European journal of preventive cardiology最新文献

Introduction: Lp(a) is an independent risk factor for a variety of cardiovascular (CV) outcomes. However, it remains unclear whether its prognostic value differs between individuals with varying baseline traditional CV risk. This study aims to evaluate the association between Lp(a) levels and all-cause & CV mortality, stratified by baseline CV risk.

Methods: Using data from NHANES III (1988-1994) with mortality follow-up through 2019, we analysed a nationally representative cohort of U.S. adults. Baseline CV risk was stratified into low, borderline-intermediate, and high groups using the PREVENT equations. Associations between Lp(a) levels and outcomes were assessed using multivariable Cox and Fine-Gray competing risk models.

Results: A total of 55,050,155 survey-weighted records (4,707 unweighted) were analysed. The mean age was 48 (±13) years, with 51% female. Over a mean follow-up of 22.4 years (±7.07), there were 17,301,805 all-cause and 4,965,456 CV deaths. Elevated Lp(a) (>50 mg/dL) was present in 15% overall, more commonly in the high-risk group (15% vs 11% in low-risk). In the high-risk group, Lp(a) >75 mg/dL was associated with higher all-cause (HR: 1.25; 95% CI: 1.02-1.53) and CV mortality (sHR: 1.21; 95% CI: 1.09-1.36). Lp(a) 50-75 mg/dL showed a borderline association with all-cause mortality (HR: 1.16; 95% CI: 1.00-1.34) but not CV mortality (sHR: 1.06; 95% CI: 0.98-1.15). No significant associations were observed in lower-risk groups.

Conclusions: Elevated Lp(a) levels (> 75 mg/dL) are associated with increased all-cause and CV mortality among individuals with high baseline traditional CV risk, as defined by the AHA's PREVENT score, independent of traditional risk factors. Our findings highlight the value of Lp(a) particularly among those with elevated baseline risk, where its prognostic utility appears greatest.

The rising prevalence of obesity poses an increasing burden on individuals, health care systems, and society. Obesity is the main risk factor for several cardiovascular diseases (CVD). Physical activity (PA) may help to reduce the risk for CVD across the lifespan independent of obesity. The obesogenic and built environment can influence obesity and PA. The primary objective of this scientific statement is to underscore the role of obesity as a risk factor for CVD and to explore how PA can be leveraged to mitigate CVD risk. A novel aspect is the examination of how environmental factors influence the feasibility and implementation of current PA guidelines. Rather than focusing exclusively on a specific age group, this scientific statement investigates how environmental determinants may affect the implementation of increasing PA throughout the lifespan by focusing on three age groups: children and adolescents (<18 years), adults (18-64 years), and older adults (≥65 years). Furthermore, this scientific statement analyses the association of the built environment on PA behaviour by conducting a scoping literature review to identify age-specific evidence regarding the relation of the built environment on PA across the lifespan. This review highlights potentially effective strategies to reduce CVD risk within the context of the built environment and provides practical implications for healthcare professionals and policymakers to increase PA behaviour on an individual and societal level. Altogether, the present work raises awareness of the broader challenges posed by obesity and advocates for PA as a key strategy to improve public health outcomes.

Cardiovascular disease causes almost four million deaths in Europe, costing the EU €282billion/annum. Future mortality rate improvements will be gained through improving secondary prevention of atherosclerotic cardiovascular disease (ASCVD) events. Wide gaps exist between ASCVD prevention/treatment guidelines and their implementation across Europe. We aim to estimate lifetime benefits available via optimised secondary prevention in patients with ASCVD in Denmark, France, Germany, Italy, Poland, Spain and the UK. A literature review identified ASCVD risk factor prevalence in ASCVD populations in seven countries. The simulation used an analytical framework and the SMART-REACH survival model to derive event probabilities over 1-year, associated with being 'at-risk' and 'risk free'. The effect of modifying four risk-factors in the SMART-REACH model - hypertension, hypercholesterolaemia, diabetes and tobacco smoking - was examined. The impact of improving treatment coverage and smoking cessation from (estimated) 43% to 70% (i.e. 70% of patients reach treatment targets/cease smoking) was analysed. Over 94,359 cardiovascular-event-free life years could be gained/year across seven countries by improving secondary ASCVD prevention: 25,333 years in Germany, 21,144 in Italy, 14,584 in France, 13,324 in the UK, 9,393 in Spain, 9,369 in Poland and 1,212 in Denmark. This is a step in better quantifying the impact of improved secondary ASCVD prevention, giving an indication of the potential of EU and national Cardiovascular Health Plans in cardiovascular survival gains. Countries should incentivise proactive identification of patients at risk and ensure subsequent, timely treatment according to guidelines. Future work should utilise updated data and modelling integrating additional cardiometabolic risk factors.

Aim: To determine whether exercise training patterns were associated with the incidence and timing of ventricular arrhythmia in veteran male endurance athletes.

Methods: One-hundred-and-six healthy male endurance athletes (cyclists/triathletes) aged >50y undertaking >10h/week of exercise for >15y underwent clinical assessment, cardiac magnetic resonance (CMR) and implantable loop recorder (ILR) implantation. Daily exercise was tracked with computerised exercise tracking devices. Athletes were followed up for ventricular arrhythmia on ILR; ventricular tachycardia (VT) and non-sustained VT (NSVT).

Results: Fifty-five ventricular arrhythmia events occurred (median follow-up 796 days); 3 (5.5%) VT and 52 (94.5%) NSVT in 25 (23.5%) athletes. Myocardial fibrosis was significantly more prevalent in athletes with ventricular arrhythmia than those without ventricular arrhythmia (19 (76.0%) vs 31 (38.3%), P<001).The incidence of exercise-related ventricular arrhythmia was 0.4/1000 hours of exercise versus non-exercise-related ventricular arrhythmia incidence of 0.01/1000 hours of non-exercise. All three sustained VT cases occurred during exercise in athletes with fibrosis and were preceded by NSVT. There were no training differences between athletes with and without ventricular arrhythmia over two years and in the month prior to each arrhythmic event.

Conclusion: A significant proportion of highly trained male veteran athletes developed ventricular arrhythmia which was predominantly NSVT and was strongly associated with myocardial fibrosis. Acute exercise exposure was associated with an increased risk of developing ventricular arrhythmia but chronic exercise load was not. Our findings therefore highlight myocardial fibrosis as a potential pro-arrhythmic substrate upon which intense exercise may trigger arrhythmogenesis in certain male veteran athletes.

Valvular heart disease poses persistent challenges for clinical decision-making, and international guidelines provide essential frameworks for its management. The American College of Cardiology/American Heart Association last issued a full update in 2020 and an expert consensus on tricuspid regurgitation in 2025. The European Society of Cardiology/European Association for Cardio-Thoracic Surgery released their updated guidelines in 2025. Although there is broad alignment in principles of intervention, prosthesis choice, and the role of Heart Teams, the European document incorporates substantial new trial evidence. Key areas of divergence include thresholds for earlier intervention in aortic stenosis and regurgitation, expanded recommendations for transcatheter edge-to-edge repair and mitral replacement, formal integration of tricuspid repair and transcatheter therapies, evolving strategies for coronary assessment in transcatheter aortic valve implantation, and sex-specific considerations. This review highlights consistencies, discrepancies, and priorities for future research.

Background and aims: To date, limited evidence has assessed the relationships of long-term exposures to PM2.5 constituents and greenness with AF incidence. This study aimed to examine the association between these exposures and incident AF, and further assess the joint effects of genetic susceptibility.

Methods: PM2.5 constituents and greenness were estimated around the residence of 411,364 UK adults. Time-varying Cox models were used to examine these associations. The polygenic risk score (PRS) assessed genetic susceptibility to AF and explore the joint effect between genes and exposures.

Results: The HRs (95% CIs) of AF for per interquartile range increase in elemental carbon (EC), organic matter (OM), ammonium (NH4+), nitrate (NO3-), and sulfate (SO42-), NDVI300m, NDVI500m, NDVI1000m, and NDVI1500m, were 1.05 (1.03, 1.07), 1.06 (1.04, 1.08), 1.07 (1.05, 1.10), 1.05 (1.03, 1.07), 1.06 (1.04, 1.09), 0.97 (0.95, 0.99), 0.96 (0.94, 0.98), 0.95 (0.94, 0.97), and 0.95 (0.93, 0.97), respectively. Among PM2.5 constituents, SO42- (43.8%) was the main contributor to AF in the mixture model. Mediation analyses found that negative association between greenness and AF risk was partially mediated by mitigating exposure to PM2.5 constituents. Moreover, there were additive interactions between EC, OM, NH4+, NO3-, SO42-, and NDVI1500m and PRS. Joint effect revealed that participants with a high PRS and high PM2.5 constituents or low greenness had the highest risk of incident AF, with HRs ranging from 3.14 (2.93, 3.37) to 3.26 (3.04, 3.51).

Conclusions: Long-term exposure to PM2.5 constituents was positively associated with the incidence of AF, whereas greenness was inversely associated with it.