Overcoming barriers to engagement and adherence to a home-based physical activity intervention for patients with heart failure:a qualitative focus group study

Clinical guidelines recommend regular physical activity for patients with heart failure to improve functional capacity and symptoms and to reduce hospitalisation. Cardiac rehabilitation programmes have demonstrated success in this regard; however, uptake and adherence are suboptimal. Home-based physical activity programmes have gained popularity to address these issues, although it is acknowledged that their ability to provide personalised support will impact on their effectiveness. This study aimed to identify barriers and facilitators to engagement and adherence to a home-based physical activity programme, and to identify ways in which it could be integrated into the care pathway for patients with heart failure. A qualitative focus group study was conducted. Data were analysed using thematic analysis. A purposive sample of 16 patients, 82% male, aged 68±7 years, with heart failure duration of 10±9 years were recruited. A 12-week behavioural intervention targeting physical activity was delivered once per week by telephone. Ten main themes were generated that provided a comprehensive overview of the active ingredients of the intervention in terms of engagement and adherence. Fear of undertaking physical activity was reported to be a significant barrier to engagement. Influences of family members were both barriers and facilitators to engagement and adherence. Facilitators included endorsement of the intervention by clinicians knowledgeable about physical activity in the context of heart failure; ongoing support and personalised feedback from team members, including tailoring to meet individual needs, overcome barriers and increase confidence. Endorsement of interventions by clinicians to reduce patients' fear of undertaking physical activity and individual tailoring to overcome barriers are necessary for long-term adherence. Encouraging family members to attend consultations to address misconceptions and fear about the contraindications of physical activity in the context of heart failure should be considered for adherence, and peer-support for long-term maintenance. NCT03677271. [Abstract copyright: © Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY. Published by BMJ.

Haemodynamic determinants of quality of life in chronic heart failure

BACKGROUND: Heart failure patients demonstrate reduced functional capacity, hemodynamic function, and quality of life (QOL) which are associated with high mortality and morbidity rate. The aim of the present study was to assess the relationship between functional capacity, hemodynamic response to exercise and QOL in chronic heart failure. METHODS: A single-centre prospective study recruited 42 chronic heart failure patients (11 females, mean age 60 ± 10 years) with reduced left ventricular ejection fraction (LVEF = 23 ± 7%). All participants completed a maximal graded cardiopulmonary exercise test with non-invasive hemodynamic (bioreactance) monitoring. QOL was assessed using Minnesota Living with Heart Failure Questionnaire. RESULTS: The average value of QOL score was 40 ± 23. There was a significant negative relationship between the QOL and peak O(2) consumption (r = − 0.50, p ≤ 0.01). No significant relationship between the QOL and selected exercise hemodynamic measures was found, including peak exercise cardiac power output (r = 0.15, p = 0.34), cardiac output (r = 0.22, p = 0.15), and mean arterial blood pressure (r = − 0.08, p = 0.60). CONCLUSION: Peak O(2) consumption, but not hemodynamic response to exercise, is a significant determinant of QOL in chronic heart failure patients

Heterogeneous abnormalities of in-vivo left ventricular calcium influx and function in mouse models of muscular dystrophy cardiomyopathy

BACKGROUND: Manganese-enhanced cardiovascular magnetic resonance (MECMR) can non-invasively assess myocardial calcium influx, and calcium levels are known to be elevated in muscular dystrophy cardiomyopathy based on cellular studies. METHODS: Left ventricular functional studies and MECMR were performed in mdx mice (model of Duchenne Muscular Dystrophy, 24 and 40 weeks) and Sgcd−/− mice (Limb Girdle Muscular Dystrophy 2 F, 16 and 32 weeks), compared to wild type controls (C57Bl/10, WT). RESULTS: Both models had left ventricular hypertrophy at the later age compared to WT, though the mdx mice had reduced stroke volumes and the Sgcd−/− mice increased heart rate and cardiac index. Especially at the younger ages, MECMR was significantly elevated in both models (both P<0.05 versus WT). The L-type calcium channel inhibitor diltiazem (5 mg/kg i.p.) significantly reduced MECMR in the mdx mice (P<0.01), though only with a higher dose (10 mg/kg i.p.) in the Sgcd−/− mice (P<0.05). As the Sgcd−/− mice had increased heart rates, to determine the role of heart rate in MECMR we studied the hyperpolarization-activated cyclic nucleotide-gated channel inhibitor ZD 7288 which selectively reduces heart rate. This reduced heart rate and MECMR in all mouse groups. However, when looking at the time course of reduction of MECMR in the Sgcd−/− mice at up to 5 minutes of the manganese infusion when heart rates were matched to the WT mice, MECMR was still significantly elevated in the Sgcd−/− mice (P<0.01) indicating that heart rate alone could not account for all the increased MECMR. CONCLUSIONS: Despite both mouse models exhibiting increased in-vivo calcium influx at an early stage in the development of the cardiomyopathy before left ventricular hypertrophy, there are distinct phenotypical differences between the 2 models in terms of heart rates, hemodynamics and responses to calcium channel inhibitors

Pathophysiology of exercise intolerance in chronic diseases: the role of diminished cardiac performance in mitochondrial and heart failure patients

Objective: Exercise intolerance is a clinical hallmark of chronic conditions. The present study determined pathophysiological mechanisms of exercise intolerance in cardiovascular, neuromuscular, and metabolic disorders. Methods: In a prospective cross-sectional observational study 152 patients (heart failure reduced ejection fraction, n=32; stroke, n=34; mitochondrial disease, n=28; type two diabetes, n=28; and healthy controls, n=30) performed cardiopulmonary exercise testing with metabolic and haemodynamic measurements. Peak exercise O2 consumption and cardiac power output were measures of exercise tolerance and cardiac performance. Results: Exercise tolerance was significantly diminished in patients compared with controls (ie, by 45% stroke, 39% mitochondria disease, and 33% diabetes and heart failure, p&lt;0.05). Cardiac performance was only significantly reduced in heart failure (due to reduced heart rate, stroke volume, and blood pressure) and mitochondrial patients (due reduced stroke volume) compared with controls (ie, by 53% and 26%, p&lt;0.05). Ability of skeletal muscles to extract oxygen (ie, arterial-venous O2 difference) was diminished in mitochondrial, stroke, and diabetes patients (by 24%, 22%, and 18%, p&lt;0.05), but increased by 21% in heart failure (p&lt;0.05) compared with controls. Cardiac output explained 65% and 51% of the variance in peak O2 consumption (p&lt;0.01) in heart failure and mitochondrial patients, whereas arterial-venous O2 difference explained 69% (p&lt;0.01) of variance in peak O2 consumption in diabetes, and 65% and 48% in stroke and mitochondrial patients (p&lt;0.01). Conclusions: Different mechanisms explain exercise intolerance in patients with heart failure, mitochondrial dysfunction, stroke and diabetes. Their better understanding may improve management of patients, their stress tolerance and quality of life