European journal of preventive cardiology最新文献

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.

Recent trends indicate a concerning increase in early-onset atherosclerotic cardiovascular disease (ASCVD) among younger individuals (men aged <55 years women aged <65 years). These findings highlight the pathobiology of ASCVD as a disease process that begins early in life and underscores the need for more tailored screening methods and preventive strategies. Increasing attention has been placed on the growing burden of traditional cardiometabolic risk factors in young individuals while also recognizing unique factors that mediate risk of pre-mature atherosclerosis in this demographic such as substance use, socioeconomic disparities, adverse pregnancy outcomes, and chronic inflammatory states that contribute to the increasing incidence of early ASCVD. Additionally, mounting evidence has pointed out significant disparities in the diagnosis and management of early ASCVD and cardiovascular outcomes based on sex and race. Moving towards a more personalized approach, emerging data and technological developments using diverse tools such as polygenic risk scores and coronary artery calcium scans have shown potential in earlier detection of ASCVD risk. Thus, we review current evidence on causal risk factors that drive the increase in early ASCVD and highlight emerging tools to improve ASCVD risk assessment in young individuals.

Aims: Elevated lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular disease, but the mechanisms of risk are debated. Studies have found inconsistent associations between Lp(a) and measurements of atherosclerosis. We aimed to assess the relationship between Lp(a), low-density lipoprotein cholesterol (LDL-C), and coronary artery plaque severity.

Methods and results: The study population consisted of participants of the Million Veteran Program who have undergone an invasive angiogram. The primary exposure was genetically predicted Lp(a) estimated by a polygenic score. Genetically predicted LDL-C was also assessed for comparison. The primary outcome was coronary artery plaque severity categorized as normal, non-obstructive disease, one-vessel disease, two-vessel disease, and three-vessel or left main disease. Among 18 927 adults of genetically inferred European ancestry and 4039 adults of genetically inferred African ancestry, we observed consistent associations between genetically predicted Lp(a) and obstructive coronary plaque, with effect sizes trending upward for increasingly severe categories of disease. Associations were independent of risk factors, clinically measured LDL-C and genetically predicted LDL-C. However, we did not find strong or consistent evidence for an association between genetically predicted Lp(a) and risk for non-obstructive plaque.

Conclusion: Genetically predicted Lp(a) is positively associated with coronary plaque severity independent of LDL-C, consistent with Lp(a) promoting atherogenesis. However, the effects of Lp(a) may be greater for progression of plaque to obstructive disease than for the initial development of non-obstructive plaque. A limitation of this study is that Lp(a) was estimated using genetic markers and could not be directly assayed nor could apo(a) isoform size.