Heart最新文献

Background: Ambient air pollution is associated with heart failure (HF), but underlying biological mechanisms remain unclear. We aimed to elucidate metabolic pathways linking air pollution exposure with HF.

Methods: This prospective cohort study analysed 229 812 UK Biobank participants with nuclear magnetic resonance metabolomics data. Air pollution score was constructed by fine particulate matter, coarse particulate matter, nitrogen dioxide and nitrogen oxides. Air pollution-associated metabolic signatures were identified using elastic net regression among 251 circulating metabolites. Cox regression evaluated associations between metabolic signatures and incident HF risk. Mediation analysis quantified metabolic signatures' role in air pollution-HF relationships.

Results: During median 13.1-year follow-up, 8986 participants (3.9%) developed HF. We identified 53 metabolic metabolites reflecting air pollution exposure, comprising lipoprotein metabolism markers (22.6%), fatty acids (17.0%) and amino acids (13.2%), which were used to construct the air pollution-related metabolic signatures score. After adjustment for confounding factors, each SD increase in the metabolic signatures was associated with 8% elevated HF risk (HR 1.08, 95% CI 1.06 to 1.11). Participants in the highest quantile showed a 24% increased HF risk compared with those in the lowest quantile (HR 1.24, 95% CI 1.16 to 1.3). The metabolic signatures mediated 13.08% (95% CI 12.15% to 15.71%) of air pollution-HF associations, with lipoprotein metabolism and fatty acid signatures as primary mediators.

Conclusions: Air pollution was associated with increased HF risk, with metabolic perturbations appearing to play a mediating role. These metabolic signatures provide insights into potential mechanisms linking air pollution to cardiovascular outcomes.

Mitral annular calcification (MAC) is a progressive, degenerative process increasingly recognised for its clinical impact. Beyond being an incidental finding, MAC contributes to mitral valve dysfunction, arrhythmias, systemic embolisation and elevated cardiovascular risk. In developed countries, it has now overtaken rheumatic disease as the leading cause of mitral stenosis.The pathophysiology of MAC involves chronic mechanical stress, pro-inflammatory activation and osteogenic differentiation of valvular cells. Progression is accelerated by age, chronic kidney disease and metabolic derangements. Diagnosing MAC-related valve dysfunction is challenging, as traditional echocardiographic measures often prove unreliable. Multimodality imaging-including 3D echocardiography and cardiac CT-is essential for assessing anatomy, function and procedural feasibility. Importantly, symptoms often reflect combined valvular (eg, aortic stenosis) and myocardial disease (eg, heart failure with preserved ejection fraction (HFpEF) phenocopy), necessitating careful haemodynamic evaluation to avoid futile interventions.Management should prioritise medical therapy for symptom control and comorbid HFpEF, reserving interventions for selected patients. Surgical and transcatheter approaches carry high risk and should be undertaken only in specialised centres. Future advances may include tailored devices and therapies targeting calcification pathways.

Background: Safety and efficacy of supervised exercise training (ET) remain unclear in left ventricular assist device (LVAD) patients. A systematic review with an individual participant data (IPD) meta-analysis was performed to determine: (1) safety, (2) the effects of ET on peak oxygen consumption (peakVO₂), 6 min walk distance (6MWT) and quality of life (QoL) and (3) the effects of ET on different subgroups of patients with LVAD (age, sex, body mass index (BMI), time post LVAD implantation, baseline exercise performance).

Methods: IPD were retrieved from all published randomised, controlled trials that compared the efficacy of ET versus standard care in LVAD patients. One-stage and two-stage (sensitivity analysis) meta-analyses were used to determine the effects of ET overall and for subgroup and ET effects interactions.

Results: Four trials that included 119 LVAD patients (89.1 % males; age: mean (SD), 53 (14) years; BMI: 28 (5) kg/m²; ejection fraction: 19 (6)%) were analysed. ET was safe and improved peakVO₂ (mean difference (95% CI) +1.43 (0.39 to 2.45) mL/kg/min, p=0.004), 6MWT distance (+48 (95% CI 24 to 73) m, p<0.001), QoL (+0.66 (95% CI 0.26 to 1.05) standardised units, p<0.001) more than standard care. Males, older patients, 1 year post LVAD implantation and those with lower baseline BMI and (sub)maximal exercise performance had larger benefit of ET.

Conclusions: ET is safe and improves (sub)maximal exercise performance and QoL in LVAD patients, and should be considered in management of LVAD.

Prospero registration number: CRD42023480119.

Myocarditis is an inflammatory disease of the heart muscle that can be triggered by various causes, including viruses, autoimmune response, molecular mimicry and exposure to immune-stimulating drugs or vaccines. Most cases of myocarditis heal, and cardiac dysfunction, if present, recovers; however, selected forms may require targeted therapy to improve outcomes. We herein review five conditions presenting with or mimicking myocarditis that require targeted diagnostic approaches, including endomyocardial biopsy, and/or targeted treatments. Giant cell myocarditis is an intense and unresolving inflammation of the heart, characterised by rapid progression, significant arrhythmias, heart failure and shock, that is unlikely to resolve without immunosuppression therapy. Myocarditis related to immune checkpoint inhibitors is a rare but potentially fatal adverse effect of the use of cancer immunotherapy with checkpoint inhibitors, requiring immunosuppressive therapy. Eosinophilic myocarditis can be triggered by allergy, hypersensitivity reactions, infections or can be idiopathic and is characterised by eosinophilic infiltrates in the heart and other organs, associated with thrombosis and necessitating targeted therapy. Myocarditis is a frequent cardiovascular manifestation of systemic immune-mediated inflammatory diseases such as systemic lupus erythematosus, and injury is caused by an autoimmune response in the myocardium and cytokine-mediated damage, requiring targeted therapy. Genetic pathogenic mutations in desmoplakin and other desmosomal genes can present with 'hot phases' mimicking myocarditis associated with an increased risk of arrhythmias, heart failure, and sudden cardiac death.

As transcatheter aortic valve implantation (TAVI) is increasingly used in younger and lower-risk patients, long-term valve durability has become a growing concern. Bioprosthetic valve degeneration (BVD) is multifactorial, encompassing calcific and non-calcific structural deterioration, non-structural deterioration, valve thrombosis and procedural or device-related factors. This review aims to provide a look across the spectrum of understanding BVD, presenting insights from fundamental and translational science through to the clinic to give a comprehensive overview of the mechanisms underlying BVD in TAVI valves. This review highlights the pivotal role of multimodality imaging in detection, classification and monitoring of degeneration and discusses the emerging pharmacological and engineering innovations aimed at preventing degeneration. Finally, reintervention strategies, including redo-TAV and surgical explantation, are explored with an emphasis on CT-based planning and bench-testing insights that have enhanced our understanding of BVD and inform ongoing procedural refinement. These perspectives support a proactive and tailored approach to managing transcatheter aortic valve degeneration across the patient's lifetime.

Cardiac device therapy has significantly evolved since the introduction of the first implantable pacemaker and the subsequent development of the implantable cardioverter-defibrillator (ICD). ICDs are highly effective; however, their main weakness lies in lead-related complications. To avoid the need for venous access and the complications associated with transvenous leads, a fully subcutaneous ICD (S-ICD) system was developed. Despite these advancements, the S-ICD system is limited by its inability to provide bradycardia pacing and antitachycardia pacing. This limitation prompted the development of a modular cardiac rhythm management system, integrating a new leadless pacemaker with an S-ICD that uses unidirectional communication to command the pacemaker to deliver antitachycardia pacing.Conduction system pacing, including His bundle pacing and left bundle branch area pacing (LBBAP), has emerged as a physiological alternative to biventricular resynchronisation therapy and conventional pacing, pending results of large clinical trials. LBBAP offers superior electrical parameters and long-term performance compared with His bundle pacing. The capability to provide defibrillation via the same lead used for LBBAP represents an unresolved challenge that is currently under ongoing research.This state-of-the-art review presents the latest developments and innovations in cardiac device therapy, offering a comprehensive overview of current technologies that increasingly enable therapy to be tailored to individual patient needs.

Background: Fluid restriction is a commonly prescribed non-pharmacological intervention in the management of heart failure (HF). However, data on its efficacy and safety are scarce. Recent randomised clinical trial (RCT) data prompt reassessment of the available evidence.

Methods: CINAHL, EMBASE, PubMed and the Cochrane Library were searched up to 1 May 2025. RCTs were included if adults with HF were randomised to fluid restriction in comparison to a liberal or unrestricted intake, less strict restriction or usual care. Outcomes of interest were mortality, HF hospitalisation, quality of life (QoL), thirst distress, New York Heart Association (NYHA) class and N-terminal pro-Brain Natriuretic Peptide (CRD42022292319). No meta-analysis was performed due to high heterogeneity of the included trials.

Results: In total, four RCTs were included, comprising 682 randomised inpatient, recently discharged and stable outpatient patients (ranging from 46 to 504 patients per trial). Only one study had a low risk of bias. None of the four trials found a significant difference in mortality or HF hospitalisations. For QoL, the results are contradictory, but overall, there is no clear benefit for fluid restriction, but it resulted in more thirst distress. No significant differences in NYHA class or (NT-pro)BNP were observed.

Conclusion: Studies on fluid restriction in patients with HF are scarce, and most of the available studies are at high risk of bias. Although power is lacking, there is no evidence indicating that fluid restriction affects mortality or HF hospitalisations, but there is a signal of harm in terms of thirst distress. Taken together, the current evidence does not support the routine use of fluid restriction in patients with HF.

Background: Ethnic inequalities exist in the management of patients with cancer with acute coronary syndrome (ACS). Given their under-representation in trials, ethnic minority patients are often studied using large registries, but the quality of ethnicity coding in these datasets remains unclear.

Methods: Agreement of ethnicity coding and outcomes for patients with cancer with ACS (2000-2018) was examined across four national datasets: National Cancer Registration and Analysis Service (NCRAS), Myocardial Ischaemia National Audit Project (MINAP), British Cardiovascular Intervention Society database (BCIS) and Hospital Episode Statistics (HES). Three linkages were performed: NCRAS-MINAP, NCRAS-MINAP-BCIS, NCRAS-MINAP-HES, with four groups based on ethnicity agreement: Concordant, Discordant, Missing (1 and ≥2 datasets). Multivariable logistic regression and Cox's Proportional Hazards models assessed 1-year and long-term (≤5 years) cardiac and cancer-related death for each agreement group.

Results: Among three linkages, just over half of the ethnicities were concordant (range: 52.4%-53.8%). Discordance was relatively low (range 1.2%-5.5%) while missingness ranged between 28.6% and 43.4% in 1 dataset and 1.6%-12.6% in ≥2 datasets. Ethnicity correlation between individual datasets was poor, lowest between NCRAS and BCIS (r=0.318). We observed higher 1-year and long-term cardiac and cancer deaths in several of the Missing (1 and ≥2 datasets) groups across the three linkages, compared with the Concordant group.

Conclusion: Across four national datasets for patients with cancer with ACS, nearly half of patients had missing ethnicity in at least one dataset, which was associated with higher cardiac or cancer mortality. Inconsistency in ethnicity coding represents a missed opportunity to examine health inequalities in this high-risk and understudied population.