Cardiac Failure Review最新文献

Heart failure (HF) is a major contributor to hospitalisations and accounts for 7% of cardiovascular-related deaths, with patients who have chronic kidney disease and type 2 diabetes at heightened risk. Existing treatment guidelines inadequately address these comorbidities. Steroidal mineralocorticoid receptor antagonists (MRAs) are commonly used in HF with reduced ejection fraction but pose risks, such as hyperkalaemia and acute kidney injury. Finerenone, a non-steroidal MRA, offers a safer alternative, with higher selectivity, reduced electrolyte disturbances and beneficial effects on heart and kidney tissues. Preclinical studies show anti-inflammatory and anti-fibrotic effects, while phase III trials (ARTS and ARTS-HF) demonstrated fewer hyperkalaemia incidents compared with spironolactone. In phase III trials (FIDELIO-DKD and FIGARO-DKD), finerenone reduced HF hospitalisations by 22% in patients with chronic kidney disease and type 2 diabetes. The FINEARTS-HF trial found that finerenone significantly reduced the risk of worsening HF events or CV death in patients with HF with mildly reduced or preserved ejection fraction. Its combination with therapies, such as sodium-glucose cotransporter 2 inhibitors, shows promise and ongoing trials, such as REDEFINE-HF, FINALITY-HF and CONFIRMATION-HF, are investigating its efficacy in other HF phenotypes. These studies will further establish the role of finerenone in managing cardio-renal-metabolic diseases.

Aldosterone is a key regulator of fluid and electrolyte balance in the body. It is often dysregulated in heart failure (HF) and is a key driver of cardiac remodelling and worse clinical outcomes. Potassium regulation is essential for normal cardiac, gastrointestinal and neuromuscular function. Serum potassium fluctuations are largely determined by aldosterone, the final step of the renin-angiotensin-aldosterone system. Dyskalaemia (i.e. hypokalaemia and hyperkalaemia) is prevalent in HF because of the disease itself, its therapies and related comorbidities such as chronic kidney disease. Prognostic implications of abnormal serum potassium follow a U-shaped curve, where both hypokalaemia and hyperkalaemia are associated with adverse outcomes. Hypokalaemia is associated with increased mortality, starting from potassium <4.0 mmol/l but especially at potassium <3.5 mmol/l. Hyperkalaemia, along with increasing arrhythmia risk, limits the use of lifesaving renin-angiotensin- aldosterone system inhibitors, which may have long-term survival implications. The advent of novel potassium binders aims to manage chronic hyperkalaemia and may allow for uptitration and optimal dosing of guideline-recommended therapy. This review discusses the impacts of dyskalaemia in HF, along with management strategies, including the relevance of potassium binder use in optimising HF treatment. Current and potential future aldosterone-modulating therapies, such as non-steroidal mineralocorticoid receptor antagonists and aldosterone synthase inhibitors, are also discussed.

Activation of the renin-angiotensin-aldosterone system is the ultimate pathophysiological hallmark in heart failure. Though aldosterone primarily appears to regulate electrolyte homeostasis by acting on distal nephrons in the kidneys, its effects are far-reaching across the cardiovascular system as its receptors are also expressed in vascular smooth muscle cells, endothelial cells, macrophages and cardiomyocytes. Aldosterone excess leads to vascular stiffness, vasoconstriction, endothelial dysfunction, inflammation, oxidative stress, cardiac fibrosis and hypertrophy, atherogenesis and thrombosis. Hence, aldosterone antagonism is an attractive proposition for heart failure management. The first-generation non-selective mineralocorticoid receptor antagonist spironolactone produced a spectacular reduction of cardiovascular outcomes in the seminal RALES study, while the selective second-generation congener eplerenone boasts two positive studies: EPHESUS and EMPHASIS-HF. The TOPCAT trial indicated that a specific subgroup of patients with heart failure with preserved ejection fraction may benefit from targeted therapy of mineralocorticoid receptor antagonists. Newer-generation non-steroidal mineralocorticoid antagonists and aldosterone synthase inhibitors are being evaluated in randomised trials.

This review examines the effects of glucagon-like peptide-1 receptor agonists (GLP-1RAs) on different heart failure phenotypes with preserved ejection fraction (HFpEF). Traditional heart failure treatment modalities have shown limited success in improving outcomes for patients with HFpEF, but new evidence suggests that GLP-1RAs could be beneficial. The positive effects of GLP-1RAs are likely due to their ability to reduce systemic inflammation, enhance metabolism and directly affect the cardiovascular system, addressing critical aspects of HFpEF pathology. However, the exact impact of GLP-1RAs on clinical outcomes for different HFpEF phenotypes is still unclear. This review highlights both the potential benefits and the current limitations of GLP-1RA therapy, suggesting a careful approach for their application in clinical practice.

Acutely decompensated heart failure is one of the leading causes of hospitalisation worldwide, with a significant majority of these cases attributed to congestion. Although congestion is commonly mistaken for volume overload, evidence suggests that decompensation can occur without significant water accumulation, being attributed to volume redistribution. Yet, the distinction between intravascular and extravascular congestion in heart failure often blurs, as patients frequently exhibit overlapping features of both, and as patients may transition between phenotypes over time. Considering that differentiation between intravascular and extravascular congestion can lead to different management strategies, the aim of this review was to delineate the pathophysiological nuances between the two, as well as their correlation with clinical, biochemical and imaging indices.

This paper delves into the significance of imaging in the diagnosis, aetiology and therapeutic guidance of heart failure, aiming to facilitate early referral and improve patient outcomes. Imaging plays a crucial role not only in assessing left ventricular ejection fraction, but also in characterising the underlying cardiac abnormalities and reaching a specific diagnosis. By providing valuable data on cardiac structure, function and haemodynamics, imaging helps diagnose the condition, evaluate haemodynamic status and, consequently, identify the underlying pathophysiological phenotype, as well as stratifying the risk for outcomes. In this article, we provide a comprehensive exploration of these aspects.

Transcatheter aortic valve replacement (TAVR) has undergone rapid expansion, emerging as a viable therapeutic option for low-risk patients in lieu of surgical aortic valve replacement. This paper aims to provide a review of the scientific evidence concerning TAVR in low-risk patients, encompassing both observational and clinical trial data. Furthermore, a substantial proportion of low-risk patients possesses a bicuspid aortic valve, necessitating careful examination of the pertinent anatomic and clinical considerations to TAVR that is highlighted in this review. Additionally, the review expands upon some of the unique challenges associated with alternate access in low-risk patients evaluated for TAVR. Last, this review outlines the pivotal role of a multidisciplinary heart team approach in the execution of all TAVR procedures and the authors' vision of 'minimalist TAVR' as a new era in low-risk TAVR.

Glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) are emerging glucose-lowering agents primarily used in managing diabetes and obesity. Recently, GLP-1 RAs have garnered attention for their cardiovascular benefits beyond glycaemic control in patients with type 2 diabetes, exhibiting patterns previously seen in cardiovascular outcomes trials on sodium-glucose cotransporter 2 inhibitors, which now receive a high level of recommendation for the treatment of heart failure (HF). GLP-1 RAs have been increasingly investigated in HF cohorts, but mainly in small-scale studies reporting inconclusive findings regarding clinical outcomes and different safety profiles in HF patients with reduced and preserved ejection fractions. This review discusses the effects of GLP-1 RAs on surrogate HF outcomes, such as cardiac structure and function, exercise capacity and quality of life, in HF patients across the spectrum of left ventricular ejection fraction, to provide insights into the potential of these agents to be investigated in large clinical trials to evaluate clinical outcomes.

Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are now recommended in the current European Society of Cardiology/American College of Cardiology guidelines for the treatment of heart failure (HF) across the spectrum of left ventricular ejection fraction (LVEF) and several large trials have documented the beneficial effects of this drug class on cardiovascular outcomes. Although the clinical efficacy of SGLT-2 inhibition in HF is now well recognised, research is still ongoing to better understand the underlying mechanistic effects of this drug class. In this paper we assess the haemodynamic effects following SGLT-2i treatment in HF patients by reviewing the current literature. We focus our review on preload of the LV in terms of filling pressure and pulmonary artery pressure, cardiac output and afterload. We discuss these variables stratified according to HF with reduced LVEF (HFrEF) and HF with preserved LVEF (HFpEF). Finally, we examine the evidence of LV remodelling in the setting of SGLT-2i-related changes in haemodynamics.