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[Figure: see text].

Objective: Although research has been conducted on how nurse staffing levels affect outcomes, there has been little investigation into how the health-related productivity of nurses is related to quality of care. Two major causes of worker presenteeism (reduced on-the-job productivity as a result of health problems) are musculoskeletal pain and mental health issues, particularly depression. This study sought to investigate the extent to which musculoskeletal pain or depression (or both) in RNs affects their work productivity and self-reported quality of care and considered the associated costs., Methods: Using a cross-sectional survey design, a random sample of 2,500 hospital-employed RNs licensed in North Carolina were surveyed using a survey instrument sent by postal mail. Specific measures included questions on individual and workplace characteristics, self-reported quality of care, and patient safety; a numeric pain rating scale, a depression tool (the Patient Health Questionnaire), and a presenteeism tool (the Work Productivity and Activity Impairment Questionnaire: General Health) were also incorporated. A total of 1,171 completed surveys were returned and used for analysis., Results: Among respondents, the prevalence of musculoskeletal pain was 71%; that of depression was 18%. The majority of respondents (62%) reported a presenteeism score of at least 1 on a 0-to-10 scale, indicating that health problems had affected work productivity at least "a little." Pain and depression were significantly associated with presenteeism. Presenteeism was significantly associated with a higher number of patient falls, a higher number of medication errors, and lower quality-of-care scores. Baseline cost estimates indicate that the increased falls and medication errors caused by presenteeism are expected to cost $1,346 per North Carolina RN and just under $2 billion for the United States annually. Upper-boundary estimates exceed $9,000 per North Carolina RN and $13 billion for the nation annually., Conclusion: More attention must be paid to the health of the nursing workforce to positively influence the quality of patient care and patient safety and to control costs.

Background: Hemodynamic load regulates myocardial function and gene expression. We tested the hypothesis that afterload and preload, despite similar average load, result in different phenotypes., Methods and Results: Afterload and preload were compared in mice with transverse aortic constriction (TAC) and aortocaval shunt (shunt). Compared with sham mice, 6 hours after surgery, systolic wall stress (afterload) was increased in TAC mice (+40%; P<0.05), diastolic wall stress (preload) was increased in shunt (+277%; P<0.05) and TAC mice (+74%; P<0.05), and mean total wall stress was similarly increased in TAC (69%) and shunt mice (67%) (P=NS, TAC versus shunt; each P<0.05 versus sham). At 1 week, left ventricular weight/tibia length was significantly increased by 22% in TAC and 29% in shunt mice (P=NS, TAC versus shunt). After 24 hours and 1 week, calcium/calmodulin-dependent protein kinase II signaling was increased in TAC. This resulted in altered calcium cycling, including increased L-type calcium current, calcium transients, fractional sarcoplasmic reticulum calcium release, and calcium spark frequency. In shunt mice, Akt phosphorylation was increased. TAC was associated with inflammation, fibrosis, and cardiomyocyte apoptosis. The latter was significantly reduced in calcium/calmodulin-dependent protein kinase IIdelta-knockout TAC mice. A total of 157 mRNAs and 13 microRNAs were differentially regulated in TAC versus shunt mice. After 8 weeks, fractional shortening was lower and mortality was higher in TAC versus shunt mice., Conclusions: Afterload results in maladaptive fibrotic hypertrophy with calcium/calmodulin-dependent protein kinase II-dependent altered calcium cycling and apoptosis. Preload is associated with Akt activation without fibrosis, little apoptosis, better function, and lower mortality. This indicates that different loads result in distinct phenotype differences that may require specific pharmacological interventions.

Background: Oxygen (O(2)) homeostasis is central to myocardial tissue functioning, and increased O(2) demand is thought to be satisfied by a vasodilatory mechanism that results in increased blood and O(2) delivery. We applied blood oxygenation level-dependent (BOLD) MRI in conjunction with vasodilatory stress to index the ability to augment intramyocardial oxygenation in hypertensive hypertrophy, the primary cause of heart failure., Methods and Results: Nine healthy controls and 10 hypertensive subjects with moderate-to-severe hypertrophy underwent imaging on a 1.5 T clinical scanner. The dipyridamole-induced change in the apparent transverse relaxation rate, R2*, which correlates with hemoglobin oxygenation, was -5.4+/-2.2 s(-1) (95% CI, -4.0 to -6.8 s(-1)) in controls compared with -1.7+/-1.4 s(-1) (95% CI, -0.8 to -2.6 s(-1)) in hypertensive patients (P=0.0003)., Conclusions: Patients with hypertensive hypertrophy demonstrate an impaired ability to increase intramyocardial oxygenation during vasodilatory stress, as indexed by BOLD MRI. The capacity to image vascular function with BOLD MRI may advance the understanding of the development of ventricular dysfunction in hypertension.