Nutrition Metabolism and Cardiovascular Diseases最新文献

Background and aims: It is well known that being overweight or obese is a risk factor for coronary artery disease (CAD). At the same time, belonging to these categories indirectly influences other risk factors like hypertension, diabetes or dyslipidemia also through a chronic inflammation condition. The aim of this study was to establish to which extent the effect of body mass index (BMI) on CAD risk can be explained by the chronic inflammation degree, using a statistical mediation model.

Methods and results: The present study used data from EPICOR, the cardiovascular branch of the EPIC Italy (European Investigation into Cancer and Nutrition) study. We employed a case-cohort design including 1416 participants with 622 incident CAD cases (major coronary events, myocardial infarction). Acute phase reactant C-reactive protein (CRP) and Plasminogen Activator Inhibitor-1 (PAI-1), were measured at baseline. A mediation analysis was performed to establish to which extent the effect of BMI on CAD risk can be explained by the inflammation degree expressed by the levels of both CRP and PAI-1. Using a fully adjusted survival model individuals in the second and third BMI categories had increased hazard ratios for CAD compared to the first BMI category. Mediation analysis revealed significant direct and indirect effects of BMI on CAD risk through inflammation, and results were consistent across gender and with waist-to-hip ratio analyses.

Conclusion: Chronic inflammation might explain part of the increased risk of CAD due to more or less severe excess weight, in a robust statistical mediation model.

Background and aims: Lipoprotein(a) [Lp(a)] emerging as a significant risk factor for coronary artery disease (CAD). However, the role and the impact of Lp(a) in the early formation and progression of complex CAD remains unclear. This study aimed to investigate the impact of Lp(a) levels on the age of first acute coronary events and CAD severity in acute coronary syndrome (ACS) patients.

Methods and results: The RELACS study, a single-center prospective observational study that included 774 consecutive ACS patients. Lp(a) levels were measured and stratified into tertiles. Primary endpoint was the correlation between Lp(a) levels and the age of first acute coronary event. Secondary endpoint was correlation between Lp(a) levels and CAD complexity (SYNTAX I and Gensini scores). The mean (SD) age was 63.2 (12.6) years and 603 (78 %) were males. The clinical presentations included 40.1 % of patients with STEMI, 46.9 % with NSTEMI, and 13 % with unstable angina. Median baseline Lp(a) level was 21.85 mg/dL. Higher Lp(a) levels were linked to a younger age of the first coronary event (B coefficient -0.83, p = 0.002). Positive correlations were found between Lp(a) levels and Gensini (r = 0.16, p = 0.011) and SYNTAX scores (r = 0.14, p = 0.004). Each tertile increase in Lp(a) corresponded to an 8.01-point increase in Gensini score (p = 0.019) and a 2.92-point increase in SYNTAX score (p < 0.001).

Conclusions: Elevated Lp(a) levels are associated with earlier onset and greater complexity of CAD in ACS patients. These findings suggest Lp(a) is a critical risk factor for early atherogenesis and may require aggressive lipid-lowering strategies in primary prevention settings.

Background and aims: Obesity represents a crucial modifiable risk factor for cardiovascular complications. Two dietary approaches, Very Low-Calorie Ketogenic (VLCKD) and Intermittent Fasting (IFD) diets, have demonstrated to reduce blood pressure (BP) and produce cardiovascular and metabolic advantages. We aimed to evaluate the effects of VLCKD or IFD compared to Free Diet (FD) on office brachial and central systolic BP levels. Secondary outcomes included changes from baseline of diastolic BP and several weight-related indexes.

Methods and results: In this single-center, open-label, prospective clinical study, post-menopausal women with treated uncomplicated hypertension and obesity were assigned to 3 dietary programs: VLCKD, IF, and FD. All patients underwent BP measurements, dietary consultation with personalized dietary program, and blood tests for metabolic parameters. All outcome variables were measured at baseline (T0), two (T1) and six months (T2). We included 18 patients in the VLCKD, 16 in the IFD and 9 in the FD groups, respectively. At T2 VLCKD patients showed significantly lower brachial systolic (p = 0.005) and diastolic (p = 0.038), central systolic (p = 0.02) and diastolic (p = 0.03) BP levels than those in other groups. VLCKD also induced reductions in weight (p = 0.03), WC (p < 0.01), WHR (p < 0.01), BFP (p < 0.01); TOT-C (p = 0.01), LDL-C (p < 0.01), and triglycerides (p = 0.02). No relevant changes were observed in IF and FD groups.

Conclusions: KD emerged as the clear front-runner in reducing brachial and central office systolic/diastolic BP levels and weight-related parameters in post-menopausal women with treated hypertension and obesity.

Backgrounds and aim: To prospectively evaluate the associations between changes in (poly)phenol intake, body weight(BW), and physical activity(PA) with changes in an inflammatory score after 1-year.

Methods and results: This is a prospective observational analysis involving 484 participants from the PREDIMED-Plus with available inflammatory measurements. (Poly)phenol intake was estimated using a validated semi-quantitative food frequency questionnaire and the Phenol-Explorer database. An inflammatory score was calculated based on 8 blood biomarkers (IL-6, IL-8, IL-18, MCP-1, C-peptide, hs-CRP, leptin, and RANTES). The association between BW, PA, (poly)phenol intake and inflammatory score was evaluated using structural equations. Mediation analyses were performed to assess the relationship between change in (poly)phenol intake and inflammatory score was mediated by the change in BW. A higher increase in total (poly)phenol intake was related to a decrease in the inflammatory score (β = -0.005mg/1000 Kcal; CI95 % = -0.100,0.000) along with a decrease in BW (β = -0.006mg/1000 Kcal; CI95 % = -0.010,-0.003). Increased PA was associated with a lower inflammatory score (β = -0.129MET-min/d; CI95 % = -0.238,-0.021) and BW (β = -0.248MET-min/d; CI95 % = -0.343,-0.152). Finally, a decrease in BW was associated with a decrease in the inflammatory score (β = 0.240 kg; CI95 % = 0.155,0.325). Mediation analyses revealed that changes in BW explained 22 % of the overall association between changes in (poly)phenol intake and inflammatory score.

Conclusions: An inverse association between changes in (poly)phenol intake and inflammatory status was observed, with BW playing a significant mediating role, emphasising the impact of BW reduction on inflammation reduction.

Front-of-pack nutrition labels (FOPNLs) have been developed since 1989 to curb the increasing prevalence of obesity and non-communicable diseases (NCDs) and to promote healthy consumption choices. While several countries have introduced their own labeling schemes on a voluntary basis, the European Commission aims to harmonize a FOPNL system that will be mandatory for all member states. This paper summarizes a contribution to the current debate on FOPNLs from Italian and Spanish researchers working in the fields of human nutrition, nutritional epidemiology and public health education and communication policy before the final decision on FOPNLs to become mandatory in Europe is taken.

Background and aims: Patients with adrenal insufficiency (AI) face elevated risks during various hospitalizations including cardiovascular related admissions. Despite this, limited data exist specifically regarding congestive heart failure (CHF) in the context of AI. This investigation leveraged a comprehensive national database to examine the association between AI and cardiovascular outcomes among patients admitted with CHF.

Methods and results: Admissions for CHF were identified in the 2016-2019 National Inpatient Sample. In-hospital outcomes were compared between patients with and without AI. The primary outcome was in-hospital mortality. Secondary outcomes included cardiogenic shock, ventricular tachycardia (VT), acute kidney injury (AKI), vasopressor use, mechanical circulatory support (MCS) use, mechanical ventilation use, hospital length of stay (LOS), and total charges. Multivariable regression models were used to adjust for potential confounders. Among 1,270,784 CHF hospitalizations, 3812 (0.3 %) had a diagnosis of AI. AI was associated with higher odds of in-hospital mortality (aOR 2.6, 95 % CI 2.1-3.7), VT (aOR 1.40, 95 % CI 1.1-1.8), AKI (aOR 1.29, 95 % CI 1.10-1.52), the need for vasopressors (aOR 3.3, 95 % CI 1.9-5.63), mechanical ventilation use (aOR 3.8, 95 % CI 2.9-4.99), cardiogenic shock (aOR 3.08, 95 % CI 2.38-3.98), and MCS (aOR 2.12, 95 % CI 1.14-3.95). Patients with AI also had a longer LOS (8.62 days vs. 5.25 days, p < 0.001) and higher total charges ($103,248 vs. $50,280, p < 0.001).

Conclusion: Patients with AI admitted for CHF had higher in-hospital mortality, non-fatal adverse outcomes, and incurred higher hospital charges compared to patients without AI.

Background and aims: Elevated total IgE levels are traditionally associated with allergic conditions; however, their potential role as biomarker for mortality risk beyond allergic diseases has not been extensively explored. Recent studies have suggested that IgE is associated with cardiovascular (CV) disease. We aimed to investigate the association between total IgE levels and the risk of all-cause and cause-specific mortality, as well as to explore the potential mediating role of vitamin status in these associations.

Methods and results: The association between IgE and mortality risk was examined in the National Health and Examination Survey 2005-2006. Weighted multivariable Cox proportional hazards model was employed. We further performed restricted cubic spline analysis to assess dose-response relationships and conducted mediation analysis to explore the influence of vitamins on IgE-related mortality risk. Individuals in the highest total IgE quantile (>107.0 kU/L) exhibited a 32 % increased risk of all-cause mortality (95 % CI: 1.07-1.64) and a 98 % elevated risk of CV mortality (95 % CI: 1.28-3.07) compared to the lowest quantile (<14.5 kU/L). Heterogeneity exists in the dose-response relationship and threshold effects among individuals with and without allergic diseases. Vitamin deficiency is associated with elevated total IgE levels, and vitamins mediated the relationship of the IgE-related all-cause mortality with the proportion of mediation ranging from 4.68 to 12.71 %.

Conclusions: Our findings introduce a novel dimension to the understanding of IgE as a biomarker for mortality beyond its traditional role in allergic diseases, challenging the current paradigm that elevated IgE levels without overt allergic symptoms are benign.

Beckground and aims: Individuals with a higher body fat percentage may have higher serum levels of caffeine and its metabolites and process caffeine more slowly than individuals with a lower body fat percentage, so the aim of this study is to compare the occurrence of positive and negative effects of caffeine in nonobese and obese women.

Methods and results: One hundred and sixty women were included in the study. Body fat was determined using the mBCA 515 SECA analyzer. Participants were divided into 4 groups: nonobese caffeine, nonobese placebo, obese caffeine and obese placebo. Caffeine groups received 6 mg/kg body weight caffeine. Placebo groups received identical starch-filled capsules. One hour after ingestion and within 24 h, participants completed a caffeine-induced effect questionnaire. Caffeine intake showed statistically significant differences compared to placebo for neutral (p ≤ 0.014; Cramér's V = 0.27; 27 % increase), negative (p ≤ 0.002; Cramér's V = 0.34; 34 % increase), and positive effects (p ≤ 0.015; Cramér's V = 0.27; 27 % increase). Further analysis revealed significant associations with increased urine output (p ≤ 0.014; Cramér's V = 0.27; 27 % increase), vigor/activeness (p ≤ 0.009; Cramér's V = 0.29; 29 % increase), and headache (p ≤ 0.033; Cramér's V = 0.24; 24 % increase) 1 h post-ingestion. No significant effects were observed in the placebo group. There was no statistically significant placebo effect.

Conclusions: Obese and nonobese women show different responses to caffeine 60 min after ingesting 6 mg/kg body weight. Obese women are more likely to report adverse effects, including increased urine output, heightened vigor/activeness, and headaches, compared to nonobese women.

Trial registration: ANZCTR12622000823774; June 10, 2022.

Aims: The association of telomere length (TL) and coronary heart disease (CHD) is still debated, and there is a lack of dose-response meta-analyses on this issue. The aim is therefore to integrate existing evidence on the association between TL and CHD risk and explore the dose-response relationship between them.

Data synthesis: PubMed, EMBASE, and Web of Science were searched for relevant studies up to September 2024. Meta-analysis was performed using a random-effects model, with data presented as RRs and 95 % CIs. Restricted cubic splines were used to assess linear and nonlinear associations. Subgroup analysis and meta-regression were performed to explore sources of heterogeneity. Fourteen articles (8 prospective cohort studies, 2 case-cohort studies, 2 case-control studies, and 2 cross-sectional studies) were finally included in the meta-analysis, with a total sample size of 199,562 participants and 25,752 cases. For CHD, the total RR for the highest TL group compared to the lowest TL group was 0.69 (95 % CI: 0.61, 0.78, I² = 64.5 %). For every 1 kilobase pair (kbp) increase in TL, the CHD risk decreased by 23 % (RR = 0.77, 95 % CI: 0.69, 0.87, I² = 89.0 %). The nonlinearity test indicated a linear association between TL and CHD risk (P_{non-linearity} = 0.930). Sensitivity analyses indicated that the results were robust.

Conclusions: The meta-analysis showed a linear relationship between TL and CHD. People with low TL may be more likely to develop CHD than those with high TL. The association between the two did not change in a wide range of populations.

Background and aims: Numerous studies have evaluated the association between baseline uric acid (UA) and heart failure (HF) outcomes. The impact of longitudinal UA on HF survival remains unknown. We aim to investigate the association between different parameterizations of longitudinal UA measurements and survival outcomes in HF patients.

Methods and results: We retrospectively included patients hospitalized for HF with multiple repeated UA measurements. Joint models were fitted to assess the longitudinal association between UA and outcomes of all-cause and cardiovascular (CV) death. The study included 1596 patients (mean age 54 years, 26.9 % women) with 7875 UA measurements. During a median follow-up of 34.7 months, 330 all-cause deaths occurred, among them 280 of CV causes. After adjusting for clinically relevant covariates, every doubling of UA at any time led to a 5.14-fold increase of all-cause death risk (95 % confidence interval [CI] 3.79-8.29) and a 4.56-fold increase of CV death risk (95 % CI 2.96-8.29) for men; for women, the corresponding hazard ratios were 4.47 for all-cause death (95 % CI 3.02-7.40) and 4.93 for CV death (95 % CI 2.78-8.58). The increase in slope and area under the UA trajectory were additionally associated with a higher risk of all-cause and CV death in both genders. All the associations remained consistent after adjusting for repeatedly measured renal function and across the ejection fraction phenotypes.

Conclusion: The longitudinally measured UA and its derived parameterizations are strong prognostic factors in hospitalized HF patients, independent of clinically relevant confounders and repeatedly assessed renal function.