搜索结果：European heart journal supplements : journal of the European Society of Cardiology

Cardiovascular diseases remain the leading cause of mortality globally and in Italy, with a growing burden exacerbated by ageing populations and underdeveloped strategies for managing chronic cardiovascular conditions. This position paper, resulting from the 2024 ANMCO General Assembly, addresses the current state of cardiovascular chronicity management in Italy, highlighting critical gaps and proposing sustainable, integrative solutions. Despite improvements in acute cardiovascular care, the lack of structured post-acute management, insufficient adoption of secondary prevention protocols, limited access to innovative therapies, and a slow digital transition continue to hinder effective chronic care. The document stresses the pivotal role of cardiologists, not only in acute intervention but also in long-term care and secondary prevention, emphasising the need for a multidisciplinary, multichannel healthcare model. The paper explores the potential of e-Health and artificial intelligence to revolutionize chronic disease management. It advocates for the widespread implementation of integrated care pathways, digital tools like electronic health records and telemedicine platforms, which together could enhance early detection, patient monitoring, and therapeutic adherence while reducing unnecessary hospitalisations. It also underscores the necessity of updating national and regional pharmaceutical policies to improve equitable access to disease-modifying therapies. Furthermore, the integration of palliative care in end-stage cardiovascular disease and the enhancement of post-acute care networks are deemed essential. Ultimately, the document advocates for a comprehensive systemic and cultural transformation spearheaded by scientific societies such as ANMCO, where technological innovation, organisational reform, and patient-centred care align to ensure a sustainable and universally accessible healthcare system. This vision is consistent with the objectives of the PNRR, the 2030 Agenda, and, most importantly, the foundational principles of the Italian Constitution.

The widespread use of coronary computed tomography (CT) to exclude significant coronary stenoses and, more broadly, to achieve a more accurate assessment of cardiovascular risk through the evaluation of atherosclerosis has gained momentum in recent years, largely driven by growing criticism of the traditional ischaemia-centred paradigm. The SCOT-HEART studies were among the first large randomized trials to promote the use of coronary CT in patients presenting with angina. The information provided by coronary CT translated into improved clinical outcomes through the adoption of more aggressive medical therapy, particularly lipid-lowering treatment, which was selectively prescribed to patients with evidence of atherosclerosis. The results of the SCOT-HEART 2 primary prevention trial are eagerly awaited and may further influence clinical practice. Finally, photon-counting CT, representing the latest technological advance, together with the application of artificial intelligence-based image analysis algorithms, may constitute an additional step forward in the use of CT imaging.

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.

Dual antiplatelet therapy (DAPT) with acetylsalicylic acid (ASA) and a P2Y12 receptor inhibitor (P2Y12i) for 12 months represents the standard of care after acute coronary syndrome (ACS). However, balancing ischaemic protection against bleeding risk remains challenging, providing the rationale for the development of de-escalation strategies. European and U.S. guidelines allow shortening the duration of DAPT in patients at high bleeding risk, whilst still maintaining 12 months as the reference recommendation. Interest in abbreviated DAPT regimens has been driven by improvements in percutaneous coronary intervention devices and techniques, as well as by a better understanding of the temporal evolution of ischaemic and bleeding risks. Several trials have shown that short-duration DAPT followed by monotherapy-particularly with a P2Y12i-is not inferior in terms of ischaemic outcomes and significantly reduces bleeding events. In this context, the NEO-MINDSET trial failed to demonstrate the non-inferiority of immediate P2Y12i monotherapy compared with standard DAPT. In contrast, the TARGET-FIRST study confirmed the safety of ASA discontinuation after 30 days in selected patients, with a clear bleeding benefit. Overall, the available evidence indicates that immediate discontinuation of ASA in patients with acute coronary syndrome is not universally safe, whereas strategies based on at least 1 month of DAPT followed by monotherapy with a potent P2Y12i currently represent the most balanced approach for selected patients. More refined personalization of antiplatelet therapy, guided by an integrated assessment of ischaemic and bleeding risks, represents the future perspective in this field.

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.

Obesity is a chronic, multifactorial condition strongly associated with increased cardiovascular and metabolic risk, as well as the development of systemic complications. Recent evidence from randomized controlled trials-including SELECT, STEP-HFpEF, STEP-HFpEF DM, SUMMIT, and SURMOUNT-5-has demonstrated the effectiveness of glucagon-like peptide-1 receptor agonists and dual glucose-dependent insulinotropic polypeptide/glucagon-like peptide-1 agonists in the treatment of obesity, with clinical benefits that appear to extend beyond weight reduction alone. In addition to substantial reductions in fat mass, these agents improve cardiovascular parameters (including reductions in major adverse cardiovascular events), functional capacity, and quality of life. Additional benefits have been observed at the metabolic level, with reductions in glycated haemoglobin, blood pressure, triglycerides, and systemic inflammatory markers such as high-sensitivity C-reactive protein. These results confirm that pharmacological modulation of the incretin axis should not be viewed merely as an adjunctive strategy for weight loss, but rather as an integrated therapeutic intervention capable of modifying overall cardiovascular risk and improving the inflammatory and metabolic profile of the obese patient. In light of these findings, a re-evaluation of the role of pharmacological therapy in the clinical management paradigm of obesity is warranted.

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.

Cardiac glycosides represent one of the oldest therapeutic pillars in medicine, although their role has progressively diminished in the modern era of neurohormonal therapy for heart failure (HF). Following publication of the Digitalis Investigation Group (DIG) trial in 1997, no randomized clinical trials evaluating this drug class were conducted for almost three decades, while observational studies and meta-analyses accumulated, often yielding conflicting results. The DIGIT-HF randomized clinical trial (2025) addressed a major unmet need by evaluating digitoxin in patients with HF with reduced ejection fraction in the contemporary era of guideline-directed medical therapy. Treatment with digitoxin was associated with favourable outcomes, including a reduction in the composite endpoint of all-cause mortality and hospitalizations for HF, thereby reopening a long-standing debate on the role of digitalis, which had remained marginal for many years. This article reviews the history of digitalis, the main evidence generated over recent decades, the evolution of clinical guidelines from 1997 to 2022, and the conceptual and clinical implications of the DIGIT-HF trial.

Tricuspid regurgitation (TR) affects approximately 4% of individuals over 75 years of age and is associated with substantial morbidity due to heart failure symptoms and frequent hospitalization. In Europe, TR prevalence is expected to rise with an ageing population, contributing to a growing burden on heart failure services. Surgical repair or replacement for isolated TR has been historically underutilized because of high operative risk, however, recent advancements in transcatheter technology have shifted the treatment paradigm. Having once been labelled the forgotten valve, the European interventional cardiology community was suddenly confronted with a number of different devices, all designed to target TR. Having the intrahospital mortality for isolated tricuspid valve surgery in mind, ranging from 8.0% to 12.3%, the initial results of transcatheter therapies with an all-cause mortality of 3.7% at 30 days were promising, although procedural success was achieved in only 62% and cardiac and cerebrovascular major adverse events were as high as 26%. Already, T-TEER constituted the majority of interventions, although miskeyed M-TEER devices were used off-label. Other systems, such as Trialign, TriCinch, FORMA, Cardioband, NaviGate, and caval valve implantation were used distinctively less often.

Vericiguat is a soluble guanylate cyclase stimulator that acts by restoring the nitric oxide-cyclic guanosine monophosphate pathway, which is markedly impaired in heart failure with reduced ejection fraction (HFrEF). The VICTORIA trial demonstrated that treatment with vericiguat leads to a significant reduction in mortality and morbidity in patients with HFrEF and a recent episode of clinical decompensation. However, the role of vericiguat in clinically stable patients had remained unexplored until the recent publication of the VICTOR trial. In a population receiving optimal medical therapy and characterized by a lower risk of events, vericiguat did not demonstrate a significant reduction in the primary composite endpoint of cardiovascular death and hospitalization for heart failure. When analysing the individual components of the primary endpoint, no benefit was observed with respect to hospitalizations, whereas significant reductions in both cardiovascular and all-cause mortality were reported. This finding, which is highly unusual in the context of recent clinical trials in patients with HFrEF, warrants further consideration when interpreting the results of the study.

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.

Tricuspid regurgitation (TR), once considered a passive marker of advanced cardiac disease, is increasingly recognized as an independent contributor to morbidity, mortality, and healthcare burden. Recent evidence, including the pivotal TRILUMINATE trial and Tri-FR, together with supporting cost-effectiveness models, suggest that the correction of TR with T-TEER systems may improve patient outcomes and offer good value for money in European healthcare settings. This article explores the clinical rationale and economic imperative for considering TR as a modifiable and actionable target in modern cardiology ([Adamo M, Chioncel O, Pagnesi M, Bayes-Genis A, Abdelhamid M, Anker SD et al. Epidemiology, pathophysiology, diagnosis and management of chronic right-sided heart failure and tricuspid regurgitation. A clinical consensus statement of the Heart Failure Association (HFA) and the European Association of Percutaneous Cardiovascular Interventions (EAPCI) of the ESC. Eur J Heart Fail 2024;26:18-33.]).

Hospital discharge is a pivotal stage in the continuum of care, marking the transition from the acute clinical episode to subsequent therapeutic management. Rather than being a purely administrative procedure, discharge is a multifaceted process that requires structured planning, clear communication, and the coordinated participation of all healthcare stakeholders, with the patient playing a central role. Inadequate discharge processes may adversely affect clinical outcomes and increase hospital readmission rates, resulting in sub-optimal utilization of healthcare resources. This issue is particularly relevant in the context of an ageing and increasingly frail population, characterized by a high burden of comorbidities and complex clinical needs. In this setting, discharge planning should be treated as an integral component of the care pathway, embedded within a comprehensive, coordinated model of care. This document proposes an updated, practical framework for hospital discharge management, grounded in current scientific evidence and multidisciplinary expertise. Its primary objective is to enhance continuity of care, support individualized treatment strategies, and ultimately improve patient outcomes. Specifically, this paper aims to provide clinical cardiologists with a structured reference tool for discharge management, including actionable recommendations to strengthen physician-patient communication, optimize therapeutic regimens, and promote better health outcomes.

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.

The haemodynamic mechanisms underlying vasovagal (reflex) syncope include hypotension and extrinsic asystole/bradycardia, corresponding to two distinct haemodynamic phenotypes of syncope, that is, the hypotensive and the bradycardic phenotypes. The hypotensive phenotype is the most prevalent, being observed in the 83% of patients. Twenty-four hours ambulatory blood pressure monitoring (ABPM) demonstrated high effectiveness in identifying the hypotensive phenotype in patients with suspected reflex syncope. The diagnosis of a hypotensive mechanism of syncope is supported by ABPM when one or more of the following criteria are present:. Constitutional hypotension: 24-h systolic blood pressure (SBP) < 105&#x2005;mmHg in men and <98 in women. Drug-related hypotension: 24-h SBP <120&#x2005;mmHg. Hypotensive episodes: &#x2265;1 daytime SBP <90&#x2005;mmHg or &#x2265;2 daytime SBP <100&#x2005;mmHg. Postprandial hypotension: symptomatic SBP fall >20&#x2005;mmHg or absolute value <90&#x2005;mmHg within 75&#x2005;min of meals. ABPM also plays a key role in guiding therapy. In hypertensive patients with hypotensive syncope, deprescribing antihypertensive medications is indicated with the goal of increasing 24-h average SBP to &#x2265; 134&#x2005;mmHg and/or by at least &#x2265;12&#x2005;mmHg, without exceeding 140&#x2005;mmHg (or <160&#x2005;mmHg in frail older patients). In patients with drug-unrelated hypotension, lower-body elastic garments, fludrocortisone, or midodrine-prescribed singularly or in combination-may be considered and targeted to achieve a 24-h average SBP &#x2265;116&#x2005;mmHg and/or an increase of at least &#x2265;9&#x2005;mmHg.

Five modifiable cardiovascular risk factors-hypertension, diabetes, smoking, hypercholesterolemia, and obesity-account for approximately 50% of the global burden of cardiovascular disease. Recent data from the Global Cardiovascular Risk Consortium show that the absence of diabetes and smoking is associated with the lowest risk in terms of life expectancy and years lived free from cardiovascular disease. A systolic blood pressure below 130&#x2005;mmHg, lower non-HDL cholesterol levels, and normal body weight are associated with a later onset of cardiovascular disease and a more modest increase in life expectancy. The absence of hypertension is correlated with the greatest number of years lived free from cardiovascular events. Smoking is confirmed as one of the most influential risk factors in terms of its impact on health and longevity. Individuals who eliminate hypertension and smoking in midlife gain the greatest number of additional years of life free from cardiovascular disease and all-cause mortality, respectively. Male sex emerges as a traditional, non-modifiable risk factor independent of modifiable risk factors. Finally, even the absence of all the risk factors considered remains associated with a residual lifetime probability of developing cardiovascular disease.

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.

In recent years, remarkable advancements in paediatric cardiology and surgical techniques have dramatically increased the survival of patients with congenital heart disease. As a result, adults with congenital heart disease (ACHD) are now living longer, and many, despite having residual lesions and sequelae, may have near-normal life expectancy. Adults with congenital heart disease patients should no longer be viewed merely as survivors; instead, medical care should shift its focus from simply prolonging life to enhancing quality of life and overall well-being. Moreover, as ACHD population ages, they are increasingly exposed to a burden of acquired cardiovascular and extracardiac disease, making early intervention on modifiable risk factors a key priority. Herewith, we provide an overview of the multiple aspects that should be considered in this holistic approach to guide everyday issues of ACHD patients, including nutrition, physical activity, sexual health, cancer prevention, respiratory disease, and infective endocarditis.

PCSK9 inhibitors represent a cornerstone of lipid-lowering therapy; however, the need for cost containment and simplified routes of administration has stimulated the development of oral small molecules and peptidomimetics capable of modulating or blocking the PCSK9-LDL receptor (LDL-R) interaction, inhibiting PCSK9 mRNA transcription, or preventing lysosomal degradation of the LDL-R. Agents in advanced development include enlicitide (MK-0616) and laroprovstat (AZD0780), while DC371739, NNC0385-0434 (development currently suspended), and CVI-LM001 should also be considered. Enlicitide decanoate, owing to improved intestinal permeability, significantly reduces free PCSK9 (>90%) and LDL-cholesterol (C) (&#x2248;60%) in Phase I-II studies, with excellent tolerability. Phase III trials (CORALreef-Lipids and CORALreef-HeFH) have confirmed LDL-C reductions of 55-60%, along with favourable effects on non-HDL-C, apolipoprotein B (apoB), and Lipoprotein(a) Lp(a), comparable to those achieved with monoclonal antibodies. AZD0780 demonstrates dose-dependent reductions in LDL-C (up to 50%) and potential synergism with rosuvastatin, whereas NNC0385-0434-despite documenting significant decreases in LDL-C and Lp(a)-has been discontinued. DC371739 (a dual PCSK9/ANGPTL3 inhibitor) and CVI-LM001 (a transcriptional modulator) may represent additional therapeutic perspectives. Overall, oral PCSK9 inhibitors show consistent efficacy and favourable safety profiles, positioning them as next-generation lipid-lowering therapies, pending cardiovascular outcome data from ongoing studies.