organelles, constantly fusing and dividing to maintain kidney homoeostasis. In diabetic kidney disease (DKD), mitochondria appear dysfunctional, but the temporal development of diabetes-induced adaptations in mitochondrial structure and bioenergetics have not been previously documented. In the present study, we map the changes in mitochondrial dynamics and function in rat kidney mitochondria at 4, 8, 16 and 32 weeks of diabetes. Our data reveal that changes in mitochondrial bioenergetics and dynamics precede the development of albuminuria and renal histological changes. Specifically, in early diabetes (4 weeks), a decrease in ATP content and mitochondrial fragmentation within proximal tubule epithelial cells (PTECs) of diabetic kidneys were clearly apparent, but no changes in urinary albumin excretion or glomerular morphology were evident at this time. By 8 weeks of diabetes, there was increased capacity for mitochondrial permeability transition (mPT) by pore opening, which persisted over time and correlated with mitochondrial hydrogen peroxide (H 2 O 2 ) generation and glomerular damage. Late in diabetes, by week 16, tubular damage was evident with increased urinary kidney injury molecule-1 (KIM-1) excretion, where an increase in the Complex I-linked oxygen consumption rate (OCR), in the context of a decrease in kidney ATP , indicated mitochondrial uncoupling. Taken together, these data show that changes in mitochondrial bioenergetics and dynamics may precede the development of the renal lesion in diabetes, and this supports the hypothesis that mitochondrial dysfunction is a primary cause of DKD