Typically, heart failure (HF) is definitively diagnosed and treated with guideline-directed medical therapy late in its natural history, with reported delays, missed investigation and inpatient diagnoses associated with poor outcomes. Accordingly, better, more decisive primary care can and should play a critical role in addressing this seemingly intractable problem. However, as reflected by a paucity of evidence to inform the recommendations of expert HF guidelines, primary care teams are rarely considered as part of the solution. In this review, we explore all the potential outcomes from more proactive screening for HF in primary care when introducing artificial intelligence-mediated portable cardiac ultrasound. Based on the strengths and weaknesses of the screening components that can now be applied, we consider the spectrum of early to late forms of HF likely to be revealed and more immediately diagnosed. Within this context, we present, as an example of what can be achieved in this space, a clinical algorithm that was developed for a prospective, multicentre project to find and manage HF earlier in the primary care setting.
The prevalence of obesity among the general population has resulted in significant overlap and complex interactions with heart failure. This review aims to describe recent changes to the definition of obesity and explore direct and indirect mechanistic links between obesity and heart failure. Diagnostic challenges presented by obesity regarding echocardiography and B-type natriuretic peptide are also explored. Treatment options and the evidence base for addressing obesity in heart failure are examined across both heart failure with preserved ejection fraction and heart failure with reduced ejection fraction. Finally, the safety profile of new incretin-based therapies is examined.
Acute heart failure (AHF) is a leading cause of hospitalisation worldwide, with the majority of cases triggered by an identifiable precipitant. Recognition of these precipitants is important for both acute management and long-term prevention, as they are frequently reversible, carry prognostic significance and directly inform targeted therapy. The epidemiology of precipitants varies across settings, and patterns are evolving as the prevalence of heart failure with preserved ejection fraction rises. In this review, we summarise the epidemiology, diagnostic evaluation and management of the most common precipitants of AHF. Globally, the leading precipitants of AHF are ischaemia/acute coronary syndrome, infection, arrhythmias, uncontrolled hypertension, nonadherence and renal dysfunction, although their relative distribution varies by geography and heart failure phenotype. Optimal medical management necessitates initial haemodynamic stabilisation, identification of the underlying precipitant and delivery of targeted therapy. Importantly, successful identification and treatment of a reversible precipitant should not preclude initiation or optimisation of guideline-directed medical therapy, which remain essential for long-term outcomes.
The interplay between sleep-disordered breathing (SDB) and cardiovascular disease, particularly arrhythmias and heart failure, is complex and bidirectional. This article examines the impact of SDB in cardiovascular disease and heart failure. It is proposed that teams interested in improving SDB diagnosis and management take ACTION (assess for risk factors/screening in each visit; collaborate with sleep colleagues for referrals/visits; test for SDB with home sleep apnoea test, polysomnography; intervene with SDB-specific treatment (oral devices, continuous positive airway pressure, bilevel positive airway pressure, phrenic nerve and hypoglossal nerve stimulators) including risk factor modification (weight reduction, alcohol abstinence); continue ongoing assessment by cardiology and sleep teams for feedback about treatment; creating niche programmes for AF, heart failure and weight loss.
Central sleep apnoea (CSA) and Cheyne-Stokes respiration are prevalent in patients with heart failure and contribute to disease progression, increased risk of death, heart failure hospitalisations and reduced quality of life. The 2025 American Academy of Sleep Medicine Clinical Practice Guideline for the Treatment of Central Sleep Apnea in Adults represents a major advance, recognising transvenous phrenic nerve stimulation as an evidence-based therapy for adults with CSA, including those with heart failure, as well as updating the clinical data on adaptive servo-ventilation. This review summarises key updates in the American Academy of Sleep Medicine 2025 guideline, examines the pathophysiological link between CSA and heart failure, and evaluates the clinical evidence and practical considerations for treatment. Current evidence indicates improvements in apnoea indices, oxygenation and quality of life, while the effect on mortality and hospitalisation needs additional prospective randomised data. Identification of patients with signs and symptoms which are likely due to central sleep apnoea is often missed in clinical practice, and treatment has a significant impact on quality of life.
Background: Exercise intolerance in heart failure reflects heterogeneous mechanisms, including coronary microvascular dysfunction (CMD), obesity and sarcopenia. The aim of this study was to investigate the relationships between cardiopulmonary exercise capacity, coronary microvascular function and body composition in patients with suspected heart failure with preserved ejection fraction (HFpEF). Methods: In this single-centre cross-sectional study, consecutive patients presenting with chest discomfort or dyspnoea and an intermediate or high probability of HFpEF were enrolled. All patients underwent body composition analysis, adenosine stress echocardiography for coronary flow reserve (CFR) and cardiopulmonary exercise testing to assess peak oxygen consumption (VO2peak). Results: Of the 101 patients (mean age 63 years; 52.0% women), CMD (CFR <2.5) was present in 40.6%. Mean VO2peak was 23.0 ± 5.3 ml/min/kg. Patients with lower VO2peak (<23 ml/min/kg) had higher visceral fat area and percentage body fat. VO2peak correlated positively with CFR (r=0.344, p<0.001) and septal e′ velocity and inversely with E/e′. Skeletal muscle mass index correlated positively with VO2peak predominantly in obese patients (BMI ≥25 kg/m2). In multivariable analysis, both CFR and degree of body fat remained independent correlates of VO2peak. Conclusion: In patients with suspected HFpEF, cardiopulmonary exercise capacity is closely associated with left ventricular diastolic function, coronary microvascular function and body composition. Preserved skeletal muscle mass may mitigate the adverse impact of obesity on exercise performance. These findings highlight the importance of integrated assessment of CMD and body composition and support targeted lifestyle and exercise interventions to improve functional capacity in HFpEF phenotypes.
Background: Cardiovascular complications are a leading cause of morbidity and mortality following non-cardiac surgery. Although the association between systolic dysfunction and perioperative outcomes is well recognised, the prognostic significance of diastolic dysfunction remains underexplored and is not incorporated into risk models. This study investigated whether preoperative diastolic dysfunction is associated with adverse in-hospital outcomes following non-cardiac surgery. Methods: This retrospective cohort study included 3,882 adults who underwent non-cardiac surgery between 2011 and 2021 and had preoperative echocardiographic assessment of diastolic function. Diastolic dysfunction was graded per 2016 American Society of Echocardiography guidelines and categorised as normal/grade 1 (normal left-sided filling pressure [NLFP]) or grade 2/3 (elevated left-sided filling pressure [ELFP]). The primary outcome was a composite of in-hospital mortality and acute heart failure. Results: The primary outcome occurred in 22.3% of patients with ELFP and 11.6% of patients with NLFP (OR 2.1; 95% CI [1.7–2.6]; p<0.001). In-hospital mortality was 9.1% in the ELFP group and 4.2% in the NLFP group (OR 2.2; 95% CI [1.6–3.0]). Pulmonary oedema (3.8% versus 0.7%; OR 4.9; 95% CI [2.9–8.4]), furosemide use (12.9% versus 5.5%; OR 2.5; 95% CI [1.9–3.2]) and vasoactive medication administration (7.9% versus 5.4%; OR 1.5; 95% CI [1.1–2]) were more frequent in the ELFP group. These associations persisted after adjustment for echocardiographic and clinical parameters. Stratified analysis showed the association was strongest in intermediate- to high-risk surgeries. Conclusion: Diastolic dysfunction is independently associated with adverse postoperative outcomes in non-cardiac surgery. Incorporating diastolic parameters into preoperative risk assessment may improve perioperative outcomes.
To determine the effects of the comprehensive disease-modifying pharmacological approach among patients with heart failure with reduced ejection fraction, a cross-trial, aggregate-data analysis was performed to estimate the expected combined effect of quintuple therapy by multiplying trial-level HRs, assuming independent and multiplicative treatment effects from Phase III randomised clinical trials: EMPHASIS-HF, PARADIGM-HF, pooled DAPA-HF and EMPEROR-Reduced, and pooled VICTORIA and VICTOR. The imputed aggregate treatment effects on the primary endpoint of cardiovascular death or first heart failure hospitalisation were favourable to the quintuple compared with conventional therapy (HR 0.34; 95% CI [0.27–0.42]). This also occurred for cardiovascular death alone (HR 0.47; 95% CI [0.35–0.63]), first heart failure hospitalisation (HR 0.31; 95% CI [0.23–0.40]) and all-cause mortality (HR 0.51; 95% CI [0.39–0.67]). The numbers needed to treat per year for the primary outcome, cardiovascular death and first heart failure hospitalisation were 10, 23 and 15, respectively. Our findings support the potential benefit of comprehensive therapy, with the incremental role of vericiguat likely greatest in higher-risk patients or those with recent worsening heart failure.
This paper discusses the considerations for multidimensional and multidisciplinary management of heart failure (HF) patients with frailty. Frailty is a multidimensional, dynamic and potentially reversible state, defined by clinical, functional, psycho-cognitive and social domains. Frailty is seldom systematically assessed in clinical practice in HF patients. Paradoxically, although the absolute benefit of HF guideline-directed medical treatment in frail HF patients seems greater, it is under-prescribed. This therapeutic gap could be related to different reasons, such as concerns about safety, polypharmacy and the lack of specific evidence-based data. Frail HF patients require a comprehensive, multidimensional therapeutic strategy that integrates available evidence-based pharmacological interventions with targeted non-pharmacological modalities across multiple clinical disciplines to optimise patient outcomes. The four domains of frailty should be objectively and routinely assessed with a multidimensional approach to facilitate a more individualised and comprehensive care plan delivered by a multidisciplinary team. In the future, we need more dedicated studies and randomised clinical trials that include frail HF patients.
Acute heart failure with preserved ejection fraction (acute heart failure-heart failure with preserved ejection fraction) is increasingly prevalent, resulting from the interaction between a dysfunctional ventricle, the patient's comorbidity burden and acute triggers. Patients are typically older, commonly female and have cardiometabolic, renal, arrhythmic, ischaemic and inflammatory comorbidities that produce vulnerability to decompensation. Acute episodes manifest with pulmonary and/or systemic congestion, from abrupt rises in left-sided filling pressures due to cardiac and arterial stiffness driven by neurohormonal activation and inflammation. Congestion and elevated blood pressure are common, but clinical presentation is more heterogeneous, reflecting the haemodynamic abnormalities, severity of triggers and comorbidity load. Diagnosis relies on integrating clinical context, echocardiography, adjusted thresholds of natriuretic peptides, and invasive and/or stress haemodynamics when diagnosis is uncertain. Management requires individualised decongestion, alongside treatment of precipitants. Early initiation of disease-modifying therapies after haemodynamic stability, including sodium-glucose cotransporter 2 inhibitors, mineralocorticoid receptor antagonists and glucagon-like peptide-1 receptor agonists, improves outcomes. Acute heart failure-heart failure with preserved ejection fraction follows a relapsing-remitting trajectory, underscoring the importance of comorbidity management, structured follow-up and preventive strategies.
Acute heart failure (AHF) is a systemic condition characterised by multiorgan involvement that varies from subclinical to overt organ failure. The liver is particularly vulnerable due to its dual blood supply and sensitivity to haemodynamic and inflammatory disturbances. Abnormal liver function tests are highly prevalent in patients with AHF, reflecting major mechanisms: passive hepatic venous congestion from elevated central venous pressure, hepatocellular ischaemia from low cardiac output, systemic inflammation and poor metabolic status associated with cachexia. In patients with AHF, liver function tests at admission, during hospitalisation and at discharge are independently associated with rehospitalisation, cardiovascular and all-cause mortality. Persistent abnormalities after hospitalisation often reflect incomplete decongestion or irreversible structural liver changes. Therapeutic strategies focus on decongestion, optimisation of cardiac output and medication adjustments to avoid hepatotoxicity. Despite significant advances in understanding cardio-hepatic interactions, major gaps remain, including the lack of standardised definitions, limited mechanistic studies and the underrepresentation of patients with heart failure with preserved ejection fraction in contemporary research. Future research should explore targeted therapies to improve cardiohepatic interactions and patient outcomes.
Heart failure (HF) continues to challenge clinicians worldwide, not only because of its high morbidity and mortality but also due to the persistent difficulty in translating therapeutic advances into routine care. Despite the availability of effective treatments, data show striking gaps in the optimal use of guideline-directed medical therapy. Among the four pillars of guideline-directed medical therapy, mineralocorticoid receptor antagonists (MRAs) remain the least prescribed. This underuse is concerning considering the evidence demonstrating consistent benefits of MRAs across different HF phenotypes. In this review, we revisit the role of MRAs across the spectrum of HF. We summarise the supporting evidence, discuss their mechanisms of action and provide practical guidance on patient eligibility and initiation strategies. In addition, we address common barriers that often limit their use. By combining mechanistic insights, trial evidence and pragmatic recommendations, this review aims to facilitate broader and earlier use of MRAs, thereby helping to close a major gap in the implementation of evidence-based HF care.
Background:The prognostic significance of obesity in patients hospitalised for acute heart failure (HF) remains uncertain, particularly among older adults. This study aimed to assess whether three obesity definitions - BMI, waist circumference and the clinical obesity framework - predict hospital length of stay (LOS) in older adults hospitalised for acute decompensated HF. Methods:This post hoc exploratory analysis used data from a prospective cohort of 250 adults aged ≥60 years hospitalised for acute decompensated HF. Obesity was defined as: BMI ≥30 kg/m²; waist circumference ≥102 cm in men or ≥88 cm in women; and clinical obesity per the Lancet Diabetes & Endocrinology Commission, applied post hoc. LOS was modelled using univariable and multivariable negative binomial regression. Results:None of the three obesity definitions were independently associated with LOS. In the multivariable models, only N-terminal pro-B-type natriuretic peptide (NT-proBNP) was an independent predictor of LOS in patients with clinical obesity (incidence rate ratio [IRR] 1.004 per 100 pg/ml; p=0.004). Among those with classical obesity, New York Heart Association class IV (IRR 2.355; p=0.004), NT-proBNP (IRR 1.004; p=0.004), and smoking history of 41-50 pack-years (IRR 1.946; p=0.022) remained independently associated with longer LOS. For central obesity, haemoglobin (IRR 0.923; p=0.029) and NT-proBNP (IRR 1.004; p<0.001) were significant predictors. Conclusion:In this cohort of older adults hospitalised for acute decompensated HF, none of the three obesity definitions - including the new clinical obesity framework - were independent predictors of LOS.
Heart failure with preserved ejection fraction (HFpEF) is associated with reduced functional capacity and quality of life, as well as with high rates of heart failure hospitalisation and mortality. Valvular heart disease (VHD) is frequently encountered in patients with HFpEF, and both conditions share common risk factors, such as age, hypertension, diabetes and coronary artery disease, which may contribute to their shared pathogenesis and progression. With recent advances in percutaneous therapies for VHD and an improved understanding of HFpEF, there is a growing interest in the relationship between VHD and HFpEF. In this review, we provide an overview of the pathophysiology, epidemiology and management strategies of tricuspid regurgitation, mitral regurgitation, aortic stenosis and aortic regurgitation in the setting of HFpEF.
There is a large spectrum of acute decompensated heart failure presentations resulting from the interaction between an acute precipitant and the patient’s underlying cardiac and non-cardiac conditions. A robust classification scheme at admission is crucial for appropriate triage and targeted treatment of high-risk populations. Such a scheme should incorporate timely actionable items to generate immediate management decisions, including characteristics that suggest life-threatening clinical presentations, the factors that could be favourably modified by in-hospital interventions, such as correctable aetiologies and congestion/hypoperfusion status, and in-hospital trajectories determined by patient responses to inpatient treatment. In-hospital trajectories determine the intensity of escalation therapies and timing for initiation/up-titration of guideline-directed medical treatment. In the long term, some patients experience a progressive downsloping course culminating in advanced heart failure, while others maintain a relatively stable remitting-relapsing trajectory. For future clinical trials, a comprehensive classification scheme integrating in-hospital and long-term trajectories could profoundly affect study design by ensuring interventions are tested in more homogeneous patient populations and facilitating nuanced patient stratification.
Hypertrophic cardiomyopathy (HCM) is a genetic disease present in 0.2% of the general population. It is defined by the presence of an increased left ventricular wall thickness (with or without right ventricular hypertrophy) or mass that is not solely explained by abnormal loading conditions. The vast majority of genes and mutations underlying HCM encode sarcomere proteins or sarcomere-associated proteins. The clinical presentation of the disease is highly heterogeneous and can present in all age groups. Most affected individuals will achieve a normal life expectancy without disability, but some patients with HCM can present significant complications, including sudden cardiac death, heart failure and AF. The selection of patients for the best therapeutic approach requires accurate diagnosis and phenotyping of the disease. In addition, differential diagnosis with other entities that can present with left ventricular hypertrophy is key to prescribing the most appropriate therapy. Multimodality imaging plays a key role in the characterisation of HCM.
Patients with chronic kidney disease and/or cardiovascular disease are at heightened risk of developing hyperkalaemia. This electrolyte disorder is prevalent and, if left untreated, typically results in fatal outcomes. The implementation of standardised, specialised management strategies represents a valuable tool for clinicians in the care of these patients. The primary objective of this study is to present a consensus document for the management of hyperkalaemia of cardiorenal origin, developed by a group of experts in cardiology and nephrology, opinion leaders in Mexico. To this end, a Delphi panel was formed, comprising a group of cardiologists and a group of nephrologists, each coordinated by a leader who concentrated the information. The panellists responded to a questionnaire that was sent to them. In a virtual meeting, the responses were reviewed and a consensus was reached by all participants based on the current literature.
Heart failure (HF) is one of the most difficult challenges in cardiology nowadays, constituting a significant global epidemiological, social and economic burden. For many years, there has been a search for new risk factors that predispose to the development of HF and biomarkers that could indicate HF patients with a poorer prognosis. Lipoprotein(a) (Lp[a]) is an estimated risk factor for atherosclerotic cardiovascular disease and aortic valve stenosis, but its causal role in HF has not been clearly defined yet. The results of the few studies regarding the influence of elevated Lp(a) on the development and course of HF are uncertain. However, most authors suggest that elevated Lp(a) increases the risk of HF and may correlate with a higher risk of major adverse cardiovascular events. The aim of this review is to present the current state of knowledge on the importance of the association between Lp(a) levels and HF, from pathophysiology to clinical practice including current management.
