Effect of exercise on depressive symptoms in patients with heart failure

Background & Aim: Depression is common among cardiac patients, especially patients with heart failure and leads to a poor prognosis. This study aimed to assess the effect of exercise on depressive symptoms in patients with heart failure, attending the Cardiac Rehabilitation Center. Methods & Materials: In this clinical trial, 60 patients with NYHA class II and III heart failure who referred to the Cardiac Rehabilitation Center of Shafa Hospital affiliated to Kerman University of Medical Sciences in 2015 were randomly assigned into two groups of 30 patients. Subjects in the intervention group participated in a supervised 8-week exercise program, 3 days per week, while those in the control group only received standard routine care. Data were collected before and after the intervention by the demographic form and the Personal Health Questionnaire Depression Scale (PHQ-8). Data analysis was done by Chi-Square, Wilcoxon, Mann-Whitney U and Nonparametric ANCOVA tests using the SPSS version 21 and R software. Results: The two groups were homogeneous in terms of depression score before the intervention. The median and interquartile range of the score of depression were 10 (5.25) in the control group and 8.5 (9.25) in the intervention group which showed a significant difference (P=0.042). By adjusting the variables of the duration of the disease and the pre-test scores of depression symptoms by non-parametric covariance test, the difference between the two groups was also significant. Conclusion: Exercise can reduce depressive symptoms in patients with heart failure. Clinical trial registry: IRCT201605107844N1

The impact of cardiac rehabilitation on pulmonary artery systolic pressure and left ventricular end-diastolic pressure in patients after coronary artery bypass graft surgery

Background: Cardiac rehabilitation program (CRP) is a useful method of modifying cardiovascular risk factors, improving life expectancy and quality of life in patients with ischemic heart disease (IHD). The present study was conducted to evaluate the effects of cardiac rehabilitation on the pulmonary artery systolic pressure (PASP) and left ventricular end-diastolic pressure (LVEDP). Methods: This Quasi-experimental study with pretest-posttest design was conducted on 80 patients with IHD who had participated in CRP after undergoing coronary artery bypass graft (CABG) surgery. Echocardiography was performed before the beginning of CRP (the 1st session) and at the end of the rehabilitation sessions, and ventricular function indices (ejection fraction), PASP (using the tricuspid regurgitation velocity), and LVEDP (using Nagueh formula: 1.24�E/e�+1.9) were measured. Results: Ejection fraction (EF) was changed from 49.3 ± 7.8 before rehabilitation to 50.7 ± 7.4 after rehabilitation, which was a statistically significant difference (P=0.003). The pulmonary artery systolic pressure altered from 30.3 ± 8.4 before rehabilitation to 27.3 ± 6.6 after rehabilitation. The left ventricular end-diastolic pressure (LVEDP) changed from 10.5 ± 3.7 before rehabilitation to 9.1 ± 2.9 after rehabilitation, which was a statistically significant difference (P=0.000). Conclusion: According to the results, LVEDP and PASP in patients with IHD who underwent CABGs decreased after cardiac rehabilitation. © 2020, Kerman University of Medical Sciences. All rights reserved

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease