Latest articles

The 2026 European Society of Cardiology (ESC) heart failure guidelines represent an important shift in how we think about this disease.¹ Heart failure (HF) is no longer simply a syndrome treated once symptoms develop; it is a continuum from cardiovascular risk to cardiac change and overt disease. The greatest gains may come from identifying patients earlier, before irreversible changes occur. The question is no longer simply, “How should we treat HF?”, but “How early should we intervene, and can we prevent it?”

It is impossible to cover every change within such comprehensive guidelines in a single opinion piece. We, therefore, focus on four clinically important developments: the prevention-focused stages A–D, revised left ventricular ejection fraction (LVEF) classification, replacement of guideline-directed medical therapy (GDMT) with more precise terminology, and earlier referral in stage D.

Cardiovascular–kidney–metabolic (CVKM) care is increasingly recognised as a more realistic way to understand and manage chronic disease. Cardiovascular disease, chronic kidney disease (CKD), type 2 diabetes, obesity, and metabolic dysfunction-associated steatotic liver disease (MASLD) frequently co-exist, share major risk factors, and influence one another biologically and clinically. Yet care delivery across the National Health Service (NHS) remains largely organised around separate pathways, disease-specific targets, and professional silos. This creates a practical mismatch between integrated disease biology and fragmented service delivery.^1–3

A coherent CVKM approach is, therefore, not simply a new label for existing practice. It is a shift in clinical reasoning and system design: away from isolated disease management and towards integrated risk reduction, prioritisation, and patient-centred decision-making.^4,5 The challenge is no longer only to identify effective therapies, but to deliver them in ways that are meaningful, equitable, and sustainable across real-world primary and secondary care.^6–8

To pace or not to pace? Clinical decision-making for older people with frailty and bradycardia is often challenging. For ambulatory, symptomatic patients a pacing strategy is clearly recommended, however, for those patients with severe frailty or limited mobility with an absence of clearcut symptoms, management strategies usually take a shared decision-making approach. How are clinicians expected to provide patients and carers with an objective picture of things to come in such an evidence-light space? The featured publication by Warraich et al., entitled “Outcomes of bradyarrhythmia device implantation: a single-centre retrospective cohort study”, from this issue at https://doi.org/10.5837/bjc.2026.052, is a call to arms to aid clinicians by providing some metrics around the likelihood of benefit. Bradycardia and bradyarrhythmias are common in older people reaching the end of their natural life, and patients, families and clinicians are reluctant to implant a pacemaker device when impact on quality of life is doubtful. This said, syncope can have devastating consequences, particularly hip fractures and head injuries, so there is a risk either way. Geriatricians are heavily invested in falls prevention, and the promotion of physical activity to improve health and wellbeing in the latter stages of life, so implantation is usually the preferred choice in the majority of cases, but where should we draw the line?

There is growing evidence for mortality with increasing age and comorbidities in implantable cardiac defibrillator receivers. We aimed to characterise how frailty and comorbidities impact mortality in patients receiving simple bradyarrhythmia device implants.

A retrospective cohort of 700 consecutive individuals who underwent novel bradyarrhythmia devices in a single centre were studied. Results were analysed using a multi-variate Cox regression model hazard ratios (HR) and Kaplan-Meier curves.

Mean implant age was 78.4 ± 10.3 years; 53.9% inpatient implants. All-cause mortality rate was 12.4% at one year. Mild-to-severe frailty measured by Rockwood frailty score (RFS) 5–9 was associated with mortality overall (HR 1.70, 95% confidence interval [CI] 1.30 to 2.21). Both inpatient (HR 1.57, 95%CI 1.19 to 2.08) and single-lead implants (HR 1.63, 95%CI 1.20 to 2.21) were associated with mortality.

Patient characteristics include male gender (HR 1.49, 95%CI 1.15 to 1.92) and age per 10-year increment (HR 1.75, 95%CI 1.46 to 2.09), heart failure syndrome (HR 1.52, 95%CI 1.13 to 2.05), valvular heart disease (HR 1.88, 95%CI 1.33 to 2.65), obesity (HR 2.97, 95%CI 1.42 to 6.21), chronic kidney disease (HR 1.34, 95%CI 1.00 to 1.79) and malignancy (HR 1.55, 95%CI 1.09 to 2.19) were associated with mortality.

In conclusion, higher RFS, male gender, heart failure syndrome, valvular heart disease, chronic kidney disease, obesity and malignancy were associated with mortality. Although advanced age does not preclude pacing, consideration should be given to frailty, which may detract from any perceived benefit bradyarrhythmia correction may offer.

The population of adults living with congenital heart disease (CHD) has expanded substantially over the last 40 years due to advances in diagnostic, transcatheter, and surgical techniques. Consequently, clinicians, regardless of their specialty, will encounter patients presenting with sequelae of both simple and complex CHD more frequently. Familiarisation with the pathophysiology and basic management of these conditions, including the role of adult congenital heart disease (ACHD) centres, is, therefore, vital. The moderately complex congenital heart defects that may present in adulthood include atrioventricular septal defects (AVSD), Ebstein’s anomaly (EA), tetralogy of Fallot (TOF) and transposition of the great arteries (TGA). Some of these defects are typically diagnosed and repaired in infancy, so clinicians must be aware of the possibility of adults presenting with post-repair complications, but some patients with unrepaired or undiagnosed defects remain asymptomatic until middle age, where they may present with heart failure, arrhythmia, endocarditis or even sudden cardiac death.

Iron deficiency (ID) is common in patients with heart failure (HF) and is independently associated with poor outcomes, such as reduced functional capacity and quality of life, increased frailty and increased risk of HF hospitalisations and mortality. Intravenous iron has been shown to be an effective and well-tolerated therapy in patients with HF with reduced and mildly reduced ejection fraction and ID, improving quality of life and functional status and reducing the risk of HF hospitalisations. This review aims to summarise the evidence behind intravenous iron therapy in HF from recent key randomised-controlled trials. This review will also discuss the evidence for intravenous iron therapy in patients with HF with preserved ejection fraction. Ultimately, we also aim to review remaining uncertainties, such as sex-specific differences in outcomes, the optimal iron repletion and maintenance strategies, and the most accurate measures of ID in HF.

Coronary artery disease (CAD) remains a leading cause of morbidity and mortality globally, with early identification and management of risk factors being crucial to its management. Patients undergoing day-case angiograms represent a relatively high-risk population, yet often lack comprehensive risk-factor evaluation. Interventions have been shown to be more consistently aligned with guideline-recommended targets when conducted in hospital. As such, the cardiac catheterisation lab offers an invaluable opportunity for cardiovascular risk factor screening and intervention.

We enrolled 585 consecutive patients attending our institution for day-case coronary angiograms. Blood samples were collected for lipid profile and glycated haemoglobin (HbA1c), in addition to blood pressure recordings and a smoking history taken. The results were available for clinician review on the day, with encouragement to intervene on off-target risk factors.

We identified high levels of patients with established CAD and risk factors outside of the target range. This included 77% and 70% with low-density lipoprotein (LDL) and non-high-density lipoprotein (non-HDL) above target, respectively. There were also 19% smoking and 14% with HbA1c above target. A number of patients with CAD and previously undiagnosed risk factors were also identified, including 18 newly diagnosed with diabetes. A considerable proportion of these had interventions made on the day of their procedure.

Our results demonstrate a clear benefit to risk-factor screening in the catheterisation lab, with a high number of patients found to have risk factors outside of the target range, or previously undiagnosed, and appropriate interventions were made as a result.

Unfractionated heparin (UFH) is routinely used in percutaneous coronary intervention (PCI). The aim of this study was to determine whether the required dose of heparin used during PCI procedures has increased over time, which was our subjective observation.

This retrospective study analysed the required heparin dosage in 100 consecutive patients undergoing isolated PCI for each year between 2016 and 2024, starting from 1 January of each year. The primary analysis compared the total heparin dose administered (a) unadjusted and (b) adjusted for weight and procedure duration, between annual populations. A secondary analysis compared heparin dosage in patients with at least one activated clotting time (ACT) value >250 seconds, the target ACT level at our centre.

The median total heparin dose rose from 9,000 units (U) in 2016 (interquartile range [IQR] 7,000–11,000 U), to 12,000 U (IQR 10,000–15,000 U) in 2024 (p<0.001). The median weight- and time-adjusted total heparin dose in 2016 was 1.95 (IQR 1.44–2.77) U/kg/min compared with 2.93 (IQR 2.1–3.8) U/kg/min in 2024 (p<0.001).

In the secondary analysis (in those who achieved a target ACT >250 seconds), the median dose was 1.81 (IQR 1.21–2.24) U/kg/min in 2016 versus 2.59 (IQR 2.03–3.22) U/kg/min in 2024 (p<0.001).

In conclusion, there has been a significant and unexplained increase in the total administered heparin dose for PCI cases in this centre between 2016 and 2024.

The most common site of origin of idiopathic premature ventricular complexes (PVCs) is the right ventricular outflow tract (RVOT). This study reports a single-centre UK National Health Service (NHS)-based experience of catheter ablation (CA) for idiopathic PVCs.

We conducted a retrospective review of the electronic patient record, searching for all patients undergoing idiopathic PVC ablation at Guy’s and St Thomas’ NHS Foundation Trust (GSTT) between January 2016 and June 2023. There were 147 procedures performed in 118 patients: 21 patients underwent repeat ablations. There were 75% originating in the RVOT and 11% from the left ventricular outflow tract (LVOT). Acute suppression of PVCs was achieved in 121 procedures (82%). Following acutely successful ablations, PVC burden reduction was greater in RVOT (85% decrease) than LVOT PVCs (44% decrease) at follow-up (p=0.03). There were 12 patients with PVC-induced cardiomyopathy identified. Following successful ablation (n=9), left ventricular ejection fraction (LVEF) increased from 38% to 49%. Symptomatic improvement after ablation was reported by 80%, with 64% having complete symptomatic resolution. Patients experiencing complete symptom resolution had a 92% decrease in PVC burden, whereas patients with residual symptoms had a 76.2% decrease (p=0.03).

Procedural complications occurred in 10 procedures (6.8%): five were classified as major, including four pericardial effusions requiring pericardiocentesis, and one cardioversion for pulseless ventricular tachycardia.

In conclusion, CA is an effective and safe strategy for PVC suppression in idiopathic PVCs, and may result in a significant symptomatic improvement even without complete PVC suppression. Among those with PVC-induced cardiomyopathy, CA results in improved LVEF.