7 research outputs found
Depression mediates physical activity readiness and physical activity in patients with heart failure
Aims Although physical activity (PA) and exercise are essential for patients with heart failure (HF), adherence to the recommended guidelines is low. Not much is known about the mediating effect of HF patients mental state with their readiness for PA and reported activity levels. The purpose of this study is to investigate the mediatory effect of depression on PA readiness (physical limitation and psychological readiness) and self-reported PA in patients with HF. Methods and results In this cross-sectional study, 163 New York Heart Association Class I and II HF patients, during their clinic visit, reported on their physical limitation (PAR-Q) and psychological readiness [self-efficacy (ESES) and motivation (RM 4-FM)] for PA, depression (HADS-D), and PA (s-IPAQ). Mediation analysis was performed to test the mediating effect of depression on PA readiness (physical limitation and psychological readiness) and self-reported PA following the steps described by Baron and Kenny (1986). Hierarchical regression models were tested for their effects. The Self-Efficacy Theory and Self-Determination theory provided the theoretical platform for the study. Depression completely mediated the effect of physical limitation (beta(dep) = 268.57; P < 0.0001) and partially mediated the effect of self-efficacy on PA (beta(dep) = 344.16; P < 0.0001). Both intrinsic (P < .0001) and extrinsic motivation (P < .0001) for PA had an independent and significant effect on PA, not mediated by depression. Conclusions Patients with HF should be screened for depression throughout the trajectory of the disease as it can impact their physical and psychological readiness to perform PA
Physical Activity Readiness in Patients with Heart Failure
The aim of this study was to explore the readiness for physical activity (PA) and its related factors in patients with heart failure. This cross-sectional study included 163 patients with heart failure (mean age 66 +/- 16, 50% female). The ability to safely engage in PA was assessed with the PA Readiness Questionnaire (PAR-Q). Psychological readiness was measured using two questionnaires, namely: Exercise Self-efficacy Scale and the Motivation for PA and Exercise/Working Out. A multivariate analysis of covariance was conducted to test the effect of background variables on readiness for PA. 64% (n = 105) of patients reported not being able to safely engage in PA, 80% (n = 129) reported low self-efficacy, and 45% (n = 74) were extrinsically motivated indicating external factors drove their motivation. Factors that positively influenced the PA readiness included lower age (p < 0.01), being male (p < 0.01), being married (p < 0.01), having higher education (p < 0.01), being in NYHA-class I compared with II (p < 0.01), less time since diagnosis (p < 0.01), lower BMI (p = 0.02), and not suffering from COPD (p = 0.02). Prior to recommending exercise, assessment of safety to engage in PA along with self-efficacy and motivation in patients with heart failure is essential
Physical activity enjoyment, exercise motivation, and physical activity in patients with heart failure : A mediation analysis
Objective To determine whether physical activity enjoyment mediated the association between motivation and physical activity in patients with heart failure. Design and setting A cross-sectional study at the cardiology clinic in the university hospital in Valencia, Spain Subjects A total of 134 patients with heart failure. Main measurements Physical activity was assessed with the International Physical Activity Questionnaire, motivation was assessed with the Exercise Motivation Index and Physical Activity Enjoyment was assessed with the Physical Activity Enjoyment Scale. Analysis Mediation analysis using Hayes PROCESS macro (Model 4) for SPSS. Results The mean age of the sample was 70 +/- 14 years, 47 patients were female (35%), and 87 patients were in New York Heart Association I/II (67%). A positive relationship was found between exercise motivation and physical activity (t = 4.57, p < .01) and physical activity enjoyment (t = 11.52, p < .01). Physical activity enjoyment was found to positively affect physical activity (t = 3.50, p < .01). After controlling for physical activity enjoyment, the effect of exercise motivation on physical activity changed from a significant to non-significant (t = 1.33, p = .89), indicating that enjoyment completely mediated the relationship between motivation and physical activity. Overall, 25% of the variation in physical activity was explained by the mediation model. Conclusions Physical activity enjoyment mediates the relationship between exercise motivation and physical activity in patients with heart failure. This means that even highly motivated heart failure patients may not be physically active if they do not enjoy the physical activity
Cardiac Allograft Rejection Induces Changes in Nucleocytoplasmic Transport: RANGAP1 as a Potential Non-Invasive Biomarker
The non-invasive diagnosis of acute cellular rejection (ACR) is a major challenge. We performed a molecular study analyzing the predictive capacity of serum RanGTPase AP1 (RANGAP1) for diagnosing ACR during the first year after heart transplantation (HT). We included the serum samples of 75 consecutive HT patients, extracted after clinical stability, to determine the RANGAP1 levels through ELISA. In addition, various clinical, analytical, and echocardiographic variables, as well as endomyocardial biopsy results, were collected. RANGAP1 levels were higher in patients who developed ACR (median 63.15 ng/mL; (inter-quartile range (IQR), 36.61–105.69) vs. 35.33 ng/mL (IQR, 19.18–64.59); p = 0.02). Receiver operating characteristic (ROC) curve analysis confirmed that RANGAP1 differentiated between patients with and without ACR (area under curve (AUC), 0.70; p = 0.02), and a RANGAP1 level exceeding the cut-off point (≥90 ng/mL) was identified as a risk factor for the development of ACR (OR, 6.8; p = 0.006). Two independent predictors of ACR identified in this study were higher RANGAP1 and N-terminal pro-brain natriuretic peptide levels. The analysis of the ROC curve of the model showed a significant AUC of 0.77, p = 0.001. Our findings suggest that RANGAP1 quantification facilitates risk prediction for the occurrence of ACR and could be considered as a novel non-invasive biomarker of ACR
Identification of gene mutations and fusion genes in patients with Sézary syndrome.
Sézary syndrome is a leukemic form of cutaneous T-cell lymphoma with an aggressive clinical course. The genetic etiology of the disease is poorly understood, with chromosomal abnormalities and mutations in some genes being involved in the disease. The goal of our study was to understand the genetic basis of the disease by looking for driver gene mutations and fusion genes in 15 erythrodermic patients with circulating Sézary cells, 14 of them fulfilling the diagnostic criteria of Sézary syndrome. We have discovered genes that could be involved in the pathogenesis of Sézary syndrome. Some of the genes that are affected by somatic point mutations include ITPR1, ITPR2, DSC1, RIPK2, IL6, and RAG2, with some of them mutated in more than one patient. We observed several somatic copy number variations shared between patients, including deletions and duplications of large segments of chromosome 17. Genes with potential function in the T-cell receptor signaling pathway and tumorigenesis were disrupted in Sézary syndrome patients, for example, CBLB, RASA2, BCL7C, RAMP3, TBRG4, and DAD1. Furthermore, we discovered several fusion events of interest involving RASA2, NFKB2, BCR, FASN, ZEB1, TYK2, and SGMS1. Our work has implications for the development of potential therapeutic approaches for this aggressive disease.This project was funded by “Retos de la Sociedad 2013: Europa Redes y Gestores” Programme from the Spanish Ministry of Economy and Competitiveness no. SAF2013-49108-R (to XE) and RD12/0036/0044 Red Temática de Investigación Cooperativa en Cancer, Fondo Europeo de Desarrollo Regional (to BE, FG, and RP), the Generalitat de Catalunya AGAUR 2014 SGR-1138 (to XE) and 2014 SGR-585 (to BE, A Puiggros, and FG), the European Commission 7th Framework Program (FP7/2007-2013) under grant agreement 282510 (A BLUEPRINT of haematopoietic Epigenomes to XE) and 262055 (European Sequencing and Genotyping Infrastructure to XE), Instituto de Salud Carlos III FEDER (PT13/0010/0005), and the “Xarxa de Bancs de tumors sponsored by Pla Director d’Oncologia de Catalunya.” We would also like to thank “Xarxa de Limfomes Cutanis de Catalunaya.” A Prasad is a Marie Curie Postdoctoral fellow supported by the European Commission 7th framework program (FP7/2007-2013) under grant agreement no. 625356. We acknowledge the support of the Spanish Ministry of Economy and Competitiveness, Centro de Excelencia Severo Ochoa 2013-2017, SEV-2012-0208