European journal of preventive cardiology最新文献

Aims: Apolipoprotein (Apo) C3 has been associated with incident coronary heart disease and major adverse cardiovascular events (MACE). Whether ApoC3 levels predict risk in patients with acute coronary syndrome (ACS) on optimized statin treatment is unknown.

Methods: ApoC3 was measured by mass spectrometry at baseline (n=11,956) and after 4 months' treatment (M4; n=11 176) with alirocumab or placebo in the ODYSSEY OUTCOMES trial. Patients with fasting triglycerides >400 mg/dL were excluded. The association of baseline ApoC3 with risk of MACE or death was assessed in post hoc adjusted Cox regression models and spline analyses adjusted for treatment and ApoB. In adjusted models in the alirocumab group we determined association of ApoC3 change from baseline to M4 with subsequent risk of MACE and death.

Results: Median (Q1, Q3) baseline ApoC3 concentration was 85 (65, 113) mg/L. With adjustment for ApoB, baseline ApoC3 showed no clinically meaningful relationship to risk of MACE or death in spline analyses and no association with MACE (P=0.89) or death (P=0.70) in Cox regression analyses. Alirocumab reduced ApoC3 modestly by median -10 (-27, -5) mg/L (P<0.0001) and reduced MACE (10.1% vs 12.1%; P=0.0006) and death (3.5% vs 4.2%; P=0.045) versus placebo. However, the change in ApoC3 on alirocumab did not predict subsequent MACE or death.

Conclusion: In patients with recent ACS on optimized statins without severe hypertriglyceridemia, neither baseline ApoC3 (accounting for ApoB) nor ApoC3 change with alirocumab predicted MACE or death. It is uncertain whether targeted therapies producing larger reductions in ApoC3 from higher baseline levels will affect cardiovascular risk.

Aims: With current, stricter lipid and blood pressure targets in patients with ischemic heart disease (IHD), secondary prevention may be insufficient and vary between patient groups and primary health care centres (PHCCs). We assessed the heterogeneity of risk-factor control and secondary prevention using contemporary Swedish primary-care data.

Methods: Cross-sectional study of IHD patients in September 2023 from QregPV, a Swedish regional primary-care register. We evaluated the proportions attaining risk-factor control (blood pressure <140/90 mmHg, LDL-cholesterol [LDL-C] <1.4 mmol/L, and non-smoking) and the use of lipid-lowering therapy (LLT) and antithrombotic therapy (ATT) by age and sex using logistic regression models. Heterogeneity among PHCCs was estimated using multilevel models and summarised as adjusted median odds ratios (aMOR).

Results: 45 771 patients (34.5% women) were included. Combined risk-factor control was low, 15.5% (95% CI 15.0-16.0), mainly due to low LDL-C attainment, 20.7% (20.3-21.1). Combined risk-factor control decreased with higher age (p<0.001) and was lower in women than in men, age-adjusted odds ratio (aOR) 0.60 (0.55-0.66). LLT and ATT were used by 77.2% (76.8-77.6) and 85.6% (85.2-85.9), with lower usage in women, aOR 0.52 (0.50-0.54) and aOR 0.58 (0.54-0.62). Substantial heterogeneity among PHCCs was observed, with combined risk-factor control aMOR 1.39 (1.32-1.48).

Conclusion: Combined risk-factor control was low, largely due to low LDL-C control, despite high LLT usage. Risk-factor control and the use of LLT and ATT varied between PHCCs and were lower in women than men. Concrete clinical strategies for attaining risk-factor goals in both sexes and for reducing PHCC variation are warranted.

Aims: Atrial fibrillation (AF) is the most common cardiac arrhythmia. Although lipoprotein(a) [Lp(a)] is known to be a well-established risk factor for atherosclerotic cardiovascular disease (ASCVD), its role in development of AF, independent of this association, remains unclear.

Methods: Adult patients from the three Mayo Clinic sites with a baseline Lp(a) and without AF history were included. Patients were categorized into two groups based on their Lp(a) levels: high Lp(a) (≥50 mg/dL) and low Lp(a) (<50 mg/dL). Survival probabilities free from incident AF were compared between Lp(a) groups, during a follow-up period up to 15 years, using the Kaplan-Meier curve and the Log-Rank test. Multivariable Cox regression analysis was also conducted.

Results: A total of 75,376 patients were included (median age: 55 years, 59% males), with a median follow-up duration of 8.8 [inter quartile range (IQR): 3.4, 14.8] years. Incident AF was detected in 5738 (7.6%) patients. Survival probability free from incident AF was significantly lower in patients with elevated Lp(a) (86%) compared with those with low Lp(a) (88%, log rank P<0.001). Multivariable analysis adjusted for potential risk factors of AF showed a statistically significant association of elevated Lp(a) with a 11% increase in AF risk (adjusted HR: 1.11, 95% CI: 1.05 to 1.18).

Conclusions: Our study suggests that elevated Lp(a) (≥50 mg/dL) is an independent risk factor for incident AF. Future prospective studies are warranted to validate our results and to test the if reducing Lp(a) could mitigate the burden of AF.

Aims: Cardiorespiratory fitness (CRF), measured by peak oxygen uptake (VO2peak), is a strong predictor of mortality. Despite its widespread clinical use, current reference equations for VO2peak show distorted calibration in obese individuals. Using data from the Fitness Registry and the Importance of Exercise National Database (FRIEND), we sought to develop novel reference equations for VO2peak better calibrated for overweight/obese individuals - in both males and females, by considering body composition metrics.

Methods: Graded treadmill tests from 6,836 apparently healthy individuals were considered in data analysis. We used the National Health and Nutrition Examination Survey equations to estimate lean body mass (eLBM) and body fat percentage (eBF). Multivariable regression was used to determine sex-specific equations for predicting VO2peak considering age terms, eLBM and eBF.

Results: The resultant equations were expressed as VO2peak (male) = 2633.4 + 48.7✕eLBM (kg) - 63.6✕eBF (%) - 0.23✕Age2 (R2=0.44) and VO2peak (female) = 1174.9 + 49.4✕eLBM (kg) - 21.7✕eBF (%) - 0.158✕Age2 (R2=0.53). These equations were well-calibrated in subgroups based on sex, age and body mass index (BMI), in contrast to the Wasserman equation. In addition, residuals for the percent-predicted VO2peak (ppVO2) were stable over the predicted VO2peak range, with low CRF defined as < 70% ppVO2 and average CRF defined between 85-115%.

Conclusions: The derived VO2peak reference equations provided physiologically explainable and were well-calibrated across the spectrum of age, sex and BMI. These equations will yield more accurate VO2peak evaluation, particularly in obese individuals.

Aims: This study aimed to investigate how nutritional exposures in early life, represented by birth weight (BW), and in later life, indicated by adult body mass index (BMI), interact to influence cardiometabolic disease (CMD) risk and to examine the underlying causal relationships.

Methods: Included were 254,224 participants of White European ancestry from the UK Biobank. To evaluate the joint associations of BW and adult BMI with CMD risk, BW was categorized as low (LBW, <2.5 kg) or high (HBW, ≥2.5 kg), and BMI as low (LBMI, <30 kg/m²) or high (HBMI, ≥30 kg/m²). Multivariable Cox proportional hazards models and 2x2 factorial Mendelian randomization (MR) analyses were employed to assess these associations and the underlying causality.

Results: Compared to the participants with HBW-LBMI, the hazard ratio (HR) for atherosclerotic cardiovascular disease (ASCVD) was 1.19 (95% CI: 1.12 to 1.26) in the LBW-LBMI group, 1.33 (1.28 to 1.38) in the HBW-HBMI group, and 1.62 (1.50 to 1.75) in the LBW-HBMI group. The LBW-HBMI group also exhibited higher risks for hypertension (HR: 2.42 [2.26-2.59]), diabetes (HR: 5.16 [4.73-5.63]), and hyperlipidemia (HR: 1.95 [1.81-2.10]). Additive interactions between LBW and HBMI were identified for metabolic diseases but not for ASCVD. The causality of these associations was confirmed by MR analysis.

Conclusions: Combined exposure to LBW and HBMI was most strongly associated with an elevated risk of CMD, underscoring the critical role of the mismatch between early-life and adult nutritional status in shaping long-term cardiometabolic health.

Aims: Both plasma levels of remnant cholesterol and low-density lipoprotein cholesterol (LDL-C) levels are independent risk factors for atherosclerotic cardiovascular disease. However, only remnant cholesterol has consistently been associated with systemic inflammation. In this study, we aimed to assess the extent to which inflammation mediates the effect of remnant and LDL cholesterol on (non)fatal major adverse cardiovascular events (MACE), comprising of coronary artery disease and ischemic stroke.

Methods and results: This prospective study included 16,445 participants without prior atherosclerotic cardiovascular disease from the EPIC-Norfolk study, with a mean age of 58.8±9.1 years, of which 9,357 (56.9%) were women. Every 1 mmol/L higher remnant cholesterol was associated with 29.5% higher high-sensitivity C-reactive protein (hsCRP) levels (95% Confidence Interval (CI): 22.1, 37.4, p<0.001), whereas LDL-C was not significantly associated with hsCRP levels in the fully adjusted model. Additionally, each 1 mmol/L higher remnant cholesterol was associated with a hazard ratio (HR) of 1.31 (95% CI: 1.14, 1.50, p<0.001) for MACE, compared to a HR of 1.21 (95% CI: 1.13, 1.31, p<0.001) for LDL-C. Mediation analysis showed that hsCRP mediated 5.9% (95% CI: 1.2, 10.6%, p<0.001) of the effect of remnant cholesterol on MACE, whereas hsCRP did not mediate the effect of LDL-C.

Conclusions: Plasma remnant cholesterol levels are independently associated with systemic inflammation and cardiovascular events. Inflammation, as measured with hsCRP, contributed minorly to the association between remnant cholesterol and MACE. This underscores the need to address both remnant cholesterol and systemic inflammation separately in the clinical management of cardiovascular disease.