European journal of preventive cardiology最新文献

Aim: To estimate the prevalence of good adherence to statin therapy and identify demographic and clinical factors associated with adherence among adults prescribed lipid-lowering therapy (LLT) for atherosclerotic cardiovascular disease (ASCVD) prevention.

Methods: We conducted a systematic search of PubMed and Scopus through May 2025 to identify randomized controlled trials, cohort, nested case-control, and cross-sectional studies evaluating adherence to statin monotherapy. Data were extracted on study design, participant demographics, comorbidities, adherence assessment method and duration, and statin type. A random-effects meta-analysis was performed. Study quality was assessed using the Newcastle-Ottawa Scale, and risk of bias in randomized trials was evaluated with the Cochrane RoB 2 tool. Subgroup and sensitivity analyses examined adherence variations by follow-up duration (<1, 1, >1 year), alternative adherence thresholds, and study quality. "Primary" non-adherence (failure to initiate prescribed therapy) was not reported in any of the included studies.

Results: Seventy-six studies encompassing 5,898,141 participants (median follow-up 24 months) were included. The pooled prevalence of good adherence (≥80% medication use) was 62.4% (95% CI: 58.3-66.5%), lower in primary (57.5%) than secondary (64.4%) prevention settings. Factors associated with lower adherence included female sex (RR=0.92), Black race (RR=0.66), smoking (RR=0.94), depression (RR=0.89), and heart failure (RR=0.96). Higher adherence was observed among older adults (RR=1.34), individuals with myocardial infarction (RR=1.28) or hypertension (RR=1.12), those with ≥2 comorbidities (RR=1.25), and patients with polypharmacy (RR=1.32). Subgroup and sensitivity analyses yielded consistent results.

Conclusions: Adherence to statin therapy remains suboptimal and is significantly influenced by demographic and clinical factors. Targeted strategies are needed to improve adherence, particularly in high-risk groups.

Aims: Atrial fibrillation (AF) is a growing public health concern, but its etiology is not well understood. A few studies investigated the association of depression and anxiety with AF and yielded mixed results. Studies analyzing the link of other psychiatric disorders (PDs) with AF risk are scarce. Herein, we investigated the association between a broad range of PDs and the risk of incident AF.

Methods and results: We studied 3,815,546 parents of live-born children registered in the Swedish Medical Birth Register during 1973-2014 and followed them from January 1, 2001 to December 31, 2023. We used Cox proportional hazard models and flexible parametric survival models to estimate the associations of overall and 14 specific PD subtypes with the risk of incident AF. We used sibling comparisons to evaluate whether shared familial factors confounded the observed associations. Altogether 806,078 (21.13%) participants had at least one PD and 213,048 (5.58%) had a diagnosis of AF during the 82.6 million person-years follow-up. Overall PD and several types of PDs were associated with increased risks of AF. The adjusted hazard ratios and 95% confidence intervals for AF according to overall PD were 1.28 (1.27-1.29) and 1.32 (1.29-1.35) in the whole cohort and in the sibling analysis, respectively. The associations were generally strongest early in the follow-up, progressively weakened over time, but persisted through the whole follow-up.

Conclusion: Several PDs were linked to increased risks of developing AF. Further studies are needed to replicate our findings and to understand the mechanisms underlying these associations.

Hypertension is the leading cardiovascular risk factor. However, despite the availability of safe and effective antihypertensive drugs, blood pressure (BP) control rates remain low worldwide. In this context, the recent European hypertension guidelines present an additional challenge by lowering the BP threshold for initiating pharmacological treatment to below 140/90 mmHg for selected high-risk patients and recommending that BP values be lowered to below 130/80 mmHg for most hypertensive patients. In this narrative review, we discuss the barriers to the implementation of guideline-defined standards of care in high-, low-, and middle-income countries and consider some possible solutions to improve this situation. We discuss strategies for detecting hypertension and monitoring its control, including new technologies and settings for BP measurement. Key issues related to the treatment of hypertension at the population level are also addressed, including lifestyle interventions, improving adherence to treatment, and organizational solutions, particularly for long-term follow-up of hypertensive patients. Finally, we identify key areas for future research into the implementation of hypertension care standards and attempt to suggest possible strategies that may be particularly relevant in the future, with the aim of improving global hypertension control rates and reducing the burden of its complications.

Aims: This study aims to investigate the role of biological aging pace and quantify its contributions in explaining sex disparities in cardiovascular disease (CVD) risk.

Methods and results: A population-based study was conducted, including 371 032 participants in the UK Biobank. Two measures of biological aging pace were assessed, including phenotypic age acceleration (PhenoAgeAccel) and telomere length. The chronological age was similar between females [56.1 (8.0) years] and males [56.1 (8.2) years]. Male participants consistently had higher CVD risks than female participants, including any CVD [hazard ratio (HR), 1.66; 95% confidence interval (CI), 1.54-1.80], atrial fibrillation (HR, 1.78; 95% CI, 1.73-1.83), coronary heart disease (HR, 2.11; 95% CI, 2.05-2.18), heart failure (HR, 1.72; 95% CI, 1.65-1.80), and stroke (HR, 1.44; 95% CI, 1.38-1.51). Females had 0.71-2.90 years longer time to CVD than males. Males had a faster biological aging pace of 1.02 (95% CI, 0.99-1.06) years in PhenoAgeAccel than females, with 17.1% explained by unhealthy lifestyles, followed by prevalent chronic diseases (8.6%) and metabolic factors (6.5%). The sex disparities in PhenoAgeAccel significantly explained 65.0% of male-associated any CVD, 64.7% of atrial fibrillation, 68.2% of coronary heart disease, 64.4% of heart failure, and 60.4% of stroke, respectively. Similar findings were observed when using the telomere length for evaluating biological aging pace or controlling for sex hormones.

Conclusion: Our findings reveal that the biological aging pace might partially explain sex disparities in CVD risk, highlighting the importance of monitoring the biological aging pace to address the huge sex gap and promote sex-specific CVD primary prevention.

Current approaches to estimate cardiovascular risk for primary prevention of cardiovascular disease (CVD) are suboptimal and novel strategies that optimise and personalise risk predictions are needed. In this review, we provide an overview of the potential use of circulating cardiovascular biomarkers - C-reactive protein, growth differentiation factor 15, N-terminal pro B-type natriuretic peptide, and cardiac troponins - to improve CVD risk prediction in the general population. We present novel statistical approaches that dynamically capture risk to further optimise and personalise cardiovascular risk estimation systems. While all studied cardiovascular biomarkers are independently associated with CVD risk when using measurements from a single time-point, the added value they provide to traditional risk factors in terms of accuracy is modest. A dynamic risk prediction approach - such as joint modelling - that can incorporate changes in biomarkers and other risk factors over time may better capture the complexities of CVD development, enhancing CVD risk estimates. With the increasing adoption of electronic health records and commercially available assays for these circulating biomarkers, deploying such systems in clinical practice has become feasible. Future research should focus on the development and validation of multi-marker biomarker-driven dynamic risk prediction models, along with development of a standardized methodological approach for comparing performance of dynamic risk estimation systems against current static models. To facilitate its implementation in clinical practice, public health impact and cost-effectiveness needs to be assessed. Finally, optimizing screening intervals through a biomarker-driven dynamic risk approach may offer further improvement in individualising primary CVD prevention strategies.

Aims: Blood proteomic profiling may model vascular biological aging with high precision. This study aimed to assess the association between blood pressure and proteomic vascular aging, and its potential mediation effects in the relationship between high blood pressure and incident cardiovascular events.

Methods: Among 45,387 UK Biobank participants, we developed a proteomic vascular aging signature (vascular age gap) using 21 heart- and artery-enriched proteins via a LightGBM model. Associations with vascular age gap were evaluated for blood pressure categories and continuous systolic/diastolic blood pressure (SBP/DBP). Mediation analyses examined the role of proteomic vascular aging in the link between high blood pressure and cardiovascular events.

Results: Compared to normotensive participants, vascular age gap was significantly higher in those with high-normal blood pressure (0.122±0.048 years, P=0.011), grade 1 hypertension (0.266±0.049 years, P<0.001), and grade 2 hypertension (0.494±0.071 years, P<0.001). Non-linear associations were observed for both SBP and DBP, with thresholds near 120/80 mm Hg. The associations were stronger in midlife adults. The vascular age gap may mediate 3.73% to 10.59% of the association between grade 2 hypertension and cardiovascular events. No mediation was observed for peripheral artery disease in grade 2 hypertension. The most influential proteins exhibited potential mediation effects, with TNFRSF11B and CRLF1 consistently contributed to mediation across blood pressure categories and outcomes.

Conclusions: High blood pressure is associated with accelerated proteomic vascular aging, which potentially mediates its link to cardiovascular events. This supports vascular age gap as a modest but significant marker of blood pressure-related cardiovascular risk.

Aims: Lipid-lowering therapy is typically initiated at high low-density lipoprotein(LDL) cholesterol marked by elevated apolipoprotein B(apoB). We tested the hypothesis that elevated apoB alternatively due to high remnant cholesterol confers equally high risk of atherosclerotic cardiovascular disease(ASCVD) but less initiation of lipid-lowering therapy, compared to elevated apoB due to high LDL cholesterol.

Methods and results: From the Copenhagen General Population Study, 94 299 lipid-lowering therapy naïve adults without a history of ASCVD were included in 2003-2015. Discordance groups were formed by median levels of remnant cholesterol, LDL cholesterol and apoB. In the national Danish health registries, individuals were followed for a prescription of lipid-lowering therapy and for incident ASCVD until December 2021. During a median follow-up of 12 years, 9269 developed ASCVD. Compared to individuals with concordant low values of remnant cholesterol, apoB, and LDL cholesterol, those with high remnant cholesterol and high apoB but low LDL cholesterol had a hazard ratio(HR) of 1.45 (95% confidence interval: 1.34-1.56) for ASCVD and an odds ratio(OR) of 3.0 (2.5-3.6) for starting lipid-lowering therapy within one year. Correspondingly, those with low remnant cholesterol but high apoB and high LDL cholesterol had a HR of 1.20 (1.11-1.30) for ASCVD and an OR of 5.1 (4.3-5.9) for starting lipid-lowering therapy.

Conclusion: In a primary prevention setting, elevated apoB due to high remnant cholesterol confers high risk of ASCVD but less initiation of lipid-lowering therapy compared to elevated apoB due to high LDL cholesterol, representing a guideline-based limitation and an unmet medical need.