European journal of preventive cardiology最新文献

Aims: Despite causal inference from genetically higher triglyceride levels and cardiovascular risk, therapeutic triglyceride lowering has yet to demonstrate cardiovascular benefits. Providing insights into the magnitude of treatment effect needed and the type of patients who might benefit, we assessed the relationship between triglyceride levels and cardiovascular events following myocardial infarction (MI).

Methods and results: Between 2005 and 2022, 51,719 MI patients in the Swedish MI registry SWEDEHEART were studied. Triglyceride change from admission to 1-year and 1-year levels was evaluated in adjusted Cox models. Outcomes were MACE (all-cause mortality, non-fatal MI, and non-fatal ischaemic stroke), all-cause mortality, and non-fatal MI. Over 5.6 years, 9008 patients experienced an MACE, and 5148 died. Median triglycerides were 1.4 mmol/L (interquartile range IQR 1.0-2.0) at MI admission and 1.2 mmol/L (0.9-1.6) at 1 year. Patients in the top quartile of triglyceride reduction (≥0.6 mmol/L, median 1.0 mmol/L) had the highest baseline triglycerides of 2.2 mmol/L (1.8-2.9). Compared to patients with minimal change, this quartile had the lowest risk of MACE (HR 0.85 95% CI 0.79-0.92), all-cause mortality (HR 0.90, 0.81-0.99), and non-fatal MI (HR 0.83, 0.74-0.94). Patients in the lowest quartile at 1-year (<0.9 mmol/L) had the lowest cardiovascular risk.

Conclusion: Among MI patients, triglyceride reductions of ∼1.0 mmol/L were associated with the lowest cardiovascular risk. Only 27% of patients achieved this reduction with baseline triglycerides ∼2.2 mmol/L. These findings may explain neutral results in prior triglyceride-lowering trials and suggest future trials should enrol patients with baseline triglycerides ≥2.2 mmol/L and target reductions ≥1.0 mmol/L.

Aims: Endothelial dysfunction is a hallmark of cardiovascular disease (CVD). Exercise effectively improves endothelial function, yet the impact of different modalities and intensities remains unclear. This study evaluated the effect of aerobic (AE), resistance (RE), and combined exercise (CE), on endothelial function measured by flow-mediated dilation (FMD).

Methods: A systematic review and frequentist network meta-analysis of randomised and non-randomised trials in adults with coronary artery disease or chronic heart failure was conducted. Electronic databases were searched up to April 2025. Interventions were classified as usual care (UC), moderate-intensity AE (MAE), high-intensity interval AE (HIIE), moderate-intensity RE (MRE), high-intensity RE (HRE), moderate-intensity CE (MCE), and high-intensity CE (HCE). Mean differences (MD) with 95% confidence intervals (CI) were used as effect size index, and interventions ranked using surface under the cumulative ranking curve (SUCRA).

Results: Thirty-seven studies (80 groups; n = 6818) were included. Compared with UC, MAE (2.04%; 95% CI: 1.01-3.07), HIIE (3.47%; 95% CI: 2.02-4.92), MCE (2.71%; 95% CI: 0.05-5.36), and HCE (8.25%; 95% CI: 3.18-13.32) significantly improved brachial FMD, whereas MRE did not. HIIE outperformed MAE (1.43%; 95% CI: 0.09-2.78). Although HCE showed the highest surface under the cumulative ranking curve (SUCRA: 98.2%), this relied on a single group. Crucially, sensitivity analyses confirmed HIIE as the most robust high-performing intervention (84.0%) compared to MRE (61.6%) and MCE (61.3%).

Conclusion: Exercise significantly enhances endothelial function in in patients with CVD. HIIE emerged as the most robust and evidence-based modality, demonstrating superior efficacy over moderate continuous exercise. While high-intensity combined protocols (HCE) show significant theoretical potential, randomised trials are urgently needed to confirm their efficacy. Current evidence supports HIIE as a primary strategy for vascular adaptation in cardiac rehabilitation.

Aims: Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality. SCORE2 may underestimate risk in those classified as low-to-moderate risk. Polygenic risk scores (PGSs) capture genetic predisposition to CVD and could enhance traditional models. This study examines whether integrating PGS with SCORE2 improves the prediction of significant subclinical coronary atherosclerosis, defined as coronary artery calcium (CAC) > 100.

Methods and results: We analysed data from 1420 participants in the Paracelsus 10 000 cohort with available PGS, SCORE2, and CAC measurements. Predictive performance was compared across SCORE2 alone, PGS alone, and their combination, assessed using the Akaike information criterion and area under the receiver operating characteristic curve (AUC). Decision curve analysis was performed to evaluate clinical utility. Polygenic risk score improved the prediction of CAC > 100 beyond SCORE2 alone, increasing the AUC from 0.662 to 0.738 in women and from 0.659 to 0.714 in men, with substantial net reclassification index (NRI: women 0.649, men 0.450). The addition of PGS, particularly in the highest quintiles, significantly enhanced classification accuracy for CAC > 100. Decision curve analysis demonstrated that using PGS as a continuous variable provided the highest net benefit at lower threshold probabilities, supporting its role in refining risk stratification, especially in low-to-moderate risk populations.

Conclusion: Polygenic risk score enhances SCORE2-based prediction of significant CAC. These findings highlight the potential of PGS to refine cardiovascular risk stratification, supporting targeted screening and prevention. Prospective validation, assessment of long-term cardiovascular outcomes, and cost-effectiveness analysis are warranted to guide clinical implementation.

Aims: Current guidelines fail to adequately guide cardiovascular prevention in young adults, even when a family history of cardiovascular disease (CVD) is known. We aim to assess the feasibility and acceptability of a routine family-based cardiovascular risk assessment in first-degree relatives of individuals with premature coronary artery disease (CAD).

Methods and results: Patients with premature CAD were prospectively asked about pre-existing CVD cases and previous cardiovascular check-ups among their first-degree relatives. They were then encouraged to invite their healthy and naïve to cardiology follow-up relatives to contact the cardiology department for consultation. The primary outcome was the eligibility of relatives for initial cardiovascular evaluation, defined by the absence of previously known CVD or active primary prevention. The cardiovascular status of first-degree relatives was evaluated in the families of 137 probands with premature CAD. Of the 626 identified first-degree relatives, 153 (24.4%) had known CVD, primarily CAD (19.6%). Among the 352 siblings and adult children, 48 (13.7%) were already diagnosed with CVD, 68 (19.3%) were being treated or followed for primary prevention, and 226 (64.2%) were eligible for initial cardiovascular check-up. Within 12 months, 11.1% of eligible relatives initiate screening.

Conclusion: This pilot study revealed (i) a significant familial burden of CVD, (ii) opportunities for proactive primary prevention in two out of three of young relatives, and (iii) challenges in engaging non-symptomatic adults in a cardiovascular screening based on family history.

Aims: Sudden arrhythmic death syndrome (SADS) refers to a sudden death, which remains unexplained despite comprehensive post-mortem examination and a toxicological screen. We aimed to investigate the impact of age and sex on the overall diagnostic yield and underlying aetiology in decedents with SADS using a combined approach of familial evaluation (FE) and molecular autopsy (MA).

Methods and results: Consecutive referrals to a single centre for FE only, MA only or both, following a SADS death were included. First-degree family members underwent comprehensive FE and decedents with post-mortem DNA were sequenced with a 36 cardiac gene panel for MA. A Bayesian framework for analysis was performed to identify associations. Among 760 SADS decedents (66% male; mean age 31 ± 12 years) the overall diagnostic yield for an inherited cardiac condition was 37% (32-42%) and 9% (6-12%) for FE and MA cohorts. In a subset where both FE and MA were performed the diagnostic yield was 45% (38-61%). The relative risk of an FE diagnosis of long QT syndrome (LQTS) or Catecholaminergic polymorphic ventricular tachycardia (CPVT) vs. remaining unexplained declined by 5.6% [RR 0.94 (0.91-0.98)] and by 11% [RR 0.89 (0.81-0.97)], for each year increase in age. Females were more likely to have a diagnosis by both FE [40% (34-45%) vs. 36% (31-41%)] and MA [15% (10-21%) vs. 6% (3-8%)]. Females [8.1% (4.1-13.4%)], were more likely to be diagnosed with LQTS than males [1.2% (0.2-2.7%)] in the MA cohort.

Conclusion: After a SADS death, the diagnostic yield of comprehensive FE, MA, or both in an expert setting can be up to 45% with a combined approach. Females had higher diagnostic yield than males, most notable with LQTS. CPVT and LQTS diagnoses declined with increasing age. These data highlight the relative utility of FE and MA depending on age and sex for determining underlying diagnoses following SADS deaths.