Heart Failure Reviews最新文献

Hypertensive acute heart failure (HT-AHF) has historically been recognized as a distinct clinical phenotype of AHF, characterized by acute pulmonary congestion in the context of elevated systolic blood pressure (SBP), typically > 140 mmHg. However, emerging evidence has begun to challenge the diagnostic accuracy, clinical utility, and relevance of this category. A main criticism of HT-AHF is its considerable overlap with other AHF clinical profiles, including acute decompensated heart failure (ADHF) and acute pulmonary oedema (APO). Clinical features such as dyspnea and pulmonary congestion are not unique to HT-AHF. Additionally, some HT-AHF patients concurrently fulfill diagnostic criteria for the ADHF phenotype, including a history of HF or signs of volume overload, leading to ambiguity in diagnosis. HT-AHF is associated with very low in-hospital mortality (0-2%) compared to other AHF phenotypes. Notably, there is no robust evidence linking high SBP to poor short- or long-term outcomes, nor are there randomized clinical trials validating distinct management strategies for HT-AHF. Often associated with the management of HT-AHF, vasodilators have shown limited benefit across trials, contributing to a downgrade in guideline recommendations. The relatively favorable short-term prognosis and the lack of a standardized, evidence-based treatment approach weaken the rationale for classifying HT-AHF as a standalone AHF category. Given the heterogeneity of clinical presentations, overlap with other AHF phenotypes, and lack of prognostic distinction or targeted therapy, the term "AHF with high SBP at presentation" offers a more flexible and clinically meaningful descriptor, encouraging a more nuanced approach to treatment.

Although congestion is present in the large majority of patients hospitalized with acute heart failure (AHF), the pharmacological options to treat it remain poorly studied, with heterogeneity in real-world practices and outcomes. The best available evidence supports that patients with AHF and congestion should be initially treated with i.v. loop diuretics with their dose tailored to early (within 2-6 h) diuretic response, as assessed by spot urine sodium and/or hourly urine output. If diuretic response is sub-optimal, the next best steps seem to be increases in i.v. loop diuretics and addition of a thiazide and/or i.v. acetazolamide. Irrespective of the above, sodium-glucose co-transporter-2 inhibitors and spironolactone should be started in all patients with AHF as early as possible. Changes in serum creatinine in this scenario do not typically represent true worsening in renal function and should, thus, not lead to de-escalation of decongestion therapy.

Heart failure (HF) and chronic kidney disease (CKD) are prevalent comorbidities that significantly impact patient outcomes, with nearly half of HF patients experiencing renal impairment. The challenges associated with implementing guideline-directed medical therapy (GDMT) for patients with HF and CKD emphasize the role of electronic medical records (EMRs) as clinical decision-support tools. Despite the proven benefits of GDMT in improving survival and reducing hospital readmissions, many eligible patients do not receive optimal therapy due to barriers such as alert fatigue, medication costs, and the complexity of managing coexisting conditions. EMR prompts and alerts can help early detection and risk stratification of CKD, utilizing biomarkers such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR). EMRs can facilitate the timely initiation and titration of GDMT, ensuring adherence to clinical guidelines. However, the effectiveness of these alerts can be compromised by irrelevant notifications and outdated information, leading to "alert fatigue". Furthermore, integrating machine learning (ML) and artificial intelligence (AI) into EMR systems can enhance personalized healthcare approaches for HF and CKD patients. Future research directions include developing noninvasive biomarkers and validating ML models to ensure they meet clinical needs. These efforts will ultimately aim to provide individualized treatment strategies for patients with HF and CKD.

Chronic obstructive pulmonary disease (COPD) and heart failure (HF) frequently coexist and interact through complex and bidirectional hemodynamic mechanisms that amplify symptoms' burden and complicate clinical management. The present review explores the impact of COPD across the HF spectrum, particularly in HF with preserved ejection fraction (HFpEF), where comorbidities, such as COPD, exert a dominant role in disease expression. COPD-induced hyperinflation reduces cardiac preload and increases right ventricular afterload, while HF-related congestion impairs pulmonary function and gas exchange, illustrating a tight cardiorespiratory coupling. Diagnostic challenges stem from overlapping symptoms and the limited specificity of biomarkers, such as natriuretic peptides, especially in HFpEF. Cardiopulmonary exercise testing (CPET) emerges as a valuable tool for distinguishing between cardiac and pulmonary limitations and guiding individualized treatment strategies. From a therapeutic standpoint, β1-selective blockers are not only safe in COPD patients but are pivotal in those with HF with reduced ejection fraction (HFrEF), where they have been demonstrated to improve survival and reduce both HF and COPD exacerbations. Concerns regarding bronchodilator safety in HF remain largely theoretical, with current evidence supporting their continued use when clinically indicated. Ultimately, optimal care for patients with coexisting COPD and HF requires a phenotype-specific approach, incorporating insights from pathophysiology, diagnostic innovation, and evidence-based pharmacotherapy to improve outcomes in this challenging patient population.

Pulmonary arterial hypertension (PAH) is a rare and progressive disease characterized by pathological remodeling of the pulmonary arteries, resulting in increased pulmonary vascular resistance and right ventricular overload. This condition triggers common symptoms such as dyspnea and exercise intolerance, compromising thus the quality of life of individuals affected by this pathology. Skeletal muscle atrophy is one of the main determinants of these symptoms, which is mediated by an imbalance between protein synthesis and degradation, triggered by adverse systemic adaptations promoted by PAH, such as decreased blood perfusion and increased inflammation. This review addresses the main cellular and molecular mechanisms that potentially trigger or inhibit protein degradation pathways, and how they interact in the context of PAH. Furthermore, we focus on physical exercise as a non-pharmacological approach capable of modulating muscle atrophy induced by PAH.

Hypoalbuminemia is commonly seen in patients with heart failure and is associated with worse outcomes. Multiple pathophysiologic mechanisms can contribute to low albumin levels in heart failure patients, such as malnutrition, hepatic congestion, inflammation, and protein-losing enteropathy. Hypoalbuminemia can exacerbate heart failure symptoms and contributes to pulmonary edema by reducing plasma oncotic pressure, thereby favoring fluid movement into the interstitial and alveolar spaces. In this sense, albumin supplementation has been used in clinical practice to stimulate diuresis. However, evidence regarding its efficacy remains controversial. Routine albumin use does not appear to improve outcomes and should not be adopted broadly. Instead, it may be considered selectively in those with refractory edema or ascites despite maximal diuretic therapy and in whom hypoalbuminemia is profound. While proper oral nutrition has clearly shown better outcomes in malnourished heart failure patients, no clear guidelines about the use of intravenous albumin therapy are currently available to guide this practice. This article aims to review the pathophysiology of hypoalbuminemia in heart failure and the current available evidence on the therapeutic role of albumin infusion.

Cardiac rehabilitation (CR) is a comprehensive, multidisciplinary approach that combines exercise training, risk factor management, and psychosocial support, contributing to managing heart failure (HF). Despite its proven benefits, CR remains underutilized due to challenges such as limited accessibility and patient adherence. This reviews the beneficial effects of exercise on HF, including improvements in peak oxygen consumption. It outlines the key steps on the patient's journey toward a CR program, such as referral processes, risk stratification, and exercise prescription. It also explores the different types of CR programs and delivery models designed to enhance patient engagement and improve long-term adherence. Furthermore, it outlines clinical scenarios needing customized exercise prescriptions, including atrial fibrillation, pacemakers, implantable cardioverter-defibrillators, ventricular assist devices, and heart transplantation.

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.