European journal of preventive cardiology最新文献

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.

Aim: We aimed to 1) investigate associations between leisure time physical activity level cumulated over 20 years and multiple plasma proteins and 2) explore if proteins significantly associated with physical activity are also associated with risk of imminent myocardial infarction (MI), long-term MI and mortality.

Methods: In the cohort Uppsala Longitudinal Study of Adult Men (ULSAM), leisure time physical activity was self-reported at ages 50, 60, and 70. At age 70, 720 plasma proteins were analyzed in 782 participants with up to 19.3 years of follow-up for MI and 26.3 years follow-up for mortality. In the nested case-cohort study Markers of Imminent Myocardial Infarction (MIMI), plasma proteins were measured in disease-free individuals from six European cohorts. Cases (n=420) were those with acute MI within 6 months of a blood draw, with up to four cohort representatives per case (n=1,598).

Results: A higher level of leisure time physical activity level was inversely associated with 12 plasma proteins after adjusting for age, education, smoking and established cardiovascular risk factors (Bonferroni corrected p<0.000069). Of these 12 proteins, IL-6 was associated with increased incidence of imminent MI (HR 1.22 95%CI [1.09-1.37]), TNFRSF11A was associated with increased long-term MI incidence (HR 1.22 [1.01-1.48]) and 11 proteins were associated with increased mortality (HR 1.14-1.30 [1.01-1.42]).

Conclusions: These findings confirm and extend our understanding of how physical activity could assert its beneficial effect on cardiovascular health through proteins involved with modulating inflammatory, immune and metabolic pathways. Further research is needed to explore the causal mechanisms behind these associations.

Aims: Obesity increases the risk of heart failure (HF), partly due to hypervolaemia and excess epicardial adipose tissue (EAT).We aimed to investigate the effect of the sodium glucose co-transporter 2 inhibitor empagliflozin on estimated extracellular volume (eECV) and ventricular EAT mass in non-diabetic patients with overweight or obesity and risk of HF to evaluate the drug's potential for HF prevention.

Methods: In this randomised, double-blind, placebo-controlled trial, we recruited non-diabetic patients with body mass index (BMI) >28kg/m2 and risk of HF. Patients were randomised 1:1 to 180-days empagliflozin 10 mg or placebo. The primary endpoints were the baseline-adjusted mean differences in change of eECV and ventricular EAT mass in the intention-to-treat population with Bonferroni-adjustment for multiplicity.

Results: From September 2021 to July 2024, we randomised 191 patients (empagliflozin: 94, placebo: 97) with median age 68 years and median BMI 31·9 kg/m2. Analyses of eECV and EAT included 191 and 165 patients, respectively. Compared to placebo, empagliflozin significantly reduced eECV [empagliflozin, mean change (SD): -0·154 L (0·257); placebo, mean change: -0·029 L (0·261); estimated treatment difference (ETD): -0·123 L, 97.5% CI: -0·211 to -0·035, padj=0·004] but did not affect EAT mass [empagliflozin, mean change: -2·3 g (13·4); placebo, mean change: -3·7 g (15·8); ETD: 1·5 g, 97·5% CI: -3·8 to 6·7, padj=1.00].

Conclusion: In high-risk patients with overweight or obesity, treatment with empagliflozin resulted in a potentially favourable reduction in eECV compared to placebo. Meanwhile, the drug did not affect EAT mass.