Heart Failure Reviews最新文献

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.

Heart failure remains one of the leading causes of mortality and hospitalizations in the US that not only impacts quality of life but also poses a significant public health burden. The majority of affected patients are admitted with signs and symptoms of congestion. Despite the initial enthusiasm, traditional remote monitoring strategies focusing primarily on weight gain failed to improve clinical outcomes. Implantable pulmonary artery pressure sensors provide earlier and actionable data, but most patients would favor forgoing an invasive procedure in favor of an alternative, non-invasive monitoring platform. Several devices utilizing different combinations of multiparameter monitoring to reliably detect congestion have recently been developed and are undergoing testing in the clinical setting. Combining these sensors with the power of artificial intelligence and machine learning has the potential to revolutionize remote patient monitoring and early congestion detection and to facilitate timely interventions by the care team to prevent hospitalization. This manuscript provides an objective review of novel, noninvasive, multiparameter remote monitoring platforms that may be tailored to individual heart failure phenotypes, aiming to improve quality of life and survival.

Leptin plays a dual role in heart failure (HF), acting as either a primary driver or a secondary phenomenon depending on the HF subtype. In HF with preserved ejection fraction (HFpEF), chronic hyperleptinemia is a primary mediator of disease initiation and progression, closely linked to obesity and metabolic dysfunction. Elevated leptin levels promote systemic inflammation, sympathetic nervous system activation, arterial stiffness, myocardial hypertrophy, fibrosis, and sodium retention, culminating in diastolic dysfunction and elevated ventricular filling pressures. Conversely, in HF with reduced ejection fraction (HFrEF), elevated leptin levels arise as a secondary response to myocardial dysfunction, systemic inflammation, and tissue hypoperfusion. Here, leptin exacerbates cardiac dysfunction by amplifying neurohormonal activation, inflammation, and cardiac remodeling. Understanding these distinct roles has potential therapeutic implications. In HFpEF, interventions such as weight loss, glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter-2 inhibitors, and mineralocorticoid receptor antagonists can improve symptoms and prognosis, partly by mitigating chronic hyperleptinemia. Furthermore, leptin-specific therapies should be investigated in clinical trials as potential approach in managing cardiometabolic HFpEF. In HFrEF, management focuses on guideline-directed therapies targeting neurohormonal activation-the key mechanism driving disease progression. However, future research should explore whether modulating leptin signaling could provide additional benefits translated in hard clinical endpoints. By framing leptin as the initiator ("chicken") in HFpEF and a consequence ("egg") in HFrEF, this manuscript highlights the need for individualized, integrated treatment strategies. Addressing both metabolic and cardiovascular components could potentially further improve patient outcomes and quality of life.

Left atrial (LA) hypertension is central in the pathophysiology of heart failure (HF) in general and of HF with preserved ejection fraction (HFpEF) in particular. Despite approved treatments, a number of HF patients continue experiencing disabling symptoms due to LA hypertension, causing pulmonary congestion, pulmonary hypertension, and right heart dysfunction, at rest and/or during exercise. LA decompression therapies, i.e., left atrial shunting through a specifically designed device (either implant-based or implant-free), are being studied in various forms of HF to alleviate LA hypertension and patients' symptoms. Despite a solid background and favorable signals from initial non-randomized clinical trials, the quest for the optimal HF candidate for interatrial shunt devices is still an area of active research that at the same time is helping to better elucidate the intricate pathophysiology of HF(pEF).

Heart failure (HF) is a growing concern, with significant implications for mortality, morbidity, and economic sustainability. Traditionally viewed primarily as a hemodynamic disorder, recent insights have redefined HF as a complex systemic syndrome, emphasizing the importance of understanding its multifaceted pathophysiology. Fluid overload and congestion are central features of HF, often leading to clinical deterioration and hospital admissions, with the role of the lymphatic system previously largely overlooked, partly due to diagnostic challenges and visualization difficulties. With the advancement of those techniques, pathophysiological changes occurring in the lymphatic system during HF, such as enlargement of the thoracic duct and the increased lymphatic flow, are now becoming apparent. This emerging research has begun to uncover the interplay between lymphatic dysfunction and HF, suggesting novel therapeutic targets. Advances in molecular biology, such as targeting vascular endothelial growth factor and promoting lymphangiogenesis, hold promise for improving lymphatic function and mitigating HF complications. This article provides a comprehensive overview of the evolving landscape of lymphatic system-targeted therapies for HF. It explores various intervention levels, from mechanical lymphatic decongestion to pharmaceutical interactions and lymphatic micro-circulation, offering insights into future directions and potential clinical implications for HF management.

Heart failure (HF) is a complex and debilitating syndrome that affects millions of people worldwide. In addition to the syndrome-related functional limitations, such as exercise intolerance and dyspnea, patients frequently suffer from various comorbidities. Neuropsychiatric conditions, including autonomic dysfunction, cognitive impairment, and depression, are important albeit underrecognized comorbidities in HF. Autonomic dysfunction, which is expressed as sympathetic predominance and decreased parasympathetic tone, is a key contributor to HF progression. Depression and cognitive impairment are highly prevalent in HF patients, affecting adherence to medical treatment and increasing morbidity and mortality risk. Stress cardiomyopathy, a usually reversible form of left ventricular dysfunction triggered by emotional or physical stress, is another clinical manifestation of the interplay between the heart and the brain. Early recognition and management of these comorbidities in HF patients are crucial for improving outcomes. This narrative review provides an overview of the pathophysiological mechanisms linking HF and brain disorders and discusses clinical perspectives of heart-brain interactions in the context of HF.

Exercise intolerance is a well-established symptom of heart failure with preserved ejection fraction (HFpEF) and is associated with impaired quality of life and worse clinical outcomes. Historically attributed to diastolic dysfunction of the left ventricle, exercise intolerance in HFpEF is now known to result not only from diastolic dysfunction, but also from impairments in left ventricular systolic function, left atrial pathology, right ventricular dysfunction, and valvular disease. Disorders of heart rate and rhythm such as chronotropic incompetence and atrial fibrillation have also been implicated in exercise intolerance in this population. Pathologic changes to extra-cardiac organ systems including the respiratory, vascular, hormonal, and skeletal muscle systems are also thought to play a role in exercise impairment. Finally, comorbidities such as obesity, inflammation, and anemia are common and likely contributory in many cases. The role of each of these factors is discussed in this review of exercise intolerance in patients with HFpEF.

For most patients with chronic heart failure (HF), the clinical course of the disease includes periods of apparent clinical stability punctuated by episodes of clinical deterioration with worsening signs and symptoms, a condition referred to as worsening heart failure (WHF). Over time, episodes of WHF may become more frequent, and patients may enter a cycle of recurrent events associated with deterioration in their quality of life and functional capacity, hospitalizations, and ultimately death. WHF is apparently an old concept but seems to have acquired new boundaries in terms of definition and clinical and prognostic value due to the fast-paced evolution of the HF treatment landscape and the emergence of new drugs in this setting. As a result, the management of WHF is being reshaped. In the present paper, a group of HF experts gathered to discuss the concept, prevention, detection, and treatment of WHF.