European journal of preventive cardiology最新文献

Aims: Fibroblast growth factor 23 (FGF23) has been implicated in the occurrence of atrial fibrillation (AF), but its prognostic value in AF patients remains unclear.

Methods and results: A total of 35 197 AF patients with available follow-up data (3.56, 0.47-8.92 years) from the UK Biobank were included. Clinical association between serum FGF23 and AF-related outcomes including mortality, heart failure (HF), ischaemic stroke, and dementia were analysed using multivariable Cox regression. In those passed quality control for array sequencing, polygenic score for FGF23 (PGSFGF23) was calculated as genetic instrument, and the association between PGSFGF23 and the occurrence of endpoints after first AF diagnosis were further explored. In 886 patients who diagnosed AF at or prior to the enrolment, elevated serum FGF23 levels were significantly associated with an increased risk of all-cause (37% increase per standard deviation) and cardiovascular (40% increase per standard deviation) mortality and HF (43% increase per standard deviation). A total of 35 197 patients were available for genetic array sequencing data. Using polygenic score including seven independent SNPs reaching genome-wide significance threshold, genetic association analysis indicated that increased PGSFGF23 is associated with reduced risk of HF but increased risk of all-cause mortality and ischaemic stroke.

Conclusion: Our findings suggest that FGF23 is a potential biomarker for accessing AF-related outcomes. The paradoxical association between genetic FGF23 and serum FGF23 level highlights the need for further investigation to elucidate the underlying mechanisms.

Aim: To evaluate whether integrating Apolipoprotein B (ApoB) into the SCORE2 cardiovascular risk prediction framework improves its predictive accuracy and clinical applicability within the UK Biobank population.

Method: A 10-year prospective cohort study was conducted with 448,303 UK Biobank participants eligible for SCORE2 calculation. Three approaches were employed: (1) threshold analysis to determine the optimal ApoB cutoff for cardiovascular disease (CVD) risk prediction using Youden's Index, (2) assessment of the synergistic effect of SCORE2 and ApoB through concordant and discordant classifications, and (3) recalibration of the SCORE2 model by incorporating ApoB as an additional predictor.

Results: Each 0.2 g/L increase in ApoB was associated with an increased subdistribution hazard for CVD events (SHR: 1.13; 95% CI: 1.11-1.14, p < 0.001), accounting for non-cardiovascular death as a competing risk. Threshold analysis identified an optimal ApoB cutoff at 1.18 g/L; however, it demonstrated limited discriminatory performance (area under the curve 0.54), with low sensitivity (32.4%) and moderate specificity (74.4%). Individuals with both low ApoB (<1.18 g/L) and low SCORE2 risk (<5%) had a lower CVD incidence rate (232.51 per 100,000 person-years) compared to those identified as low risk by SCORE2 alone (253.69 per 100,000 person-years). Integration of ApoB into the SCORE2 model did not significantly improve the model discrimination, calibration and net reclassification improvement.

Conclusion: ApoB exhibited a dose-response relationship with cardiovascular risk but had limited standalone predictive utility within the UK Biobank population. However, combining ApoB with SCORE2 thresholds improved the identification of low-risk individuals, suggesting a complementary role for ApoB in refining cardiovascular risk stratification.

Aim: Sleep apnoea syndrome (SAS) is a common sleep disorder associated with heightened cardiovascular risks, yet sex-specific differences in these risks remain unclear.

Methods: This retrospective observational cohort study utilized the JMDC Claims Database, covering >5 million individuals in Japan. We analyzed data from 4,173,702 individuals (2,406,930 men, 1,766,772 women) after excluding those with central SAS, cardiovascular disease, and incomplete lifestyle questionnaire data. SAS was identified using ICD-10 codes and treatment records. Cox regression models adjusted for multiple factors examined the association between SAS and cardiovascular outcomes.

Results: Among the participants, 39,078 men (1.62%) and 3,960 women (0.22%) were diagnosed with SAS. Over a mean follow-up of 1,290±1,000 days, SAS was associated with an increased risk of composite cardiovascular events, with a hazard ratio (HR) of 1.27 (95% CI, 1.23-1.31) in men and 1.72 (95% CI, 1.54-1.92) in women compared to those without SAS. The association was significantly stronger in women than in men (P-value for interaction< 0.001) and this sex difference was validated by various sensitivity analyses.

Conclusions: Despite the lower prevalence of SAS among women, there was a gender disparity in the cardiovascular impact of SAS, with women demonstrating a significantly higher risk compared to men. This underscores the importance of tailored management strategies aimed at early detection and cardiovascular disease prevention specifically in female patients with SAS.

Aim: To assess the relationship between body mass index (BMI), subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), epicardial adipose tissue (EAT), pericardial adipose tissue (PAT) and clinical outcomes in dilated cardiomyopathy (DCM) patients.

Methods: Non-ischemic DCM patients were prospectively enrolled. Regional adipose tissue, cardiac function, and myocardial tissue characteristics were measured by cardiac magnetic resonance (CMR). The primary endpoint included all-cause mortality and heart transplantation (HTX).

Results: This study enrolled 1042 DCM patients (68% men, mean age 48 ± 15 years, mean BMI 23.9 ± 4.0 kg/m2). Underweight patients were more frequently women, had lower blood pressure, worse New York Heart Association (NYHA) class, reduced biventricular ejection fraction, and higher native T1 and extracellular volume fraction (ECV) value. Similarly, reduced regional adipose tissue was associated with adverse heart remodeling, worse cardiac function, and higher diffuse myocardial fibrosis. After a median follow-up of 41 months, primary endpoint occurred in 237 patients. BMI (HR: 0.94, 95% CI: 0.90 - 0.98, P = 0.006), VAT thickness (per 1 mm: HR 0.94, 95% CI: 0.91 - 0.97, P < 0.001), and EAT volume (per 1 mL: HR 0.96, 95% CI: 0.95 - 0.97, P < 0.001) were independent predictors of primary endpoint. EAT volume showed highest predictive value for heart failure death/HTX (C-index: 0.70). BMI was the best predictor of arrhythmia endpoint (C-index: 0.64).

Conclusions: Lower BMI and thinner regional adipose tissue represented the worse clinical phenotype and adverse remodeling, and were associated with worse clinical outcomes in patients with DCM.

Aims: Children of patients with early-onset myocardial infarction (MI) are at increased risk, but the importance of concordant vs. discordant parent-offspring risk factor profiles on MI risk is largely unknown. We quantified the long-term absolute risk of MI according to shared risk factors in adulthood.

Methods and results: We sampled data on familial predisposed offspring and their parents from the Framingham Heart Study. Early MI was defined as a history of parental MI onset before age 55 in men or 65 in women. Individuals were matched 3:1 with non-predisposed offspring. Cardiovascular risk factors included obesity, smoking, hypertension, high cholesterol, and diabetes. We estimated the absolute 20-year incidence of MI using the Aalen-Johansen estimator. At age 40, the 20-year risk of MI varied by cholesterol level [high cholesterol 25.7% (95% confidence interval 11.2-40.2%) vs. non-high cholesterol 3.4% (0.5-6.4)] among predisposed individuals, and this difference was greater than in controls [high cholesterol 9.3% (1.5-17.0) vs. non-high cholesterol 2.5% (1.1-3.8)]. Similar results were observed for prevalent hypertension [26.7% (10.8-42.5) vs. 4.0% (0.9-7.1) in predisposed vs. 10.8% (3.2-18.3) and 2.1% (0.8-3.4) in controls]. Among offspring without risk factors, parental risk factors carried a residual impact on 20-year MI risk in offspring [0% (0-11.6) for 0-1 parental risk factors vs. 3.3% (0-9.8) for ≥2 parent risk factors at age 40, vs. 2.9% (0-8.4) and 8.5% (0-19.8) at age 50 years].

Conclusion: Children of patients with early-onset MI have low absolute risks of MI in the absence of midlife cardiovascular risk factors, especially if the parent also had a low risk factor burden prior to MI.

Aims: In recent years, mortality from ischaemic heart disease and diabetes has decreased. There is an inequality in mortality reduction between urban and non-urban areas. This study aims to estimate the trend in mortality from ischaemic heart disease and diabetes mellitus in urban and non-urban areas in Italy and Spain throughout the first two decades of the 21st century.

Methods and results: Deaths and population data by age and sex, according to the area of residence, were obtained from the National Institute of Statistics of Italy and National Institute of Statistics of Spain. The annual age-standardized mortality rates from ischaemic heart disease and diabetes mellitus were calculated from 2003 to 2019 for each of the two areas of residence in both countries. The average annual percentage change (APC) in the mortality rate in each area was estimated using linear regression models and taking age-standardized mortality rates as a dependent variable. The mortality rates from both causes of death decreased between the beginning and the end of the period analysed. In Italy, the APC was -4.0 and -3.6% in the mortality rate from ischaemic heart disease and -1.5 and -1.3% in the mortality rate from diabetes mellitus in urban and non-urban areas, respectively. In Spain, the APC in was -4.4 and -3.7% in the mortality rate from ischaemic heart disease and -3.3 and -2.0% in the mortality rate from diabetes mellitus in urban and non-urban areas, respectively.

Conclusion: Mortality from both ischaemic heart disease and diabetes have shown a greater reduction in urban areas compared with non-urban areas since the first years of the 21st century in Spain and Italy.