Heart Failure Reviews最新文献

Chemotherapy-induced cardiomyopathy (CHIC) represents a growing clinical challenge due to the increasing use of cardiotoxic treatments. These therapies can lead to progressive myocardial dysfunction, ultimately resulting in heart failure. Cardiac resynchronization therapy (CRT) has been widely investigated in selected patients with chronic heart failure; however, those with CHIC remain underrepresented in CRT trials. Current evidence is largely based on retrospective and observational studies, with MADIT-CHIC being the only prospective trial to date. No randomized controlled trials are currently available. Despite encouraging findings, existing data remain limited by small sample sizes and short follow-up durations. In particular, the impact of CRT on left ventricular dyssynchrony, arrhythmic burden, and long-term survival in this population has not been fully elucidated. A multidisciplinary cardio-oncology approach is essential not only for the comprehensive management of these complex patients, but also to guide appropriate timing of CRT implantation. Further research is warranted to refine patient selection criteria and to fully assess the long-term benefits and risks of CRT in patients with CHIC.

Transthoracic echocardiography has a central role in the diagnosis and monitoring of cancer therapy-related cardiac dysfunction, offering a reliable, non-invasive, and cost-effective tool for the early detection of myocardial damage and the timely and effective management of cardiotoxicity. This review provides a practical and comprehensive framework for the echocardiographic assessment of oncology patients, focusing on both traditional and emerging ultrasound parameters of left and right ventricular function, and their diagnostic and prognostic value in the field of cardio-oncology. Moreover, the review discusses key aspects of pericardial disease, valvular heart disease, and intracardiac masses, which may be consequences of cancer therapy or tumor progression. Finally, the role of multimodal imaging, in particular cardiac magnetic resonance and computed tomography, is examined, especially in selected cases to supplement echocardiographic findings or when echocardiography presents limitations. Based on current guidelines and clinical experience, this review aims to provide both cardiologists and oncologists with a practical tool for interpreting echocardiographic reports in cancer patients. Additionally, a therapeutic algorithm is proposed to guide decisions on cancer treatment management and timely initiation of cardioprotective strategies in selected contexts. Close collaboration between cardiologists and oncologists remains essential to reduce cancer patients' cardiovascular risk, allowing them to access the best possible treatment and optimize outcomes by balancing anticancer therapy efficacy with cardiovascular safety.

Hypertrophic cardiomyopathy (HCM) is a genetic heart disorder defined by the presence of a maximal wall thickness of at least 15 mm with two main forms: obstructive (oHCM) and nonobstructive (nHCM). While oHCM is characterized by left ventricular (LV) outflow tract obstruction (LVOTO), nHCM lacks this feature and shows significant variability in its hemodynamic and anatomical traits. In nHCM, LV hypertrophy (LVH) presents diverse morphologies, including apical hypertrophy and reverse septal curvature, the latter potentially causing mid-ventricular obstruction and near-complete LV emptying. Apical hypertrophy is associated with the risk of LV aneurysms, potentially leading to arrhythmias and thromboembolism. These findings challenge the belief that nHCM is a more benign phenotype than oHCM and highlight the necessity for improved diagnostic and therapeutic strategies. Symptoms in nHCM, such as fatigue and dyspnea, are often attributed to diastolic dysfunction, whereas symptoms like angina are attributed to microvascular dysfunction. However, current treatment options remain limited, as traditional heart failure therapies frequently fail to provide substantial benefits. Given its heterogeneity, a more personalized treatment approach is warranted, including optimizing comorbidities, assessing coronary microvascular dysfunction, and considering alternative pharmacologic strategies. Emerging therapies, such as myosin inhibitors mavacamten and aficamten, target sarcomeric hypercontractility and show promise in early trials, but their clinical impact on nHCM is still under investigation. Gene therapies also hold potential, though their applicability to nHCM is limited by the high rate of mutation-negative cases and the potential irreversibility of advanced disease states. This review critically analyzes the pathophysiological mechanisms of nHCM, evaluates current and emerging therapeutic strategies, and provides guidance on contemporary management approaches for this complex and often underrecognized condition.

Heart failure with preserved ejection fraction (HFpEF) is characterized by elevated left-ventricular (LV) filling pressures largely owing to diastolic dysfunction and stiffness. The measurement of filling pressure presents unique challenges as cardiac structures live within the context of the thorax. The heart and pulmonary vasculature are therefore subjected to the same changes in external volume as the lung. Here, we review the mechanisms by which LV filling pressure interacts with the thoracic space, with a particular focus on patients with HFpEF during rest and exercise. Specifically, we discuss the means by which intrathoracic volume impacts ventricular filling and function. We outline the interacting compliances within the thoracic cavity which can alter intrathoracic and therefore cardiac filling pressures. We also detail means by which intrathoracic pressure can be modulated by different conditions and body positions, such as supine posture, gravity, and obesity. Throughout, we highlight gaps in the literature as well as perspective towards possible future directions.

Device-based therapies have become integral in the management of heart failure (HF). By targeting structural or neurohormonal pathways, these therapies provide additional benefits beyond those provided by pharmacologic therapies or correct structural abnormalities that may not be amenable to drug therapy. However, a comprehensive framework for device selection tailored to individual clinical profiles and comorbidities has not yet been proposed, and many potentially effective approaches are underutilized among eligible patients in clinical practice. The availability of such a framework could help maximize the benefits of available therapies for the broad population of patients with HF. In this review, we explore the current role of device-based HF therapies in clinical practice based on available evidence from clinical trials and propose a phenotype-driven framework to guide device selection in HF patients with reduced and preserved ejection fraction. We also outline future directions, emphasizing opportunities to improve HF care.

Atrial fibrillation (AF) and heart failure with a preserved ejection fraction (HFpEF) frequently co-exist and are associated with high cardiovascular morbidity and mortality. The management of AF in HFpEF requires a multifaceted and integrated approach that includes the initiation of evidence-based medical therapies for heart failure, control of arrhythmia symptoms and burden with rhythm or rate control, assessment of thromboembolic risk with treatment, and aggressive control of common clinical comorbidities. The optimal management strategy of AF is uncertain though subanalyses of randomized trials and retrospective studies suggest an improvement in cardiovascular outcomes with a catheter ablation-based rhythm control strategy, especially in patients with HFpEF and paroxysmal or early persistent AF. In this review, we summarize this integrated approach to the management of AF in HFpEF, examine the evidence for recommending first-line rhythm versus rate control, and highlight key areas in need of further study.

In contemporary clinical practice, pulmonary hypertension (PH) is most commonly caused by heart failure with preserved ejection fraction (HFpEF). This high prevalence of HFpEF-related PH has contributed to complexity in diagnosis and evaluation of PH in the context of other diseases such as the presence of risk factors for group 1 PH. In this review, we discuss emerging concepts guiding the evaluation, pathobiology, and treatment of PH in patients with HFpEF or HFpEF-associated risk factors.

The pathogenesis of heart failure (HF) is complex, and from an immunological perspective, the "gut-heart axis" plays a pivotal role in its development. The composition of gut microbiota differs significantly between HF patients and healthy individuals, with variations observed across different nations, HF etiologies, and stages defined by the New York Heart Association (NYHA) classification. Moreover, gut-derived metabolites such as short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO), bile acids, and lipopolysaccharides (LPS) influence HF progression through specific mechanisms and signaling pathways. Notably, medications recommended in cardiovascular diseases and advanced interventions applied in HF, such as heart transplantation requiring immunosuppressive therapy or the implantation of mechanical circulatory support devices, are associated with significant alterations in gut microbiota composition. However, these mechanisms are still not well-established. This review aims to summarize current data on the impact of the gut microbiome on HF progression and treatment, encompassing both standard medical treatment and advanced therapies of HF.

Heart failure with preserved ejection fraction (HFpEF) accounts for nearly 50% of all heart failure cases and remains a significant clinical challenge. It is characterized by a complex pathophysiology involving multiple comorbidities and overlapping symptoms between heart failure and these comorbid conditions (e.g., obesity). Due to this complexity, several pharmacological treatments that have proven effective in heart failure with reduced ejection fraction (HFrEF) have failed to improve outcomes in HFpEF. More recently, mineralocorticoid receptor antagonists, sodium-glucose co-transporter 2 (SGLT2) inhibitors, and glucagon-like peptide-1 (GLP-1) receptor agonists have shown potential benefits in symptom relief and prognosis improvement in patients with HFpEF. In recent years, artificial intelligence has demonstrated the ability to identify distinct HFpEF phenotypes associated with varying risks of cardiovascular outcomes. In this context, clinicians should be able to recognize patients who require closer monitoring and more intensive follow-up. Given the frequent scarcity of healthcare resources, which can negatively impact patient management, remote monitoring may serve as a valuable tool in the follow-up of HFpEF patients. This review aims to describe and highlight these key aspects of HFpEF, with a particular focus on recent evidence and emerging strategies in disease management.