Heart Failure Reviews最新文献

Tricuspid regurgitation (TR) is a common valvular dysfunction following heart transplantation (HT), with reported prevalence rates ranging from 19 to 84%, primarily depending on the duration of follow-up. Its etiology is multifactorial and includes surgical technique, ischemic time, primary graft dysfunction, pulmonary hypertension, pacemaker leads, and endomyocardial biopsies. Severe TR can significantly impair graft function, exercise capacity, and patient survival. This mini-review explores current management strategies, including surgical techniques such as annuloplasty and tricuspid valve replacement. HT patients are often high-risk surgical candidates due to factors such as immunosuppressive therapy, prior surgeries, and various comorbidities. Therefore, we primarily focus on the evidence regarding emerging interventional methods, such as transcatheter edge-to-edge repair. Although these interventions show promising early results, they remain relatively novel in HT recipients, and the current evidence is based on case reports and small studies. Further research is essential to evaluate the long-term efficacy and safety of these management strategies to enhance outcomes for HT recipients with TR.

We examined current evidence regarding the effects of anti-inflammatory therapies in patients with acute heart failure (AHF) on the risk of cardiovascular outcomes, inflammatory markers, natriuretic peptides, and renal function. Despite growing evidence that inflammation plays a pivotal role in both the development and progression of heart failure, including AHF, only a few trials have been conducted to date in patients with AHF. A systematic literature search of PubMed, Medline, the Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov was conducted in November 2024 to identify randomized controlled trials (RCTs) evaluating anti-inflammatory therapies in adult patients with AHF. Meta-analyses were conducted to estimate effects on clinical outcomes (death, HF readmission, or worsening HF) and inflammatory and other markers. Five RCTs were identified that enrolled a total of 289 patients to an anti-inflammatory intervention and 273 to a control. Prednisone was examined in two RCTs, anakinra in two, and colchicine in one. Three of the five trials required elevated C-reactive protein (CRP) level for entry. Anti-inflammatory therapy was associated with a reduced risk of the composite outcome (hazard ratio 0.55 [95% CI 0.35-0.86]) and an overall 54% greater reduction in CRP to end of therapy (ratio of geometric mean ratios 0.46 [95% CI 0.29-0.73]), which varied across studies. NT-proBNP and creatinine were not significantly affected. The analysis is limited by the small number of studies but suggests that anti-inflammatory therapy reduces inflammation and may reduce the risk of adverse clinical outcomes in patients with AHF.

The increasing recognition of cardiac amyloidosis (CA) as a cause of heart failure, coupled with advancements in therapeutic options, has underscored the need for early detection. Positron emission tomography (PET) imaging emerged as a promising non-invasive tool for diagnosing and managing CA. This review provides a comprehensive analysis of current PET imaging techniques, focusing on radiotracers, including [¹¹C]Pittsburgh Compound B, [¹⁸F]Flutemetamol, [¹⁸F]Florbetapir, [¹⁸F]Florbetaben, [¹⁸F]-sodium fluoride, and [¹²⁴I]Evuzamitide. PET imaging's ability to differentiating CA subtypes and quantify amyloid burden contributes defining prognosis and aids in monitoring treatment response. However, standardizing imaging protocols and establishing definitive diagnostic thresholds remain challenging. As PET imaging continues to evolve, it promises to improve patient outcomes by facilitating earlier diagnosis, more accurate subtype differentiation, and better treatment monitoring in CA.

Mineralocorticoid receptor antagonists (MRAs) are a cornerstone of guideline-directed medical therapy for heart failure with reduced ejection fraction (HFrEF), offering significant benefits in reducing mortality and hospitalizations. However, their use is often constrained by the risk of hyperkalemia, particularly in patients with chronic kidney disease. Patiromer and sodium zirconium cyclosilicate (SZC), two novel potassium binders, have emerged as highly effective and safe tools for managing hyperkalemia and enabling the optimization of MRA therapy. This mini-review critically examines the findings of the recently published REALIZE-K (Randomized Withdrawal Trial Evaluating Sodium Zirconium Cyclosilicate for the Management of Hyperkalemia in Patients With Symptomatic Heart Failure With Reduced Ejection Fraction and Receiving Spironolactone) trial, placing it within the broader context of current evidence on potassium binders and their potential role in mitigating hyperkalemia to optimize MRA treatment. Moreover, it explores other significant barriers to MRA optimization, including clinician concerns over the risk of hyperkalemia, a consistent and pervasive issue that often leads to treatment inertia. By addressing both physiological and psychological barriers, this review aims to provide a comprehensive understanding of how to enhance MRA utilization and potentially improve clinical outcomes in patients with HFrEF.

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.

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), a chronic and progressive disease, is increasing in prevalence worldwide and is associated with increased hospitalizations and death. Despite notable improvements in medical therapy for HF, patients are still at risk of future negative outcomes. Current guidelines recommend four classes of medication for treating patients with HF, deemed guideline-directed medical therapy (GDMT). The use and adherence of these GDMTs serve as a major predictor of outcomes in those with chronic HF; however, implementation of therapy remains poor, despite substantial evidence of benefit. The acute hospitalization for HF and the subsequent vulnerable period serve as important milestones for adequate disease modification, and implementing a strategy for aggressive medical therapy can improve HF outcomes. Current guidelines also recommend that follow-up with multidisciplinary chronic disease management specific to HF be provided to those living with heart failure, which is essential for improving readmissions and mortality. This follow-up, although important by itself, serves as an important avenue for disease modification through medication titration, and implementing such structured follow-up is essential for further population-wide improvements in HF mortality. In this context, the STRONG-HF trial investigators developed an implementation trial providing evidence for the rapid inpatient initiation and subsequent titration of HF GDMT, demonstrating the importance of implementation strategies in the care of HF patients. In this narrative review, we review the evidence base for treating patients with HF, highlight deficits in our current real-world experience, and provide support for trial evidence like STRONG-HF in the global fight to reduce the burden of HF.

Heart failure with preserved ejection fraction (HFpEF) and atrial fibrillation (AF) are increasingly prevalent cardiovascular conditions, particularly among the elderly population. These two conditions share common risk factors and often coexist, leading to a complex interplay that alters the clinical course of each other. The pathophysiology of HFpEF is multifaceted and intricately linked, with atrial disease serving as a common pathophysiological pathway. Diagnosis of HFpEF in the setting of AF, and vice versa, can be challenging; thus, effective screening and diagnostic strategies are needed. Understanding the complex relationship between HFpEF and AF is crucial for optimal patient management by timely disease recognition and identification of therapeutic interventions or treatment strategies.

With rising incidence, mortality and limited therapeutic options, heart failure with preserved ejection fraction (HFpEF) remains one of the most important topics in cardiovascular medicine today. Characterised by left ventricular diastolic dysfunction partially due to impaired Ca²⁺ homeostasis, one ion channel in particular, SarcoEndoplasmic Reticulum Ca²⁺-ATPase (SERCA2a), may play a significant role in its pathophysiology. A better understanding of the complex mechanisms interplaying to contribute to SERCA2a dysfunction will help develop treatments targeting it and thus address the growing clinical challenge HFpEF poses. This review examines the conflicting evidence present for changes in SERCA2a expression and activity in HFpEF, explores potential underlying mechanisms, and finally evaluates the drug and gene therapy trials targeting SERCA2a in heart failure. Recent positive results from trials involving widely used anti-diabetic agents such as sodium-glucose co-transporter protein 2 inhibitors (SGLT2i) and glucagon-like peptide-1 (GLP-1) agonists offer advancement in HFpEF management. The potential interplay between these agents and SERCA2a regulation presents a novel angle that could open new avenues for modulating diastolic function; however, the mechanistic research in this emerging field is limited. Overall, the direct role of SERCA2a dysfunction in HFpEF remains undetermined, highlighting the need for well-designed pre-clinical studies and robust clinical trials.

Strong evidence supports the importance of rapid sequence or simultaneous initiation of quadruple guideline-directed medical therapy (GDMT) for heart failure with reduced ejection fraction (HFrEF) for substantially reducing risk of mortality and hospitalization. Barring absolute contraindications for each individual medication, employing the strategy of rapid sequence, simultaneous, and/or in-hospital initiation at the time of HF diagnosis best ensures patients with HFrEF have the opportunity to benefit from proven medications and achieve large absolute risk reductions for adverse clinical outcomes. However, despite guideline recommendations supporting this approach, implementation in clinical practice remains persistently low, with less than one-fifth of eligible patients being prescribed the quadruple GDMT regimen. Additionally, for heart failure with mildly reduced or preserved ejection fraction (HFpEF), sodium-glucose co-transporter 2 inhibitors (SGLT2i) and non-steroidal mineralocorticoid receptor antagonists (MRA) constitute foundational therapy for all eligible patients with significant clinical benefits within just weeks of medication initiation. Nonetheless, the burden of symptoms, functional limitations, and hospitalizations remains substantial for many of these patients, even with SGLT2i and non-steroidal MRA therapy. Additional evidence supports consideration of adjunctive therapies for HF with EF > 40% that can be tailored to the patient phenotype, including glucagon-like peptide-1 receptor agonists (GLP-1 RA) for patients with obesity, as well as angiotensin receptor-neprilysin inhibitors (ARNI) for patients with EF below normal. This article reviews the evidence-based sequencing of GDMT for HF across the spectrum of EF, emphasizing the rationale and benefits of early up-front initiation of quadruple medical therapy for HFrEF, rapid initiation of SGLT2i for HF regardless of EF, and prompt phenotype-specific tailored approach to adjunctive therapies for HF with EF > 40%.