European journal of preventive cardiology最新文献

Aims: To evaluate phenotypic progression in a large cohort of patients with arrhythmogenic cardiomyopathy (ACM) using cardiac magnetic resonance (CMR), and to assess the prognostic impact of baseline structural abnormalities and to investigate the impact of exercise performed after diagnosis.

Methods: We retrospectively analysed individuals with a definitive diagnosis of ACM or identified as carriers of pathogenic or likely pathogenic (P/LP) ACM-related genetic variants, all of whom underwent at least one CMR. Longitudinal data on structural remodelling were available for a subset of patients with at least two CMRs. Patients were stratified into higher- and lower-exercise groups based on exercise performed after diagnosis. The primary composite endpoint included major ventricular arrhythmias (MVA), appropriate implantable cardioverter-defibrillator (ICD) interventions, sudden cardiac arrest, and sudden cardiac death.

Results: A total of 202 patients (mean age: 41.7 ± 16.4 years, 59% males) were included. Over a mean follow-up of 5.2 years, 32 patients (16%) reached the primary endpoint. Baseline myocardial fibrosis (MF) and reduced right ventricular ejection fraction independently predicted arrhythmic events [HR 4.9, (95% CI: 1.8-12.9), p < 0.001 and HR 2.6, (95% CI: 1.2-5.4), p = 0.002, respectively]. Among the 97 patients with at least 2 CMR scans, 32% developed de novo fibrosis, and 41% showed progression of MF. Patients with longer intervals between CMR scans demonstrated more pronounced structural remodelling, evidenced by greater increases in biventricular end-diastolic volumes and progressive declines in ventricular function. Significant left ventricular dilation was observed in the higher-exercise group, with an increase in indexed end-diastolic volumes. Carriers of PKP2 variants engaging in moderate-to-intense exercise exhibited a higher incidence of arrhythmic events.

Conclusions: MF and right ventricular systolic dysfunction emerge as independent predictors of arrhythmic risk in ACM. Serial CMR assessments demonstrate that structural progression is common, supporting the concept that ACM represents a dynamic rather than a static disease process. Patients carrying PKP2 variants may exhibit heightened susceptibility to exercise-related arrhythmic risk.Arrhythmogenic cardiomyopathy (ACM) is a heart condition that can lead to dangerous arrhythmias and structural remodeling. In this study, we followed one of the largest groups of ACM patients with repeated cardiovascular magnetic resonance (CMR) scans to better understand how the disease evolves and how exercise after diagnosis affects outcomes.

Aims: The impact of social determinants of health (SDoH) on cardiovascular disease (CVD) risk in cancer survivors remains unclear. We examined the association between SDoH and subsequent CVD risk among cancer survivors.

Methods and results: This retrospective cohort study included 18 992 cancer survivors and 75 968 propensity score matched non-cancer controls from the UK Biobank. A composite SDoH score was generated using 17 components across 5 domains, classifying participants into favourable, medium, and unfavourable SDoH groups. Cox models were used to assess associations between SDoH and incident CVD, including ischaemic heart disease (IHD), heart failure (HF), stroke, and CVD mortality. Compared with cancer survivors with favourable SDoH, those with medium and unfavourable SDoH had higher CVD risks: hazard ratio (HR) 1.17 (95% CI: 1.09-1.27) and HR 1.32 (95% CI: 1.23-1.43), respectively. Unfavourable SDoH was also associated with increased risk of IHD (HR: 1.31; 95% CI: 1.15-1.49), HF (HR: 1.58; 95% CI: 1.30-1.92), stroke (HR: 1.47; 95% CI: 1.18-1.84), and CVD mortality (HR: 1.54; 95% CI: 1.25-1.90). Cancer survivors with favourable SDoH had overall CVD risks similar to matched non-cancer controls (HR: 1.07; 95% CI: 1.00-1.13). In joint analysis, cancer survivors with favourable SDoH had a higher risk (HR: 1.22; 95% CI, 1.15-1.28) than their non-cancer counterparts.

Conclusion: Among cancer survivors, unfavourable SDoH was associated with elevated CVD risk, whereas favourable SDoH attenuated this risk to levels comparable with non-cancer population. That may partly reflect the increased risk observed among non-cancer with unfavourable SDoH. Targeted interventions and policy measures addressing social determinants are needed to mitigate cardiovascular disparities in cancer survivorship.

Aims: The Framingham risk score (FRS), a tool primarily used for atherosclerotic cardiovascular disease (ASCVD) risk stratification, incorporates factors like age, obesity, and smoking. However, its role in predicting cancer and heart failure (HF) risk remains unclear, while emerging data suggest these two conditions coincide frequently.

Methods and results: We conducted a post hoc analysis using data from the PREVEND study and validated our findings in the UK Biobank. We examined the association between FRS tertiles at baseline and incident cancer or HF. Fine-Gray regression models were used to calculate subdistribution hazard ratios (sHRs), adjusting for estimated glomerular filtration rate and urinary albumin excretion with all-cause mortality as a competing risk. In PREVEND, we included 8123 participants (mean age 49 ± 13 years, 50% female). Over follow-up periods of 17.46 years [interquartile range (IQR) 17.15-17.80] (cancer) and 23.39 years (IQR 13.78-23.81) (HF), 1176 participants developed new-onset cancer and 758 developed new-onset HF. In a multivariable analysis, participants in the highest FRS tertile compared with the lowest had a higher hazard for both cancer (sHR 2.32, P < 0.001) and HF (sHR 10.08, P < 0.001). Participants in the highest FRS tertile also had the worst survival (log-rank P < 0.001). We validated these findings in the UK Biobank (n = 389942) wherein individuals in the highest FRS tertile also had a higher hazard for both cancer (sHR 2.05, P < 0.001) and HF (sHR 5.99, P < 0.001) compared with the lowest tertile.

Conclusion: The FRS associates with new-onset cancer or HF, implicating a broader clinical application of the FRS beyond ASCVD risk stratification in cardio-oncology.