European journal of preventive cardiology最新文献

Aim: To investigate associations between psychosocial burden and biomarkers reflecting pathophysiological pathways in patients with chronic coronary syndrome.

Methods: Psychosocial (PS) factors were collected from self-assessed questionnaires and biomarkers representing inflammation (high-sensitivity [hs]-C-reactive protein [CRP], interleukin-6 [IL-6], lipoprotein-associated phospholipase A2 [Lp-PLA2]) and cardiac injury/stress (hs-troponin T [hs-TnT], N-terminal pro-B type natriuretic peptide [NT-proBNP]) were measured in 12,492 patients with chronic coronary syndrome in the STABILITY trial. Associations between level of each psychosocial factor (never-rarely (reference), sometimes, often-always) and biomarkers were evaluated using linear models with adjusted geometric mean ratios (GMR). A score comprising four factors ('feeling down', 'loss of interest', financial stress', 'living alone') that previously demonstrated association with cardiovascular (CV) outcome was created, and categorized into three levels: low, moderate and high PS burden. Associations between PS score and biomarkers were evaluated similarly.

Results: Greater PS burden was significantly associated with a gradual increase in inflammatory biomarkers (GMR [95% CI] for moderate vs low PS burden; and high vs low PS burden): hs-CRP (1.09 [1.04-1.14]; 1.12 [1.06-1.17]), IL-6 (1.05 [1.02-1.07]; 1.08 [1.05-1.11]), LpPLA2 (1.01 [1.00 - 1.02]; 1.02 [1.01-1.04]) and cardiac biomarkers hs-TnT (1.03 [1.01-1.06]; 1.06 [1.03-1.09]) and NT-proBNP (1.09 [1.04-1.13]; 1.21 [1.15-1.27]).

Conclusions: In patients with chronic coronary syndrome, greater psychosocial burden was associated with increased levels of inflammatory and cardiac biomarkers. While this observational study does not establish causal nature of these associations, the findings suggest inflammation and cardiac injury/stress as plausible pathways linking psychosocial burden to an elevated CV risk, that needs to be further explored.

Aims: Sex differences in the long-term prognosis of heart failure (HF) remain controversial, and there is a lack of comprehensive pooling of the sex differences in outcomes of HF. This study aims to characterize the sex differences in the long-term prognosis of HF and explore whether these differences vary by age, HF course, left ventricular ejection fraction, region, period of study, study design, and follow-up duration.

Methods and results: A systematic review was conducted using Medline, Embase, Web of Science, and the Cochrane Library, from January 1, 1990, to March 31, 2024. The primary outcome was all-cause mortality (ACM), and the secondary outcomes included cardiovascular mortality (CVM), hospitalization for HF (HHF), all-cause hospitalization, a composite of ACM and HHF, and a composite of CVM and HHF. Pooled hazard risks (HRs) with corresponding 95% confidence intervals (CIs) were calculated using random effects meta-analysis. 94 studies (comprising 96 cohorts) were included in the meta-analysis, representing 706,247 participants (56.5% were men, the mean age was 71.0 years). Female HF patients had a lower risk of ACM (HR: 0.83, 95% CI: 0.80, 0.85; I2=84.9%), CVM (HR: 0.84, 95% CI: 0.79, 0.89; I2=70.7%), HHF (HR: 0.94, 95% CI: 0.89, 0.98; I2=84.0%), and composite endpoints (ACM+HHF: HR: 0.89, 95% CI: 0.83, 0.95; I2=80.0%; CVM+HHF: HR: 0.85, 95% CI: 0.77, 0.93; I2=87.9%) compared to males. Subgroup analysis revealed that the lower risk of mortality observed in women was more pronounced among individuals with long-course HF (i.e., chronic HF, follow-up duration >2 years) or recruited in the randomized controlled trials. (P for interaction <0.05).

Conclusions: Female HF patients had a better prognosis compared to males, with lower risks of ACM, CVM, HHF, and composite endpoints. Despite the underrepresentation of female populations in HF clinical trials, their mortality benefits tended to be lower than in real-world settings.

Registration: PROSPERO: CRD42024526100.

Aims: Women are less likely to receive lipid-lowering therapy (LLT) after acute myocardial infarction (AMI). We analysed whether this under-prescription currently persists and has an impact on long-term outcomes.

Methods and results: The FAST-MI programme consists of nationwide registries including all patients admitted for AMI ≤ 48 h from onset over a 1 month period in 2005, 2010, and 2015, with long-term follow-up. This analysis focused on high-intensity LLT (atorvastatin ≥ 40 mg or equivalent, or any combination of statin and ezetimibe) in women and men. Women accounted for 28% (N = 3547) of the 12 659 patients. At discharge, high-intensity LLT was significantly less prescribed in women [54 vs. 68% in men, P < 0.001, adjusted odds ratio (OR) 0.78(95% confidence interval (CI) 0.71-0.87)], a trend that did not improve over time: 2005, 25 vs. 35% (P = 0.14); 2010, 66 vs. 79% (P < 0.001); 2015, 67 vs. 79.5% (P = 0.001). In contrast, female sex was not associated with a lack of other recommended treatments at discharge: beta-blockers [adjusted OR 0.98(95% CI 0.88-1.10), P = 0.78], or renin-angiotensin blockers [adjusted OR 0.94(95% CI 0.85-1.03), P = 0.18]. High-intensity LLT at discharge was significantly associated with improved 5 year survival and infarct- and stroke-free survival in women [adjusted hazard ratios (HR) 0.74(95% CI 0.64-0.86), P < 0.001 and adjusted HR: 0.81(95% CI: 0.74-0.89); P < 0.001, respectively]. Similar results were found using a propensity score-matched analysis [HR for 5 year survival in women with high-intensity LLT: 0.82(95% CI 0.70-0.98), P = 0.03].

Conclusion: Women suffer from a bias regarding the prescription of high-intensity LLT after AMI, which did not attenuate between 2005 and 2015, with potential consequences on both survival and risk of cardiovascular events.

Introduction: Inclisiran, an siRNA targeting hepatic PCSK9 mRNA, administered twice-yearly (after initial and 3-month doses), substantially and sustainably reduced LDL-cholesterol (LDL-C) in Phase III trials. Whether lowering LDL-C with inclisiran translates into a reduced risk of major adverse cardiovascular events (MACE) is not yet established. In-silico trials applying a disease computational model to virtual patients receiving new treatments allow to emulate large scale long term clinical trials. The SIRIUS in-silico trial programme aims to predict the efficacy of inclisiran on CV events in individuals with established atherosclerotic cardiovascular disease (ASCVD).

Methods: A knowledge-based mechanistic model of ASCVD was built, calibrated, and validated to conduct the SIRIUS programme (NCT05974345) aiming to predict the effect of inclisiran on CV outcomes.The SIRIUS Virtual Population included patients with established ASCVD (previous myocardial infarction (MI), previous ischemic stroke (IS), previous symptomatic lower limb peripheral arterial disease (PAD) defined as either intermittent claudication with ankle-brachial index <0.85, prior peripheral arterial revascularization procedure, or vascular amputation) and fasting LDL-C ≥ 70 mg/dL, despite stable (≥ 4 weeks) well-tolerated lipid lowering therapies.SIRIUS is an in-silico multi-arm trial programme. It follows an idealized crossover design where each virtual patient is its own control, comparing inclisiran to 1) placebo as adjunct to high-intensity statin therapy with or without ezetimibe, 2) ezetimibe as adjunct to high-intensity statin therapy, 3) evolocumab as adjunct to high-intensity statin therapy and ezetimibe.The co-primary efficacy outcomes are based on time to the first occurrence of any component of 3P-MACE (composite of CV death, nonfatal MI or nonfatal IS) and time to occurrence of CV death over 5 years.

Perspectives/conclusion: The SIRIUS in-silico trial programme will provide early insights regarding a potential effect of inclisiran on MACE in ASCVD patients, several years before the availability of the results from ongoing CV outcomes trials (ORION-4 and VICTORION-2-P).

Background: Numerous studies have shown inverse associations between serum magnesium (Mg) and risk of cardiovascular disease (CVD), but studies of dietary Mg have not been consistent.

Aim: To examine the association of a Mg-rich diet score with risks of CVD, coronary heart disease (CHD), and ischemic stroke in the Atherosclerosis Risk in Communities (ARIC) study.

Methods: There were 15,022 Black and White adults without prevalent CVD at baseline (1987-89) included in this analysis. Diet was assessed at two visits 6 years apart using an interviewer-administered 66-item food frequency questionnaire. A Mg-rich diet score was created that included servings of whole grain products, nuts, vegetables, fruit, legumes, coffee, and tea. Cox proportional hazard regression evaluated associations of incident CVD, CHD and stroke across quintiles of Mg-rich diet score, adjusting for demographics, lifestyle factors, and clinical characteristics.

Results: Over >30 years of follow-up, there were 3,531 incident CVD events (2,562 CHD, 1,332 ischemic stroke). Participants who consumed more Mg-rich foods were older, female, White, had lower blood pressure, fewer were not current smokers, and more reported being physically active. A Mg-rich diet was inversely associated with incident CVD (HRQ5 vs Q1=0.87, 95%CI: 0.77-0.98, ptrend=0.02) CHD (HRQ5 vs Q1=0.82, 95%CI: 0.71-0.95, ptrend=0.01); however, the diet-stroke association was null (HRQ5 vs Q1=1.00, 95%CI: 0.82-1.22, ptrend=0.97).

Conclusions: Consuming a diet including Mg-rich foods, such as whole grains, nuts, vegetables, fruits, legumes, coffee and tea, is associated with lower risk of CVD and CHD, but not ischemic stroke.

Aims: To investigate the association of accelerometer-measured intensity-specific physical activity (PA) with all-cause and cause-specific mortality among individuals with cardiovascular disease (CVD).

Methods: In this prospective cohort study, 8,024 individuals with pre-existing CVD (mean age: 66.6 years, female: 34.1%) from the UK Biobank had their PA measured using wrist-worn accelerometers over a 7-day period in 2013-2015. All-cause, cancer, and CVD mortality was ascertained from death registries. Cox regression modelling and restricted cubic splines were used to assess the associations. Population-attributable fractions (PAFs) were used to estimate the proportion of preventable deaths if more PA were undertaken.

Results: During an average of 6.8 years of follow-up, 691 deaths (273 from cancer and 219 from CVD) were recorded. An inverse non-linear association was found between PA duration and all-cause mortality risk, irrespective of PA intensity. The hazard ratio (HR) of all-cause mortality plateaued at 1800 minutes/week for light-intensity PA (LPA), 320 minutes/week for moderate-intensity PA (MPA) and 15 minutes/week for vigorous-intensity PA (VPA). The highest quartile of PA associated lower risks for all-cause mortality, with HRs of 0.63 (95% confidence interval [CI]: 0.51-0.79), 0.42 (0.33-0.54) and 0.47 (0.37-0.60) for LPA, MPA, and VPA, respectively. Similar associations were observed for cancer and CVD mortality. Additionally, the highest PAF were noted for VPA, followed by MPA.

Conclusion: We found an inverse non-linear association between all intensities of PA (LPA, MPA, VPA, and MVPA) and mortality risk in CVD patients using accelerometer-derived data, but with larger magnitude of the associations than that in previous studies based on self-reported PA.