Heart Failure Reviews最新文献

Worsening heart failure (WHF) is a major clinical and economic challenge, contributing to high rates of hospitalization and significant healthcare costs. While WHF has traditionally been managed through hospitalization, recent approaches are shifting toward outpatient care to maximize patient time spent at home and optimize allocation of hospital resources. Emerging treatments like subcutaneous furosemide and intranasal bumetanide offer promising alternatives for safe, well-tolerated, and effective diuresis outside the hospital. However, these novel strategies face several challenges, including the need for clinician/staff training, patient education, logistical difficulties, and a lack of evidence in diverse populations. To ensure equitable management, it is also essential to address healthcare disparities, particularly in socioeconomically disadvantaged and rural populations. While these new treatments have the potential to improve care delivery, additional research is necessary to assess their comparative effectiveness and overcome current limitations fully.

The prevalence of HFpEF is rising, especially among older females. Females possess unique attributes in their cardiovascular risk factor profiles, cardiac remodeling patterns, and sex hormonal composition that predispose them to an increased risk of developing HFpEF in comparison to males. Although comorbidities play an important role in driving the cardiac and extracardiac abnormalities manifested in HFpEF, there are ventricular-vascular properties that cannot be explained by comorbidities alone. The "hypertension, arterial stiffness and cardiac remodeling" and "obesity, chronic inflammation and microvascular dysfunction" phenotypic profiles represent two pathophysiological mechanistic pathways that are predominant in the HFpEF syndrome among females. While females exhibit worse symptoms and signs of congestion as well as poorer quality of life, they generally have better clinical outcomes in comparison to males. In this review, we will discuss the available evidence on the sex differences that exist in HFpEF including its pathophysiology, clinical presentation, and outcomes, while concurrently highlighting gaps in the existing literature. We will also mention features of HFpEF that are common to both sexes.

Heart failure (HF) affects nearly 8 million individuals in the USA, with approximately half diagnosed with heart failure with preserved ejection fraction (HFpEF). HFpEF is associated with high morbidity and mortality, with fewer than 25% of patients surviving beyond 5 years after diagnosis. Historically, poor outcomes have been largely attributed to a lack of effective disease-modifying therapies. However, the past 5 years have marked a transformative era in HFpEF management, with multiple landmark clinical trials demonstrating benefits for novel therapeutic classes. These include sodium-glucose cotransporter 2 inhibitors (SGLT2i), non-steroidal mineralocorticoid receptor antagonists (Ns-MRAs), and glucagon-like peptide-1 (GLP-1) receptor agonists, particularly for the obesity-related HFpEF phenotype. In this review, we summarize the evolution of HFpEF therapeutics, from traditional heart failure treatments with limited efficacy to emerging targeted therapies, highlighting the latest evidence shaping a modern, comprehensive approach to HFpEF management.

Diuretics are essential for managing fluid overload in heart failure (HF) and controlling blood pressure in hypertension. However, their use is often associated with complications such as electrolyte imbalances and neurohormonal dysregulation, which can limit their effectiveness and contribute to adverse outcomes. These challenges underscore the need for alternative or adjunctive strategies to better manage fluid retention and congestion. Osmolytes are small molecules that help counteract increases in extracellular osmotic and hydrostatic pressure and are naturally present at high concentrations in the renal medulla. Notably, elevated serum levels of osmolytes such as trimethylamine N-oxide (TMAO) and betaine have been observed in patients with HF, although their role in the pathophysiology of the disease remains unclear. Given the known diuretic properties of osmolytes such as urea-historically used in the management of HF-it is plausible that other osmolytes may similarly modulate diuresis and volume status. This review examines the biological actions of several key osmolytes, including urea, TMAO, betaine, and taurine. Emerging evidence supports the need for further preclinical and clinical studies to investigate the potential diuretic and cytoprotective effects of TMAO, betaine, and taurine in the prevention and treatment of HF and hypertension.

Congestive heart failure (CHF) remains a leading cause of hospitalization and mortality worldwide. Continuous monitoring is crucial for early detection of decompensation, potentially reducing hospital admissions and improving outcomes. Cardiac implantable electronic devices (CIEDs) have been established as useful therapeutic interventions that also support continuous monitoring in order to detect early signs of decompensation. However, prior to CIED implantation, effective continuous monitoring solutions are lacking. They exist at two extremes: deep implantable intravascular solutions such as pulmonary artery pressure sensors, which are effective but costly and complex, and wearables, which are inexpensive but lack evidence of their effectiveness and depend on ongoing active patient adherence. Subcutaneous sensors may represent a promising intermediate solution-offering continuous monitoring with lower invasiveness and cost, while maintaining higher adherence compared to wearables. This review explores the role of subcutaneous sensors in CHF management, comparing existing daily trend data to deep implantable sensors measuring direct filling pressure and CIEDs for multi-parametric risk scoring. We discuss their feasibility, limitations, and future integration into routine clinical practice.

Cirrhotic cardiomyopathy (CCM) is a cardiac dysfunction linked to chronic liver disease, primarily characterized by impaired cardiac response to stress, despite normal baseline function. It presents with both systolic and diastolic dysfunction, along with electrophysiological changes such as QT interval prolongation. CCM is driven by a combination of systemic inflammation, nitric oxide-induced vasodilation, and neurohormonal dysregulation, leading to myocardial impairment and abnormal vascular responses. Clinically, CCM often remains asymptomatic at rest, but patients may experience exercise intolerance or heart failure during stress. Diagnosis includes echocardiographic evaluation, biomarker analysis (NT-proBNP, troponins), and electrocardiography for detecting electrophysiologic abnormalities. Management is complicated by cirrhosis, limiting the use of conventional heart failure treatments, with liver transplantation being the most definitive intervention in severe cases. Early detection of CCM is vital, particularly for patients undergoing liver transplantation or major surgery, where cardiac complications can increase mortality. Further research is necessary to refine diagnostic criteria and treatment strategies.

Transthyretin amyloid cardiomyopathy (ATTR-CM) is a progressive, life-threatening disease caused by the pathological deposition of misfolded transthyretin (TTR) protein in the myocardium, leading to restrictive cardiomyopathy and heart failure. While TTR stabilizers such as tafamidis and acoramidis are the only FDA-approved treatments, novel gene-modulating therapies are emerging as transformative approaches. Small interfering RNA (siRNA) and antisense oligonucleotide (ASO) therapies effectively reduce TTR production and have demonstrated promising clinical outcomes, though their use in cardiac amyloidosis remains investigational. CRISPR-Cas9 therapies represent a paradigm shift, offering a potential one-time treatment by permanently silencing the TTR gene. Recent clinical trials have shown significant TTR reduction and stabilization of disease biomarkers, although long-term safety and efficacy require further evaluation. Despite the lack of direct comparisons among these modalities, their emergence highlights a promising future for ATTR-CM management. This review discusses the pathogenesis of ATTR-CM, mechanisms of novel gene-modulating therapies, clinical evidence, challenges, and the future outlook for advancing treatment options.

Renal Denervation (RDN) has emerged over the last decade as a third pillar in the treatment of arterial hypertension, alongside pharmacotherapy and lifestyle modifications. Mechanistically, it reduces central sympathetic overactivation, a process also relevant to heart failure. In this mini-review, we summarize the development of RDN for heart failure, discuss the current evidence supporting its effects, and provide an outlook on future developments.