Current Heart Failure Reports最新文献

Purpose of review: Heart failure (HF) is a complex clinical syndrome of progressive cardiac dysfunction, posing a major global burden on public health. The coupling between cardiomyocyte electrophysiology and energy metabolism is critical for sustaining cardiac electromechanical function. This review aims to elucidate the role of disrupted metabolic-electrophysiological coupling in disease progression and summarize emerging therapeutic targets.

Recent findings: Currently, drugs that correct electrical or metabolic issues are proving effective in patients, while theoretical research and preliminary experiments have corroborated electro-metabolic coupling and its regulatory crosstalk among metabolic signaling, electrical activity, and energy utilization. These foundational studies have established a viable basis for multi-target interventions in HF. Restoring the disrupted integration between metabolism and electrophysiology emerges as a promising strategic direction in HF therapy. Interventions targeting this integration, such as metabolic modulators and mitochondrially targeted agents, may suppress arrhythmias, reverse adverse remodeling, and improve contractile function. This integrated approach may ultimately lead to more effective treatments that improve clinical outcomes for HF patients.

Heart failure (HF) remains a leading cause of morbidity and mortality worldwide, with a growing need for improved understanding of disease mechanisms and better strategies for risk stratification. Among the key systems involved in maintaining cardiovascular homeostasis is the natriuretic peptide pathway, which is dependent on two critical enzymes: Corin, a cardiac-restricted serine protease, and Furin, a ubiquitous convertase. These enzymes activate pro-atrial and pro-brain natriuretic peptides that facilitate natriuresis, vasodilation, and neurohormonal balance. Disruption of the corin-furin axis impairs peptide activation and contributes to the maladaptive processes that lead to the progression of heart failure (HF). While several studies have reported altered expression of corin and furin in different HF phenotypes, their value as clinical biomarkers remains limited. Current diagnostic performance shows only modest sensitivity and specificity compared to established markers such as BNP and NT-proBNP, and incremental benefit has yet to be demonstrated in clinical settings. Nonetheless, their ability to reflect upstream enzymatic processes offers important mechanistic insight into HF pathophysiology. Looking ahead, corin and furin may hold promise as adjunctive or mechanistic biomarkers to guide therapies targeting natriuretic peptide-related pathways. This review provides a critical overview of the physiological and pathological roles of corin and furin in heart failure and evaluates current evidence for their potential as biomarkers. It also discusses key limitations and highlights future directions for research and therapeutic translation.

Purpose of review: This review examines why substantial disparities persist in the management of cardiogenic shock (CS) despite advances in therapy and the existence of clinical guidelines. We synthesize structural, clinical, and ethical mechanisms that shape access to timely and advanced care and highlight equity-oriented solutions.

Recent findings: Across contemporary cohorts, women, older adults, racial/ethnic minorities, and socioeconomically disadvantaged patients remain less likely to receive early coronary angiography, revascularization, or mechanical circulatory support (MCS) and experience longer inter-hospital transfer delays. Reported gaps typically range from ~ 20-40% lower use of guideline-recommended therapies compared with reference groups, independent of comorbidity and presentation severity. Drivers include implicit bias, variable institutional resources, uneven protocol activation, and discretionary triage under time pressure.  Equity in CS care cannot be achieved by protocols alone. It requires deliberate measurement, culturally responsive decision-making, and system-level accountability. Equity-minded implementation of protocolized care, regionalized hub-and-spoke networks, multidisciplinary shock teams, and disparity-sensitive metrics shows promise. Success in CS should be defined not only as survival but also as equitable inclusion in the full spectrum of recognition, triage, escalation, and shared decision-making.

Purpose of review: While left ventricular (LV) remodeling has been associated with poor prognosis in heart failure with reduced ejection, a variable degree of LV remodeling can be reversed upon the removal of the initial insult and with appropriate therapies. Hence, better prediction of LV reverse remodeling would not only help prognostically, but also could illuminate potential therapeutic targets. Herein, we provide a comprehensive review on the latest evidence on the predictors of LV reverse remodeling.

Recent findings: Several predictors of LV reverse remodeling have been identified including certain baseline parameters of underlying cardiomyopathy, myocardial structure and function assessed by multi-modality imaging, and biomarkers. Beyond improving clinical outcomes, many of the established and emerging heart failure therapies have been also demonstrated to promote reverse remodeling, likely reflective of the mechanistic underpinning of their therapeutics benefits. With the ongoing development of novel diagnostics and therapies of heart failure, our understanding of LV reverse remodeling continues to evolve. Furthermore, with the growing evidence between reverse remodeling and clinical outcomes, reverse remodeling may prove to be a clinically useful marker of myocardial recovery and potential therapeutic target.

Purpose of review: To examine the role of endosomal dysfunction in heart failure pathophysiology and evaluate its potential as a therapeutic target, particularly focusing on its regulation of cardiac metabolism.

Recent findings: Endosomal dysfunction, driven by v-ATPase disassembly and loss of acidification, emerges as a key contributor to metabolic perturbations in heart failure. This dysfunction leads to uncontrolled CD36 translocation, resulting in lipotoxicity and inflammatory signaling through CD36-TLR4 complex formation. These mechanisms are especially relevant in diabetic cardiomyopathy and heart failure with preserved ejection fraction. The endosomal system represents a promising therapeutic target in heart failure, though its contribution varies among patients and disease stages. Recent advances in molecular imaging and biomarker analysis enable better patient stratification, opening new avenues for personalized endosome-targeted therapies in heart failure treatment.

Purpose of review: Frailty is a prevalent and clinically significant condition affecting up to 45% of adults with heart failure (HF). Frailty reflects a state of reduced physiologic reserve and vulnerability to stressors, which profoundly influences health outcomes including health care utilization and survival. Frailty and HF interact through multiple overlapping pathophysiologic mechanisms, including chronic inflammation, neurohormonal abnormalities, and multiorgan dysfunction. This synergy, for the patient leads to poor physical performance, reduced independence, and a greater susceptibility to complications.

Recent findings: Evidence from recent clinical trials focused on frailty in HF underscores the potential benefits of multicomponent interventions combined with medication optimisation target physical dysfunction, poor nutrition, psychological disorders, and social isolation. Multidisciplinary care teams - including cardiologists, nurses, physical therapists, dieticians, occupational therapists, and social workers - can implement tailored strategies to reverse or slow the progression of frailty to improve health outcomes of patients with HF. Interventions such as resistance and balance training, individualised nutritional supplementation, medication review, cognitive and psychological support, and caregiver education have demonstrated a range of benefits in HF, from enhanced physical capacity and reduced hospital readmissions to improved health-related quality of life. Managing frailty in patients with HF requires a personalised, holistic and multicomponent approach. Successful intervention involves addressing not only physical dysfunction but also psychological, nutritional, and social factors that collectively undermine health and independence. Integrating multicomponent care into routine practice has the potential to improve clinical outcomes, reduce health care utilisation, and enhance the overall well-being of patients. Future research should aim to identify the most effective combinations of interventions, clarify mechanisms of action, and determine cost-efficiency in health care delivery.

In patients experiencing acute heart failure, acute cardiogenic pulmonary edema (ACPE) can emerge due to a surge in pulmonary capillary hydrostatic pressure. This escalation triggers a fluid build-up beyond the lymphatic interstitial drainage system's ability to eliminate, leading to a swift increase in interstitial and alveolar fluid volumes. Such accumulation subsequently results in intrapulmonary shunting and an advancing state of respiratory failure. Contemporary evidence hints at the potential of non-invasive ventilation (NIV) to cut back on the reintubation rate, along with the reduction of ICU and hospital mortality rates, particularly among patients scheduled for extubation. The aim of this review is to critically analyze the existent body of evidence concerning the application of NIV in managing ACPE. It seeks to explore the practical aspects of utilizing NIV within an emergency department environment, addressing crucial considerations such as patient selection, commencement of treatment, monitoring protocols, problem-solving strategies, and weaning processes. In addition, our review will also explore the data available on high flow nasal cannula, a relatively recent therapeutic intervention, discussing its role and effectiveness in treating respiratory insufficiency associated with ACPE.

Purpose of review: Heart failure (HF) remains a leading cause of morbidity and mortality worldwide. Increasing evidence highlights that systemic low-grade inflammation is a key pathophysiological driver of HF. This review seeks to examine the diagnostic and therapeutic relevance of inflammatory biomarkers - specifically interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) - and evaluate their potential for improving risk stratification and enabling personalized treatment approaches in HF.

Recent findings: IL-6 and hsCRP have emerged as important markers of residual inflammatory risk in HF. Elevated levels of these biomarkers are associated with increased risk of incident HF and adverse outcomes in established disease. While hsCRP is as a downstream marker of inflammation with no causal involvement, Mendelian randomization studies support a causal role of IL-6 signaling in the development of HF and coronary artery disease. Recent and ongoing clinical trials support the concept of targeting inflammatory pathways as a therapeutic strategy in selected HF populations. Inflammatory biomarkers, particularly IL-6 and hsCRP, are promising tools for advancing precision medicine in HF by improving individual risk assessment and guiding anti-inflammatory interventions. Further large-scale studies are needed to validate the integration of inflammatory biomarkers into clinical algorithms for HF and explore their potential role in future guideline recommendations and personalized prevention strategies.

Purpose of review: The global obesity epidemic has precipitated a surge in obesity-related heart failure with preserved ejection fraction (HFpEF), a distinct clinical phenotype characterized by exacerbated symptom burden, systemic inflammation, and impaired quality of life compared to non-obese HFpEF. While lifestyle modifications remain foundational, suboptimal adherence limits their efficacy. Bariatric surgery leads to the most dramatic and sustained weight loss but lacks a randomized trial for HFpEF-specific outcomes.

Recent findings: Recent landmark trials (STEP-HFpEF, STEP-HFpEF DM, SUMMIT) demonstrate that incretin-based therapies-glucagon-like peptide-1 receptor agonists (GLP-1RAs) and dual glucose-dependent insulinotropic polypeptide/GLP-1 receptor agonists-significantly ameliorate heart failure symptoms, attenuate heart failure worsening, and induce weight loss in obese HFpEF patients, irrespective of diabetes status. However, long-term cardiovascular mortality benefits and safety profiles require further validation. Sodium-glucose cotransporter-2 inhibitors and nonsteroidal mineralocorticoid receptor antagonists MRAs exhibit prognostic benefits in HFpEF, with post hoc analyses suggesting enhanced efficacy in higher BMI subgroups. Conversely, angiotensin receptor-neprilysin inhibitors and the controlled metabolic accelerator HU6 lack randomized trials to support routine use. A combination of incretin-based therapies, SGLT2 inhibitors, and non-steroidal MRAs may represent the optimal evidence-based strategy for obesity-related HFpEF at present. Future research should prioritize standardized definitions of obesity, BMI thresholds, weight loss targets, optimal combination strategies, and long-term outcome assessments.