European Heart Journal Supplements最新文献

Coronary computed tomography angiography (CCTA) has become a cornerstone in the non-invasive evaluation of coronary artery disease (CAD). Beyond defining stenosis severity, CCTA enables detailed quantification of total atherosclerotic burden, plaque composition, and imaging markers of plaque vulnerability. Recent advances-including artificial intelligence (AI)-enhanced algorithms-now allow automated and highly reproducible plaque phenotyping, with major implications for risk stratification and therapeutic monitoring. Concurrently, imaging of pericoronary adipose tissue has introduced novel biomarkers of vascular inflammation, particularly the Fat Attenuation Index and pericoronary adipose tissue attenuation. These indices independently predict adverse cardiovascular events beyond traditional risk factors. Serial imaging studies further demonstrate that lipid-lowering and anti-inflammatory therapies modulate plaque biology, promoting regression or stabilization. Integration of coronary plaque analytics, adipose tissue biology, and AI-driven risk prediction is redefining preventive cardiology and enabling increasingly individualized management strategies.

The management of chronic total coronary occlusions (CTOs) remains one of the most debated areas in interventional cardiology because of its technical complexity and the relatively high risk of procedural complications. Although the effectiveness of percutaneous coronary intervention for CTOs (CTO-PCI) in improving symptoms has been demonstrated, its impact on hard clinical outcomes remains controversial. The International Study of Comparative Health Effectiveness with Medical and Invasive Approaches (ISCHEMIA Trial) and the ISCHEMIA CTO sub-study provide important insights: in patients with stable coronary artery disease and moderate-to-severe ischaemia, an initial invasive strategy does not reduce cardiovascular mortality or myocardial infarction compared with optimized medical therapy. However, the trial was not designed to specifically assess the effectiveness of CTO-PCI, and only a minority of enrolled patients had a CTO, which was revascularized in only few cases. In addition, the ISCHEMIA trial excluded high-risk patients who are frequently encountered in everyday clinical practice, such as those with left main coronary artery disease, severe symptoms, or recent acute coronary syndromes. This article critically analyses the results of the ISCHEMIA Trial in the context of CTOs, comparing them with evidence from dedicated CTO-PCI studies, and proposes an integrated decision-making model based on symptom control, objective demonstration of inducible ischaemia and myocardial viability, multimodal imaging, and discussion within the Heart Team.

Transthyretin amyloidosis (ATTR) is a systemic disease characterized by the deposition of misfolded transthyretin (TTR) fibrils. It most commonly presents as cardiomyopathy (ATTR-CM), particularly in elderly patients with the wild-type form, whereas hereditary variants may manifest with polyneuropathy (ATTRv-PN) and/or cardiac involvement. The widespread adoption of non-invasive diagnostic pathways has increased disease recognition and facilitated the early initiation of disease-modifying therapies. Stabilizers limit dissociation of the TTR tetramer and the formation of new amyloid fibrils. Tafamidis demonstrated a benefit on mortality and cardiovascular hospitalizations in the ATTR-ACT trial and remains the treatment supported by the most robust evidence, with greater efficacy when initiated at earlier disease stages. Acoramidis, a next-generation stabilizer, improved a hierarchical composite end-point in the ATTRibute-CM trial and has been approved for ATTR-CM treatment, too. Gene-silencing therapies (small interfering RNA and antisense oligonucleotides) reduce hepatic TTR synthesis and circulating protein levels. Patisiran is approved for ATTRv-PN and, in the APOLLO-B trial, showed a functional benefit in ATTR-CM, although it has not been approved for this indication in the United States. Vutrisiran, a subcutaneously administered siRNA given every 12 weeks, reduced mortality and recurrent cardiovascular events in the HELIOS-B trial and has been approved for ATTR-CM treatment. This review summarizes the rationale and principal clinical evidence supporting tetramer stabilizers and gene-silencing therapies, which are now central to the management of ATTR-CM.

Leadless pacemakers (LPMs) constitute a significant advancement in the management of bradyarrhythmias by eliminating complications associated with transvenous leads and subcutaneous pockets. Accumulating evidence demonstrates substantial clinical benefits, including a marked reduction in complications, particularly infections, and fewer system revisions as compared with transvenous pacemakers (TVPMs). However, several limitations preclude their widespread adoption. Cardiac tamponade occurs in up to 2% of cases, requiring sternotomy in approximately one third. Management of devices at the elective replacement interval through intracardiac abandonment raises concerns, particularly in younger patients; experience with extraction remains limited and entails substantial risks, with severe complications occurring in up to 3% of cases. Limitations in atrioventricular synchronization persist despite technological advances, and cardiac resynchronization therapy remains unavailable. LPMs are emerging as the preferred option for selected populations at high risk of infection, whereas TVPMs maintain a predominant role owing to their versatility and capacity to deliver advanced therapies. LPMs are gaining traction in specific high-risk subgroups and may expand their indications as technology evolves; however, they are likely to coexist with TVPMs rather than supplant them entirely in the medium term.

Cardiogenic shock (CS) is a life-threatening syndrome characterized by systemic tissue hypoperfusion due to inadequate cardiac output. Despite advances in cardiovascular care, mortality remains high, particularly during the first hours and within the first month after onset, underscoring the need for early recognition and tailored therapeutic strategies. The marked heterogeneity of CS has prompted the development of phenotyping approaches encompassing clinical, haemodynamic, aetiological, and emo-metabolic dimensions. Clinically, patients may present as cold and congested, cold and dry, warm and congested, or warm and dry. From an aetiological perspective, CS may be ischaemic, related to de novo heart failure, acute decompensation of chronic heart failure, secondary, or mixed. Mixed shock-characterized by the coexistence of pump failure and inappropriate systemic vasodilation-is associated with higher mortality and rapid clinical deterioration. Advanced phenotyping strategies, including machine learning-based approaches, have identified additional CS subgroups with distinct prognostic profiles and therapeutic requirements. The Society for Cardiovascular Angiography and Interventions classification provides a practical framework for severity stratification and longitudinal monitoring, emphasizing the importance of frequent reassessment, particularly in early-stage patients at risk of rapid progression. Management of CS integrates pharmacological therapy-including inotropes and vasopressors-with mechanical circulatory support, tailored to the patient's phenotype and haemodynamic profile. Optimal care of cardiogenic shock relies on accurate phenotyping, dynamic risk assessment, and personalized therapeutic strategies to improve outcomes while minimizing complications.

Two randomized trials, the ALONE-AF and OCEAN, have provided valuable evidence to guide the management of oral anticoagulation therapy after ablation of atrial fibrillation. In the ALONE-AF study, amongst patients with no documented atrial fibrillation recurrence at 1 year after transcatheter ablation, the 2-year incidence of the composite endpoint of stroke, systemic embolism, and major bleeding was significantly lower in those who discontinued oral anticoagulation compared with those who continued therapy. This difference was driven by a reduction in major bleeding events, with similar rates of stroke between groups. In the OCEAN study, amongst patients without atrial fibrillation (AF) recurrence during the year following transcatheter ablation, rivaroxaban 15 mg, compared with acetylsalicylic acid (ASA), did not significantly reduce the 3-year incidence of stroke, systemic embolism, or new silent embolic cerebral infarction, but was associated with an increased risk of clinically relevant non-major bleeding. The annualized incidence of thromboembolic events was low (0.3-0.6 events per 100 patient-years). Taken together, data from these two trials suggest that discontinuation of oral anticoagulation (OAC) may be a clinically reasonable option in patients without AF recurrence for at least 1 year after ablation. This strategy should be limited to patients at low thromboembolic risk, comparable to those enrolled in the two trials. Furthermore, the implementation of optimal and sustainable rhythmmonitoring strategies is essential to support decisions regarding OAC discontinuation after AF ablation.

The widespread adoption of coronary computed tomography angiography (CCTA) has led to a growing detection of coronary artery anomalies in contemporary clinical practice, often as incidental findings during the evaluation of suspected or known coronary artery disease. Among these, anomalous aortic origin of a coronary artery (AAOCA) represents the most clinically debated entity, historically associated with myocardial ischaemia and sudden cardiac death, yet increasingly identified in asymptomatic or minimally symptomatic adults. Accumulating evidence indicates that most AAOCA diagnosed in adulthood are not associated with functionally relevant ischaemia and frequently follow a benign clinical course, highlighting the limitations of anatomy-based risk stratification alone. In this context, CCTA plays a pivotal role by accurately defining coronary origin and course, characterizing proximal vessel morphology, and assessing concomitant atherosclerotic disease, which often represents the predominant determinant of symptoms and prognosis in adult patients. Recent studies have demonstrated that quantitative CCTA-derived parameters can reliably exclude hemodynamically significant AAOCA and reduce unnecessary downstream testing. In selected cases, invasive functional assessment and intracoronary imaging provide incremental value by clarifying the presence and mechanisms of ischaemia but should be reserved for carefully selected patients. This review summarizes current evidence on coronary artery anomalies with a specific focus on AAOCA and proposes a pragmatic, stepwise approach integrating anatomical and functional assessment to guide clinical decision-making in daily practice.

Despite the use of oral anticoagulants, the residual risk of recurrent ischaemic stroke in patients with atrial fibrillation (AF) is ∼4% per year; however, in patients who experience a stroke despite oral anticoagulant therapy (OAT), this risk approaches 9% per year. It is therefore essential to identify patients at higher risk and to develop new strategies for secondary prevention. These strategies include the exclusion of non-AF-related causes, optimization of OAT and its early initiation after stroke, as well as an aggressive rhythm-control approach. Additional non-pharmacological options include surgical or percutaneous left atrial appendage occlusion, although its effectiveness in secondary prevention after ischaemic stroke is still under evaluation. Novel pharmacological therapies targeting factors XI and XIa are currently under investigation and may provide comparable efficacy with improved safety compared with direct oral anticoagulants. Conversely, switching from one anticoagulant to another or adding antiplatelet therapy is completely ineffective. The mechanisms underlying recurrent stroke despite anticoagulant therapy are therefore complex, making an individualized, patient-specific approach mandatory.

Heart failure with preserved ejection fraction (HFpEF) is a systemic syndrome driven by inflammation, with a substantial contribution from comorbidities, ageing, lifestyle factors, and genetic predisposition. Heart failure with preserved ejection fraction accounts for ∼50% of hospital admissions for heart failure. Mortality ranges from 15% at 1 year to up to 75% at 5-10 years. This paper provides an overview of HFpEF, spanning epidemiological to therapeutic aspects, with particular focus on diagnostic challenges and strategies to overcome them. The diagnostic pathway leading to HFpEF requires extensive exclusion of potentially confounding conditions. Indeed, the identification of some of these conditions allows for targeted therapies that may improve survival. Diagnostic suspicion begins with the recognition of symptoms and signs of heart failure, followed by the assessment of natriuretic peptides and supported by scoring systems and instrumental investigations performed at rest or during exercise. Heart failure with preserved ejection fraction remains a challenging condition to diagnose due to the lack of uniform definitions in the literature, the presence of symptoms and signs shared with other diseases, and the absence of a universally recognized pathognomonic marker.

In the field of heart failure, sodium-glucose cotransporter 2 inhibitors (SGLT2-i) have demonstrated robust efficacy and have received a Class I, Level A recommendation for reducing the risk of heart failure hospitalizations and cardiovascular mortality across the entire spectrum of left ventricular ejection fraction. The therapeutic effect occurs early, with the first statistical significance observed as soon as 12-28 days after treatment initiation. Evidence suggests that early introduction during hospitalization may reduce the short-term risk of cardiovascular death or worsening heart failure. SGLT2 inhibitors display a favourable safety and tolerability profile, without an increased incidence of adverse events compared with placebo. Furthermore, they are indicated for the treatment of type 2 diabetes mellitus and chronic kidney disease, irrespective of the presence of heart failure. Therefore, we propose that in patients presenting with signs and/or symptoms of heart failure and elevated natriuretic peptide levels, SGLT2 inhibitors may be initiated even before echocardiographic confirmation of the diagnosis. Given the favourable risk-benefit profile, this approach may help avoid therapeutic delay, which could otherwise be associated with an increased risk of early adverse events, and may ultimately improve prognosis.