Heart最新文献

Background: Acute coronary syndrome (ACS) is a global leading cause of morbidity, with residual inflammation contributing to recurrent events. Colchicine has been proposed as an adjunct therapy, but its efficacy remains uncertain.

Methods: We performed a systematic review and meta-analysis. PubMed, Embase and Cochrane databases were searched for randomised controlled trials (RCTs) data comparing colchicine versus placebo in ACS. Risk ratio (RR) and mean difference with 95% CIs were computed for binary and continuous outcomes, respectively. Primary outcomes were adverse cardiovascular events (ACEs), mortality and safety. Random-effects models were used for pooled estimates.

Results: Seventeen RCTs comprising 14 794 patients were included, of whom 7390 (50%) were randomised to colchicine. The mean patient age across the studies ranged from 54 to 63 years, in a follow-up period ranging from 5 days to 12 months. Colchicine reduced the incidence of recurrent ACS (RR 0.41, 95% CI 0.19 to 0.92; p=0.03; I²=55%) and unstable angina (RR 0.27, 95% CI 0.11 to 0.63; p<0.01; I²=0%). No meaningful differences were observed in all-cause mortality (RR 0.95, 95% CI 0.79 to 1.14; I²=12%), cardiovascular death (RR 1.03, 95% CI 0.82 to 1.30; I²=0%) or ACE (RR 0.77, 95% CI 0.59 to 1.01; p=0.05; I²=58%). Subgroup analyses suggested a dose-dependent effect, with 0.5 mg/day potentially reducing ACE (RR 0.63, 95% CI 0.45 to 0.88; I²=41%), but higher doses increasing gastrointestinal symptoms.

Conclusion: Low-dose colchicine may reduce recurrent ischaemic events in ACS, but evidence remains uncertain due to heterogeneity and limited long-term data. Safety and efficacy in women and optimal dosing require further investigation.

Trial registration number: CRD42024627348.

Background: Aortic stenosis (AS) frequently coexists with heart failure (HF), but its prevalence, prognostic impact and management across the full HF spectrum remain incompletely characterised.

Methods: In this retrospective cohort study, we analysed 22 906 patients with HF undergoing echocardiography between 2010 and 2020. AS was classified as mild, moderate, low-gradient (LG) or severe according to guideline criteria. Outcomes were assessed using Cox regression, stratified by HF subtype and adjusted for clinical confounders. The primary endpoint was event-free survival, defined as all-cause mortality or aortic valve replacement (AVR).

Results: Moderate AS was present in 5.5%, LG AS in 2.5% and severe AS in 6.5% of HF patients, with HF with preserved ejection fraction (HFpEF) being the most common HF subtype across all AS grades. Increasing AS severity was associated with a stepwise increase in adverse outcomes compared with HF patients without AS (adjusted HR 2.20 (95% CI 2.00 to 2.41) for moderate AS; 3.32 (95% CI 2.97 to 3.72) for LG AS and 6.20 (95% CI 5.74 to 6.69) for severe AS). These associations were consistent across HFpEF, HF with mildly reduced EF and HF with reduced EF. Despite established guideline indications, only 59.5% (95% CI 57% to 62%) of HF patients with severe AS underwent AVR within 2 years.

Conclusions: AS is common in HF and is associated with substantially worse long-term outcomes across all HF subtypes, even at non-severe stages. The high mortality risk and frequent lack of intervention highlight major treatment gaps and underscore the need for prospective trials evaluating earlier intervention strategies.

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.