Nutrition Metabolism and Cardiovascular Diseases最新文献

Background and aims: Metabolic dysregulation is closely associated with coronary artery diseases (CAD). Exploring the relationship between metabolites and CAD is helpful in identifying changes in energy metabolism during disease progression.

Methods and results: We use Mendelian Randomization (MR) analysis to assess the relationships between 275 serum metabolites and CAD such as angina pectoris, post-myocardial infarction complications, coronary atherosclerosis, myocardial infarction (MI), and unstable angina pectoris (UA). The inverse variance-weighted method (IVW) served as the primary approach for causal analysis, with MR-Egger and weighted median (WM) as supplementary methods. Sensitivity analyses were conducted to assess heterogeneity and multiple effects. We also analyzed potentially related metabolic pathways.We identified causal relationships between 42 known metabolites and CAD. Among them, the genetic susceptibility to elevated levels of amino acid Isobutyrylcarnitine is associated with an increased risk of coronary artery atherosclerosis; but it provides protection against the development of MI. Genetic susceptibility to elevated levels of fatty acids Stearate, Caprylate is associated with higher risk of angina pectoris, while Threonate has a protective effect in the development of angina; Stearate is associated with an increased risk of UA, whereas higher levels of the lipids Choline, 1-arachidonoylglycerophosphoinositol∗, Hexadecanedioate, Tetradecanedioate play a protective role in UA.Metabolic pathway analysis identified 6 pathways that may be associated with CAD.

Conclusion: We identified causal relationships between 42 serum metabolites and CAD. Specifically, changes in metabolites such as Isobutyrylcarnitine, Caprylate, and Stearate were associated with risks of CAD. These findings provide new insights into the metabolic mechanisms of CAD.

Aims: We conducted this systematic review to comprehensively assess the impact of CRT on health-related outcomes among patients with HF.

Data synthesis: In order to find studies investigating the effect of CRT on health-related outcomes among patients with HF, we performed a systematic search of PubMed, Cochrane Library, Embase, and Cumulative Index to Nursing and Allied Health Literature databases (inception until February 12th, 2023). A total of 10 studies including 933 individuals met the inclusion criteria. The systematic review indicated that 8 to 24 weeks of CRT intervention offered some health advantages for patients with HF. CRT significantly reduced patients' body weight (SMD = - 0.52, 95 % CI = - 0.99 to -0.04, P = 0.03, I² = 77 %) and improved their quality of life (SMD = 0.35, 95 % CI = 0.12 to 0.58, P = 0.003, I² = 0 %). However, CRT significantly increased the risk of mortality and HF-related rehospitalization, including combined events of all-cause mortality and HF-related rehospitalization within a year (CRT group: 20 % vs. control group: 5 %), mortality rate within 1.52 years (CRT group: 34 % vs. control group: 22 %), readmission rate (CRT group: 52 % vs. control group: 17 %), and length of stay after readmission (CRT group: 124 days vs. control group:18 days).

Conclusion: CRT provides no significant benefits in terms of health-related outcomes among patients with HF, hence most patients with HF might not be eligible for CRT treatments. Meanwhile, there are several methodological issues among the studies included in the review, resulting in a low-to-moderate quality of evidence.

Registration: The PROSPERO registration number of this review is CRD 42023413992.

Background and aim: Our aim was risk estimation for cardiovascular disease (CVD) across obesity phenotypes over 18 years of follow-up using both time-invariant and time-varying approaches.

Methods and results: This prospective cohort study included 9752 participants aged ≥30 years examined in the first and second phases of the Tehran Lipid and Glucose Study (1999-2001 and 2002-2005). Six phenotypes [i.e., metabolically healthy normal weight (MHNW), overweight (MHOW), and obese (MHO), as well as metabolically unhealthy normal weight (MUNW), overweight (MUOW), and obese (MUO)] were defined based on the body mass index (BMI) and metabolic status. Incident CVD was documented until March 2018. Time-invariant and time-varying Cox regression models were used to estimate CVD hazard ratio (HRs) for obesity phenotypes. Mean age of the participants was 46.6 ± 12.0 years, and 53.9 % of them were women. During 18 years of follow-up, 1083 new CVD events occurred. In metabolically unhealthy individuals, but not metabolically healthy people, multivariable-adjusted HRs for CVD events increased by BMI according to time-varying (HR = 1.6, 95 % CI = 1.13-2.26 for MUNW; HR = 1.92, 95 % CI = 1.43-2.58 for MUOW; HR = 1.94, 95 % CI = 1.4-2.68 for MUO) and time-invariant (HR = 1.85, 95 % CI = 1.01-3.39 for MUNW; HR = 2.75, 95 % CI = 1.63-4.63 for MUOW, and HR = 3.26, 95 % CI = 1.95-5.47 for MUO) models.

Conclusion: Metabolically unhealthy overweight and obese individuals are at increased risk of CVD and should be regularly screened to prevent possible cardiovascular events.

Background and aim: Dilated cardiomyopathy is a major cause of heart failure, and hypertrophic cardiomyopathy is a common cause of sudden cardiac death in young adults. Epidemiological studies reporting the association between these cardiomyopathies and common cardiovascular risk factors, including smoking, alcohol, and obesity, are limited, and the published studies are mostly observational, making them vulnerable to bias.

Methods and results: We performed a two-sample Mendelian randomization analysis to assess whether cardiovascular risk factors were causally associated with dilated and hypertrophic cardiomyopathies. Independent genetic variants associated with body mass index, smoking, and alcohol were selected as instrumental variables, with two sets of instrumental variables utilized for alcohol. Dilated cardiomyopathy data on 355,318 samples and hypertrophic cardiomyopathy data on 489,727 samples were obtained from a European population-based genome-wide association study (GWAS) meta-analysis. The large GWAS data sample size improved the statistical power. Our results showed significant associations between a genetic predisposition for smoking and the risk of dilated cardiomyopathy (odds ratio (OR) = 1.33; 95 % confidence level (CI): 1.07-1.67; p = 0.012) and between a genetic predisposition for obesity and the risk of dilated cardiomyopathy (OR = 1.62; 95 % CI, 1.30-2.02; p = 1.51 × 10^-5). The results of the other associations were not significant.

Conclusions: This study suggests that smoking and obesity are causally associated with an increased risk of dilated cardiomyopathy.

Background and aims: Stair climbing, a straightforward and impactful form of physical activity, has shown potential in reducing risks of cardiovascular disease and mortality. However, its association with the development of atrial fibrillation (AF) remains largely unexplored.

Methods and results: 451,089 participants (mean age 56.5 years) without cardiovascular disease (year 2006-2010) were included from the UK Biobank study. Stair climbing data was collected through touchscreen questionnaire. AF cases were identified using ICD-10 code: I48 and were followed until February 1, 2022. Models adjusted for traditional cardiovascular risk factors. Over a median follow-up of 12.6 years, 23,660 (5.2 %) participants experienced new-onset AF. In multivariable-adjusted models, climbing 10-50, 60-100, 110-150, and ≥160 steps of stairs per day were associated with significant reductions in the risk of AF, compared to not climbing any stairs. The risk reduction appeared more pronounced in women than in men (P for interaction = 0.09). When compared to participants who climbed no stairs, the HRs for those who climbed 110-150 steps of stairs per day were 0.69 (95 % CI: 0.58-0.82) among those with low cardiorespiratory fitness, 0.71 (95 % CI: 0.57-0.88) among those with intermediate cardiorespiratory fitness, and 0.83 (95 % CI: 0.64-1.07) among those with high cardiorespiratory fitness.

Conclusions: Climbing stairs was associated with a reduction in AF risks. Significant interaction between cardiorespiratory fitness and stair climbing associated with incident AF was observed. Findings suggest that promoting regular stair climbing could be a potential target for preventing AF onset.

Background and aim: The World Health Organization (WHO) recommends that countries reduce industrially produced TFA (iTFA) in the food supply. However, New Zealand (NZ) has no mandatory regulation to control amounts of iTFA in foods. The objectives of this study were to assess within the NZ packaged food supply in recent years (2015-19 and 2022): i) the availability of products displaying information on TFA content on nutrition information panels (NIPs), ii) the content of TFA declared, and iii) the presence/potential presence of iTFA (n = 85,892 products).

Methods and results: A database of packaged foods from major NZ supermarkets was used. TFA contents declared on NIPs were benchmarked against limits recommended by the WHO and the Canadian Trans Fat Task Force. Proportions of products listing specific ingredients (containing iTFA) or non-specific ingredients (potentially containing iTFA) were examined. Trends in proportions were assessed (Mantel-Haenszel tests). Among all products and years examined (n = 81,591), 84.0 % did not display information on TFA content. Across all products declaring TFA contents and years 15.4 % and 6.4 %, respectively, were above the WHO and Canadian TFA limits. Across all products and years, 0.8 % and 13.6 % listed ingredients that contained or potentially contained iTFA, respectively. Across 2015-2019, there was a trend of decrease in the proportions of products listing specific (0.9 %-0.7 %; P = 0.018) and non-specific ingredients (15.1 %-12.8 %; P < 0.001).

Conclusion: Information on the TFA content and ingredients containing iTFA in NZ packaged foods is lacking and ambiguous and government-led interventions to control and reduce TFA in the food supply are warranted.

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: 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.

Background and aim: The Naples Prognostic Score (NPS) predicts outcomes in various diseases, but its impact on cardiovascular disease (CVD) is understudied. This study investigates the association between NPS and CVD prevalence and mortality among US adults.

Methods and results: This study utilized data from the Continuous National Health and Nutrition Examination Survey (NHANES) conducted between 1999 and 2016, with mortality follow-up data available through December 31, 2019. NPS was calculated using serum albumin, total cholesterol, neutrophil to lymphocyte ratio, and lymphocyte to monocyte ratio. Participants were stratified into low, moderate, and high NPS groups. Multiple logistic regression estimated odds ratios (OR) for CVD prevalence, while Cox proportional regression estimated hazard ratios (HR) for mortality. Of 39,572 participants, 20.24 % were in the low group, 69.79 % in the moderate group, and 9.96 % in the high group. After adjusting for confounders, the CVD prevalence ORs for moderate and high groups were 1.19 (95 % CI: 1.05, 1.34) and 1.78 (95 % CI: 1.53, 2.07), respectively (P for trend <0.001). Compared to the low group, the high group had adjusted HRs of 1.92 (95 % CI: 1.54, 2.41) for all-cause mortality, 1.61 (95 % CI: 1.12, 2.34) for cardiovascular mortality, and 1.83 (95 % CI: 1.11, 3.02) for cancer-related mortality (all P for trend <0.01). These associations remained significant across all subgroups.

Conclusion: NPS is an independent risk factor for CVD and is positively associated with all-cause and cardiovascular mortality in individuals with CVD.

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.