Heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF) are subtypes of heart failure with overlapping clinical features but have some distinct functional characteristics and cellular and molecular mechanisms. Exercise training is an accessible, non-pharmacological therapy recommended for the management of HFrEF and is increasingly showing promise for treating HFpEF. This review summarises the underlying pathophysiology of HFrEF and HFpEF and the evidence from clinical and preclinical studies showing that exercise training can improve cardiac function. The authors also summarise the underlying cellular and molecular mechanisms between HFrEF and HFpEF, with respect to cardiac remodelling, fibrosis, mitochondrial adaptations and metabolism, inflammation and inter-organ crosstalk, and provide evidence that exercise training elicits protective adaptations in HFrEF and HFpEF through some different signalling pathways targeted by exercise. Finally, the authors discuss the use of exercise training as a therapeutic intervention for HFrEF and HFpEF through personalised training by phenotype and in combination with emerging pharmacological treatments.
Obstructive sleep apnoea and central sleep apnoea are common disorders, particularly in people with congestive heart failure. Continuous positive airway pressure provides transformative benefits for some patients, but is not always well tolerated. Thus, considerable focus is now being placed on alternative therapies for sleep-disordered breathing, including non-positive airway pressure therapy. Advances in pharmacology have led to a variety of options to treat both obstructive and central sleep apnoea. In addition, these approaches may have major benefits from the perspective of preventing the complications of sleep-disordered breathing. In the case of tirzepatide, the Food and Drug Administration recently approved this medication for the treatment of moderate-to-severe sleep apnoea in people with obesity. However, further data are required regarding how best to improve both subjective and objective hard outcomes in people with congestive heart failure and sleep-disordered breathing.
Typically, heart failure (HF) is definitively diagnosed and treated with guideline-directed medical therapy late in its natural history, with reported delays, missed investigation and inpatient diagnoses associated with poor outcomes. Accordingly, better, more decisive primary care can and should play a critical role in addressing this seemingly intractable problem. However, as reflected by a paucity of evidence to inform the recommendations of expert HF guidelines, primary care teams are rarely considered as part of the solution. In this review, we explore all the potential outcomes from more proactive screening for HF in primary care when introducing artificial intelligence-mediated portable cardiac ultrasound. Based on the strengths and weaknesses of the screening components that can now be applied, we consider the spectrum of early to late forms of HF likely to be revealed and more immediately diagnosed. Within this context, we present, as an example of what can be achieved in this space, a clinical algorithm that was developed for a prospective, multicentre project to find and manage HF earlier in the primary care setting.
The prevalence of obesity among the general population has resulted in significant overlap and complex interactions with heart failure. This review aims to describe recent changes to the definition of obesity and explore direct and indirect mechanistic links between obesity and heart failure. Diagnostic challenges presented by obesity regarding echocardiography and B-type natriuretic peptide are also explored. Treatment options and the evidence base for addressing obesity in heart failure are examined across both heart failure with preserved ejection fraction and heart failure with reduced ejection fraction. Finally, the safety profile of new incretin-based therapies is examined.
