Heart Failure Reviews最新文献

Unplanned admissions for worsening heart failure (WHF) are the largest resource cost in heart failure (HF) management. Despite advances in pharmacological agents and interventional therapy, HF remains a global epidemic. One crucial-and costly-gap in HF management is the inability to obtain objective information to identify and quantify congestion and personalize treatment plans to effectively manage WHF events without resorting to expensive, invasive methods. Although the causes of WHF are varied and complex, the universal effect of HF decompensation is the significant decline in quality of life due to symptoms of hypervolemic congestion and the resultant reduction in cardiac output, which can be quantified via increased pulmonary venous congestion due to high intracardiac filling pressures. Accessible and reliable markers of congestion could more precisely quantify the severity of WHF events and stabilize patients earlier by interrupting and reversing this process with timely introduction or modification of evidence-based treatments. Pulmonary artery and cardiac pressure sensing tools have gained evidential credence and increased clinical uptake in recent years for the prevention and treatment of WHF, as studies of implantable hemodynamic devices have iteratively and reliably demonstrated substantial reductions in WHF events. Recent advances in sensing technologies have ranged from single-parameter invasive pulmonary artery monitors to completely non-invasive multi-parameter devices incorporating multi-sensor concept technologies aided by machine learning or artificial intelligence, although many remain investigational. This review aims to evaluate the potential for novel pulmonary artery and cardiac pressure sensing technology to reshape the management of WHF from within the hospitalized and ambulatory care environments.

Heart failure (HF) remains a leading cause of morbidity and mortality worldwide, with inflammation playing a pivotal role in its pathogenesis. This comprehensive review aims to elucidate the intricate mechanisms by which inflammation contributes to the development and progression of HF. The review synthesizes current research on the involvement of both innate and adaptive immune responses in HF, highlighting the roles of cytokines, chemokines, and other inflammatory mediators. Recent studies have demonstrated that chronic inflammation, driven by factors such as oxidative stress, neurohormonal activation, and metabolic disturbances, leads to adverse cardiac remodeling and impaired myocardial function. The review explores how systemic inflammation, characterized by elevated levels of inflammatory biomarkers like C-reactive protein (CRP) and interleukin-6 (IL-6), correlates with HF severity and outcomes. Additionally, it discusses the impact of comorbid conditions such as diabetes, obesity, and hypertension on inflammatory pathways and HF risk. The review also delves into the therapeutic implications of targeting inflammation in HF. Despite mixed results from early clinical trials, emerging evidence suggests that anti-inflammatory therapies offer benefits in specific HF phenotypes. The potential of novel therapeutic strategies, including the use of biologics and small molecule inhibitors, is examined in the context of their ability to modulate inflammatory responses and improve clinical outcomes.

ZOLL Heart Failure Management System (ZOLL HFMS) is a non-invasive, remote monitoring device that employs radiofrequency signals transmitted through an adhesive patch embedded with integrated sensors to evaluate lung fluid levels. By analyzing trends in lung fluid status and related parameters, ZOLL HFMS may facilitate the early detection of heart failure (HF) decompensation and enable timely interventions. Insights from the recent BMAD trial (Impact of heart failure management using thoracic fluid monitoring from a novel wearable sensor: Results of the Benefits of Microcor [µCor™] in Ambulatory Heart Failure) highlight its promise in those with recent HF hospitalization, demonstrating a reduction in time to first HF readmission and improvement in quality of life. In this review, we summarize data on the ZOLL HFMS, with a focus on its lung fluid analysis mechanism for early HF decompensation detection and the accuracy of its measurements compared to other modalities. Then, we examine key outcomes from the recent BMAD trial, highlighting their clinical relevance and identifying gaps that warrant further investigation in future clinical trials. Lastly, we outline potential directions for integrating this technology into routine HF management.

Recombinant proteins, cell, and gene therapies are collectively defined as biological drugs or biologics. These therapies have transformed the lives of millions of patients over the past decades, with the number of FDA-approved biologics increasing exponentially in recent years. However, out of approximately 700 biological therapies approved by the FDA in the last 20 years, less than 1% are indicated for cardiac pathologies. The application of biologics in cardiovascular disease has faced significant challenges, including short plasma half-life, the multifactorial complexity of cardiac disease, and the lack of efficient, non-invasive, and patient-friendly drug-delivery routes. This translational gap is particularly pressing given the immense socioeconomic burden of cardiovascular disease, which remains the leading cause of death globally and accounts for billions in annual healthcare costs and lost productivity. Inhalation-based drug delivery has recently emerged as a promising strategy for treating cardiovascular disease, with several proof-of-concept studies demonstrating its potential in heart failure, the most prevalent cardiac condition. This narrative review summarizes the latest experimental evidence in the novel field of Cardiovascular Inhalation, i.e., the lung-to-heart route for biologics. We discuss translational challenges, preclinical evidence, and future perspectives for bringing this innovative approach to clinical practice.

This review explores the critical role of exercise as a non-pharmacological intervention in managing ischemic cardiomyopathy (ICM), a leading cause of heart failure. It highlights the profound cardiovascular benefits of exercise, such as improved cardiopulmonary parameters, decreased morbidity and mortality, and enhanced functional capacity. It also critically evaluates existing literature on the efficacy of various exercise types and intensities, including aerobic, resistance, and high-intensity interval training. There is a significant gap in current clinical guidelines, which lack specific exercise prescriptions tailored to the unique pathophysiology of ICM. By synthesizing data from both older and contemporary studies, this review highlights specific, evidence-based exercise regimens and promotes supervised cardiac rehabilitation programs. This review also addresses potential barriers to cardiac rehabilitation participation and proposes future directions, which include the use of technology to improve adherence and outcomes.

Chronic venous insufficiency (CVI) is a prevalent disorder, arising from venous valve incompetence and vein wall weakness, which impairs blood return and leads to venous stasis and hypertension in the lower extremities. This condition, affecting up to 40% of older adults, has been primarily considered a peripheral issue. However, growing evidence indicates its systemic impacts, notably its contribution to cardiovascular dysfunction and heart failure (HF). CVI exacerbates central venous pressure and cardiac preload, placing strain on the right heart and predisposing at-risk patients to HF. Moreover, a feedback loop exists where HF worsens CVI through increased venous stasis and fluid overload, highlighting a complex bidirectional relationship. Emerging research reveals that CVI-driven inflammation and endothelial dysfunction may accelerate adverse cardiac dysfunction. This review provides a comprehensive analysis of CVI's systemic effects, emphasizing the need for integrated cardiovascular and venous management strategies to address the reciprocal influences of CVI and HF. Such an approach could reduce disease progression and enhance outcomes for affected patients.

Cancer treatments like chemotherapy, radiotherapy, and combined immunotherapies have significantly increased patient survival. However, these treatments are frequently linked to cardiovascular toxicity, which has a significant impact on clinical outcomes and patient well-being. Chemotherapy, targeted therapy, and radiotherapy induce significant cellular stress in cardiomyocytes and endothelial cells, causing DNA damage, activating pro-inflammatory and pro-apoptotic signalling pathways. Cumulative damage causes cardiomyocyte loss, followed by fibrosis, resulting in pathological structural and functional remodelling of the myocardium. Endothelial cell damage disrupts vascular integrity, increasing the risk of atherosclerosis, coronary artery disease, and ischaemia. Over time, these changes can lead to clinical conditions like dilated and restrictive cardiomyopathy, which are frequently accompanied by arrhythmias and can result in heart failure and sudden cardiac death. To overcome this problem, the novel field of cardio-oncology aims to provide effective cancer treatments with a multifaceted cardioprotection approach involving pharmacological, diagnostic, natural compounds, and lifestyle interventions during and after cancer therapy. In this review, we cover the important cancer therapies, and their cardiotoxic mechanisms and detail different cardioprotective strategies aimed at mitigating these adverse effects and improve patient outcomes.

Iron is essential for the production of myocardial energy and proteins critical for metabolism. Iron deficiency is common in patients with heart failure and reduced ejection fraction (HFrEF) and is associated with a poor prognosis. However, whether intravenous iron replacement reduces the risk of adverse clinical events in HFrEF patients remains uncertain, despite several outcome trials being conducted. Furthermore, significant uncertainties persist in this setting regarding the most appropriate definition of iron deficiency and the optimal dosing regimen. Here, we critically discuss the findings of the recently published FAIR-HF2 (Ferric Carboxymaltose Assessment of Morbidity and Mortality in Patients with Iron Deficiency and Chronic Heart Failure) trial, which investigated the efficacy and safety of ferric carboxymaltose in patients with HF and iron deficiency, while positioning these results within the broader context of current evidence on intravenous iron supplementation in patients with HFrEF.

Guideline-directed medical therapy is the backbone of heart failure treatment. However, patients continue to experience heart failure symptoms, impaired quality of life, and reduced functional status despite guideline-directed medical and device treatment. There is a void in treatment alternatives between guideline-directed therapy and the advanced heart failure surgical options of heart transplant (HT) and left ventricular assist device (LVAD). Cardiac contractility modulation and baroreceptor activation therapies are shown to improve heart failure symptoms, quality of life, and exertional capacity in select patients and complement our current treatment paradigm. The purpose of this paper is to review these novel Food and Drug Administration (FDA)-approved heart failure therapies and facilitate the identification of appropriate candidates.

Heart failure with preserved ejection fraction (HFpEF) is a growing public health burden, contributing to significant morbidity, mortality, and healthcare costs. Exercise intolerance, a hallmark of HFpEF, stems from central (cardiac and pulmonary) and peripheral (vascular and skeletal muscle) factors that result in reduced oxygen delivery and utilization by active muscles. With relatively few effective therapies, exercise training has emerged as a reliable and proven therapeutic intervention to improve exercise capacity and physical function in HFpEF. This review synthesizes evidence from the existing literature to describe and evaluate various exercise modalities in HFpEF. Moderate-intensity continuous training significantly improves peak oxygen consumption and symptom burden and is supported by a large evidence base in patients with HFpEF. High-intensity interval training has shown potential as an alternative regimen with particular benefit in highly selected populations. Multi-modality regimens and low-intensity training approaches are potentially suitable for patients with limited exercise tolerance or those who are more vulnerable or frail. The addition of resistance training may further improve muscle strength and functional capacity. Integrating exercise interventions with complementary dietary approaches has also shown potential for enhancing exercise capacity response. Lastly, emerging modalities, such as inspiratory muscle training and functional electrical stimulation, offer additional unique options. Despite robust evidence, challenges in the long-term durability of benefits, poor responder rates (~ 1/3 of participants), and implementation persist. Ongoing and future efforts can focus on evaluating long-term clinical outcomes (i.e., mortality and hospitalizations), developing more personalized exercise protocols, and applying sustainable implementation strategies in clinical practice.