Background: Physical training currently constitutes an important part of treatment of heart failure patients. So far, no data are available on the effects of regular exercise in elderly (aged > 65 years) heart failure patients.
Methods: In a prospective trial, patients with chronic heart failure (New York Heart Association class II and III) were randomly assigned to a training group and a control group. Patients in the training group performed additional exercises three times a week, while patients in the control group continued regular treatment. To analyse the influence of age, both groups were subdivided into subjects younger than and older than 65 years. The effect of training on exercise parameters was evaluated by means of a treadmill test. Quality of life aspects were evaluated with the help of the Heart Patients Psychological Questionnaire and a single-question Self Awareness of General Well-Being test.
Results: Comparison of changes between groups revealed that training increased the duration of the exercise test and improved aspects of quality of life in the trained patients aged both younger than and older than 65 years.
Conclusion: Exercise training is equally effective in patients aged younger than and older than 65 years.
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http://dx.doi.org/10.1097/00019501-199809110-00010 | DOI Listing |
Can J Physiol Pharmacol
January 2025
Dalhousie University, Department of Physiology and Biophysics, Halifax, Canada;
A growing body of evidence suggest that the stem cell antigen-1 expressing (Sca-1) cells in the heart may be the cardiac endothelial stem/progenitor cells. Their endothelial cell (EC) functions, and their role in RV physiology and pathophysiology of right heart failure (RHF) remains poorly defined. This study investigated EC characteristics of rat cardiac Sca-1 cells, assessed spatial distribution and studied changes in Sca1 cells during RV remodelling in monocrotaline (MCT) model of pulmonary hypertension and RV remodeling.
View Article and Find Full Text PDFJ Cardiovasc Med (Hagerstown)
February 2025
Division of Cardiology, Department of Systems Medicine, Tor Vergata University, Rome.
Atrial cardiomyopathy (AC) has been defined by the European Heart Rhythm Association as "Any complex of structural, architectural, contractile, or electrophysiologic changes in the atria with the potential to produce clinically relevant manifestations".1 The left atrium (LA) plays a key role in maintaining normal cardiac function; in fact atrial dysfunction has emerged as an essential determinant of outcomes in different clinical scenarios, such as valvular diseases, heart failure (HF), coronary artery disease (CAD) and atrial fibrillation (AF). A comprehensive evaluation, both anatomical and functional, is routinely performed in cardiac imaging laboratories.
View Article and Find Full Text PDFJ Cardiovasc Med (Hagerstown)
February 2025
Cardiology Unit, Azienda Ospedaliera Universitaria di Ferrara, Cona, Ferrara, Italy.
Introduction: Cardiac amyloidosis typically causes restrictive cardiomyopathy, in which the impairment of diastolic function is dominant. Echocardiography provides prognostic information through some important parameters: left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS). However, LVEF often remains preserved despite disease progression, and GLS is not routinely performed as it is limited by suboptimal image quality.
View Article and Find Full Text PDFSci Adv
January 2025
Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Protein homeostasis is crucial for maintaining cardiomyocyte (CM) function. Disruption of proteostasis results in accumulation of protein aggregates causing cardiac pathologies such as hypertrophy, dilated cardiomyopathy (DCM), and heart failure. Here, we identify ubiquitin-specific peptidase 5 (USP5) as a critical determinant of protein quality control (PQC) in CM.
View Article and Find Full Text PDFSci Transl Med
January 2025
Center for Transplantation Sciences, Department of Surgery, Massachusetts General Hospital, Boston, MA 02114, USA.
Long-term, immunosuppression-free allograft survival has been induced in human and nonhuman primate (NHP) kidney recipients after nonmyeloablative conditioning and donor bone marrow transplantation (DBMT), resulting in transient mixed hematopoietic chimerism. However, the same strategy has consistently failed in NHP heart transplant recipients. Here, we investigated whether long-term heart allograft survival could be achieved by cotransplanting kidneys from the same donor.
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