Heart Failure Reviews最新文献

Clinical congestion remains a major cause of hospitalization and re-hospitalizations in patients with chronic heart failure (HF). Despite the high prevalence of this issue and clinical concern in HF practice, there is limited understanding of the complex pathophysiology relating to the "congestion" of congestive HF. There is no unifying definition or clear consensus on what is meant or implied by the term "congestion." Further, the discordance in study findings relating congestion to physical signs and symptoms of HF, cardiac hemodynamics, or metrics of weight change or fluid loss with diuretic therapy has not added clarity. In this review, these factors will be discussed to add perspective to this issue and consider the factors driving "congestion." There remains a need to better understand the roles of fluid retention promoting intravascular and interstitial compartment expansions, blood volume redistribution from venous reservoirs, altered venous structure and capacity, elevated cardiac filling pressure hemodynamics, and heterogeneous intravascular volume profiles (plasma volume and red blood cell mass) with a goal to help demystify "congestion" in HF. Further, this includes highlighting the importance of recognizing that congestion is not the result of a single pathway but a complex of responses some of which produce symptoms while others do not; yet, we confine these varied responses to the single and somewhat vague term "congestion."

Congenital heart disease (CHD) is the most common global congenital defect affecting over 2.4 million individuals in the United States. Ongoing medical and surgical advancements have improved the survival of children with CHD leading to a shift where, as of 2010, adults constitute two-thirds of the CHD patient population. The increasing number and aging of adult congenital heart disease (ACHD) patients present a clinical challenge due to heightened complexity, morbidity, and mortality. Studies indicate that 1 in 13 ACHD patients will develop heart failure (HF) in their lifetime. ACHD-HF patients experience more frequent emergency department visits, higher hospitalization rates, longer hospital stays, and higher mortality compared to non-ACHD patients with heart failure (non-ACHD-HF). Despite HF being the leading cause of death in ACHD patients, there is a notable gap in evidence regarding treatment. While guideline-directed medical therapy (GDMT) has been extensively studied in non-ACHD-HF, research specific to ACHD-HF individuals is limited. This article aims to comprehensively review available literature addressing the pharmacological treatment of ACHD-HF.

Cardiovascular disease is a major non-communicable disease globally, with increasing prevalence, posing a significant public health challenge. It is the leading non-obstetric cause of perinatal morbidity and mortality, with a substantial number of cardiac fatalities occurring in individuals without any known pre-existing cardiovascular disease. Peripartum cardiomyopathy is a type of de novo heart failure that occurs in pregnant women in the late stages of pregnancy or following delivery. Despite extensive research, diagnosing and managing peripartum cardiomyopathy remains challenging, resulting in significant morbidity and mortality. Recent advancements and novel approaches have been made to better understand and manage peripartum cardiomyopathy, including molecular and non-molecular biomarkers, genetic predisposition and risk prediction, targeted therapies, multidisciplinary care, and improved patient education. This narrative review provides a comprehensive overview and new perspectives on peripartum cardiomyopathy, covering its epidemiology, updated pathophysiological mechanisms, diagnosis, management, and future research directions for healthcare professionals, researchers, and clinicians.

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.

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.

With over 1 million primary heart failure (HF) hospitalizations annually, nearly 80% of patients who present to the emergency department with decompensated HF (DHF) are hospitalized. Short stay units (SSU) present an alternative to hospitalization, yet the effectiveness of the SSU strategy of care is not well known. This study is to determine the effectiveness of a SSU strategy compared with hospitalization in lower-risk patients with DHF. Our primary outcome was a composite of 30-day mortality and re-hospitalization. Key secondary outcomes included 90-day mortality and re-hospitalization, costs, and 30-day days-alive-and-out-of-hospital (DAOOH). This is a systematic review and meta-analysis, following PRISMA guidelines. MEDLINE, EMBASE, CENTRAL, CINAHL, SCOPUS, and Web of Science were searched from inception through February 2024. Either randomized trials or comparative observational studies were included if they compared outcomes between low-risk ED DHF patients admitted to an SSU (defined as an observation unit with expected stay ≤ 48 h) vs. admitted to the hospital. Two authors independently screened all titles and abstracts and then identified full texts for inclusion. Data extraction and risk of bias assessments were performed by two authors in parallel. The primary outcome was a composite of death or readmission within 30 days, reported as relative risk (RR), where a RR < 1 favored the SSU strategy. Secondary outcomes included 90-day mortality and re-hospitalization, costs, and 1-month days-alive-and-out-of-hospital (DAOOH). Of the 467 articles identified by our search strategy, only 3 full text articles were included. In meta-analysis for the primary outcome of 30-day death or readmission, the RR was 0.95 (95% CI = 0.56 to 1.63; I² = 0%) for patients randomized to SSU vs hospitalization (2 studies, 241 patients). There were only 2 total deaths at 30 days in the 2 studies (total N = 258) which reported 30-day mortality, both in hospitalized patients. Only one study reported 90-day outcomes, showing no significant differences. Costs were lower in the SSU arm from one study, and 30-day DAOOH also favored SSU based on a single randomized trial. Based on very limited evidence, SSU provides similar efficacy for 30-day and 90-day mortality and readmission compared to hospitalization. An SSU strategy appears safe and may be cost effective.

Echocardiography represents an essential tool for imagers and clinical cardiologists in the management of patients with heart failure. Advanced heart failure (AdHF) is a more severe and, typically, later stage of HF that exposes patients to a high risk of adverse outcomes, with a 1-year mortality rate of around 50%. Currently, several therapies are available to improve the outcomes of these patients, reduce their mortality rate, and, possibly, delay the need for advanced therapies such as heart transplant and long-term mechanical circulatory support. When accurately performed and interpreted, echocardiography provides crucial information to properly tailor medical and device therapy of patients with AdHF and to identify those at even higher risk. In this review, we present the state of the art of echocardiography applications in the clinical management of patients with AdHF. We will discuss the role of echocardiography chronologically, beginning with the prediction of AdHF, proceeding through diagnosis, and detailing how echocardiography informs clinical decision-making, before concluding with indications for advanced therapies.

Graphical Abstract

The role of echocardiography in the management of patients with advanced heart failure. Echocardiography is a useful method for predicting the occurrence of AdHF during follow-up of patients with HF (top line). The diagnosis of AdHF requires an echocardiographic criterion for AdHF (middle line). In patients with AdHF, echocardiography is useful to identify patients who will benefit most from medical therapy adjustment, device therapy, and LVAD implantation. HF, heart failure; LA, left atrium; RV, right ventricle; LVEF, left ventricular ejection fraction. HF, heart failure; LA, left atrium; LVEF, left ventricular ejection fraction; RV, right ventricle

Heart failure with preserved ejection fraction (HFpEF) is rapidly growing as the most common form of heart failure. Among HFpEF phenotypes, the cardiometabolic/obese HFpEF — HFpEF driven by cardiometabolic alterations — emerges as one of the most prevalent forms of this syndrome and the one on which recent therapeutic success have been made. Indeed, pharmacological approaches with sodium-glucose cotransporter type 2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA) have proved to be effective due to metabolic protective effects. Similarly, lifestyle changes, including diet and exercise are crucial in HFpEF management. Increasing evidence supports the important role of diet and physical activity in the pathogenesis, prognosis, and potential reversal of HFpEF. Metabolic derangements and systemic inflammation are key features of HFpEF and represent the main targets of lifestyle interventions. However, the underlying mechanisms of the beneficial effects of these interventions in HFpEF are incompletely understood. Hence, there is an unmet need of tailored lifestyle intervention modalities for patients with HFpEF. Here we present the current available evidence on lifestyle interventions in HFpEF management and therapeutics, discussing their modalities and potential mechanisms.

Background

The latest guidelines advocate for catheter ablation (CA) over standard medical therapy (SMT) for managing atrial fibrillation (AF) in patients with heart failure with reduced ejection fraction (HFrEF). However, significant knowledge gaps exist regarding the effectiveness of CA vs. SMT in patients with heart failure with preserved ejection fraction (HFpEF).

Methods

PubMed, Scopus, and Embase until February 2024 were systematically searched. Given the limited number of randomized studies, propensity score-matched observational studies comparing CA with SMT in AF patients with HFpEF were also included. The primary outcome was a composite endpoint of all-cause mortality and HF hospitalization.

Results

Eight studies that enrolled 17,717 SMT and 2537 CA patients were included. CA was associated with a significantly lower risk of the composite endpoint of all-cause mortality and HF hospitalization (HR 0.61; 95% CI, 0.43–0.85). The risk of HF hospitalization (HR 0.44; 95% CI, 0.23–0.83), cardiovascular mortality (HR 0.43; 95% CI, 0.22–0.84), and AF recurrence (HR 0.53; 95% CI, 0.39–0.73) were also lower in the CA group.

Conclusion

CA demonstrated significant cardiovascular morbidity and mortality benefits compared to SMT in the HFpEF population.

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with various phenotypes, and obesity is one of the most common and clinically relevant phenotypes of HFpEF. Obesity contributes to HFpEF through multiple mechanisms, including sodium retention, neurohormonal dysregulation, altered energy substrate metabolism, expansion of visceral adipose tissue, and low-grade systemic inflammation. Glucagon-like peptide-1 (GLP-1) is a hormone in the incretin family. It is produced by specialized cells called neuroendocrine L cells located in the distal ileum and colon. GLP-1 reduces blood glucose levels by promoting glucose-dependent insulin secretion from pancreatic β cells, suppressing glucagon release from pancreatic α cells, and blocking hepatic gluconeogenesis. Recent evidence suggests that GLP-1 receptor agonists (GLP-1 RAs) can significantly improve physical activity limitations and exercise capacity in obese patients with HFpEF. The possible cardioprotective mechanisms of GLP-1 RAs include reducing epicardial fat tissue thickness, preventing activation of the renin–angiotensin–aldosterone system, improving myocardial energy metabolism, reducing systemic inflammation and cardiac oxidative stress, and delaying the progression of atherosclerosis. This review examines the impact of obesity on the underlying mechanisms of HFpEF, summarizes the trial data on cardiovascular outcomes of GLP-1 RAs in patients with type 2 diabetes mellitus, and highlights the potential cardioprotective mechanisms of GLP-1 RAs to give a pathophysiological and clinical rationale for using GLP-1 RAs in obese HFpEF patients.