Nutrition Metabolism and Cardiovascular Diseases最新文献

Background and aim: Blood pressure variability (BPV) is an emerging risk factor for cardiovascular disease (CVD). However, the association between the magnitude of systolic blood pressure (SBP) fluctuations per unit time (utBPV) and CVD remains unclear. This study aimed to investigate the relationship between utBPV and incident CVD in a middle-aged and elderly population.

Methods and results: Using data from the China Health and Retirement Longitudinal Study (CHARLS), we enrolled 6134 participants aged ≥45 years without baseline CVD between 2011 and 2015. utBPV was defined as the sum of the absolute differences between consecutive SBP measurements divided by the time interval (mmHg/min). Multivariable logistic regression and restricted cubic spline analyses were employed to examine the association between utBPV and incident CVD, with subgroup analyses stratified by baseline hypertension status.During a median follow-up of 4 years, 657 incident CVD cases were observed. The results demonstrated that utBPV was a risk factor for CVD (OR: 1.018, 95 % CI: 1.005-1.031). In the non-hypertensive population, each 1-unit increase in utBPV was associated with a 2.8 % higher risk (P = 0.002). When analyzed by quartiles, the Q4 group had a 29.5 % increased risk compared to the Q1 group (95 % CI: 0.919-1.825), though the trend was not statistically significant (P = 0.166). No significant association was observed in hypertensive individuals.

Conclusions: utBPV is an independent risk factor for incident CVD in non-hypertensive adults aged 45 years and older. Given its convenience for clinical measurement, utBPV may serve as a practical tool for early CVD risk assessment.

Background and aims: Cardiovascular mortality is the leading cause of death among elderly hypertensive patients. However, the reference indicators for nutritional management in this population remain a subject of debate. The aim of this study is to explore and compare the predictive value of three commonly used nutritional assessment indicators for cardiovascular mortality in elderly hypertensive patients.

Methods and results: This study included 3611 elderly hypertensive patients aged 60 and above from seven cycles of NHANES (2005-2018). The population was categorized into two groups (malnourished vs. non-malnourished) using reference cutoff values for three nutritional assessment indicators: PNI, GNRI, and CONUT score. Multivariate Cox regression and competing risk analysis were employed to compare the predictive abilities of these three indicators for cardiovascular mortality risk. Subgroup analyses were also conducted to explore whether kidney dysfunction, cardiovascular disease, or gender interacted with the three nutritional indicators. Additionally, restricted cubic splines (RCS) curves were used to explore the dose-response relationship. Decision curve analysis was applied to assess the clinical value of these three indicators in predicting cardiovascular mortality risk. Time-dependent receiver operating characteristic (ROC) curves were used to calculate the area under the curve (AUC) for each indicator's prediction of cardiovascular mortality risk at different follow-up times. Furthermore, Net Reclassification Improvement (NRI) and Integrated Discrimination Improvement (IDI) were calculated based on multivariate Cox regression models to compare the predictive ability of these models over different follow-up durations. Malnourished patients diagnosed by PNI had a 2.70 times higher risk of cardiovascular death compared to non-malnourished patients (HR: 3.70, 95 % CI: 2.54-5.38), representing the highest cardiovascular mortality risk among the three groups. Patients diagnosed with malnutrition using GNRI and CONUT score had cardiovascular mortality risks increased by 1.39 times (HR: 2.39, 95 % CI: 1.58-3.63) and 0.84 times (HR: 1.84, 95 % CI: 1.33-2.55), respectively. In the multivariate competing risks model, the results were similar to those from the Cox regression analysis. The non-restricted cubic spline plot demonstrates an L-shaped association between GNRI and PNI with cardiovascular mortality, while the COUNT score shows an inverse L-shaped association. In addition, both the Time-ROC curve's AUC and NRI support that PNI's predictive advantage for cardiovascular mortality risk gradually increases with longer follow-up time.

Conclusion: PNI has superior predictive value for cardiovascular mortality risk compared to GNRI and COUNT score, especially for long-term prognosis.

Background and aims: The triglycerides, total cholesterol and body weight index (TCBI) is a novel nutritional marker that has shown prognostic value in various cardiovascular conditions, with low TCBI indicating poor nutritional status and being associated with adverse outcomes. However, limited data exist on the relationship between TCBI and cardiac function and outcomes in patients hospitalized with acute heart failure (AHF). This study aimed to investigate whether low TCBI is associated with impaired cardiac function and adverse outcomes in AHF.

Methods and results: We performed a post-hoc analysis of a prospective, dual-center observational cohort study of patients admitted with AHF (2022-2024). Transthoracic echocardiography, lung ultrasound and laboratory testing were performed shortly after admission. Outcomes evaluated were all-cause mortality and the composite of all-cause mortality or heart failure (HF) readmission. Unadjusted and adjusted Cox regression and Fine-Gray analyses were conducted to assess the relationship between TCBI and outcomes. The study included 487 patients, stratified into TCBI tertiles (T1: TCBI<949.6, T2: 949.6≤TCBI≤1690, T3: TCBI>1690). Low TCBI was associated with echocardiographic signs of higher filling pressures, impaired right ventricular function, higher pulmonary pressure and more B-lines on LUS. Low TCBI was associated with a higher risk of all-cause mortality compared with moderate TCBI (T1 vs T2: HR 1.54, 95 % CI [1.06-2.24], p = 0.024). Low TCBI was not independently associated with HF readmission and the composite of all-cause mortality or HF readmission.

Conclusion: Low TCBI is associated with greater signs of congestion and increased all-cause mortality risk.

In August 2025, the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS) released an update of the dyslipidaemia management guidelines, including a brief statement on lipid-lowering dietary supplements. The document states that dietary supplements or vitamins lacking documented safety and significant LDL-cholesterol-lowering efficacy are not recommended to reduce ASCVD risk. This sentence has been interpreted by some as a broad discouragement against the use of nutraceuticals; however, the corresponding class of recommendation is "C", indicating reliance on expert opinion and routine practice rather than robust randomized evidence. The negative interpretation is further influenced by the recent EFSA opinion on red yeast rice, which raised safety concerns but does not extend to other nutraceuticals. Concerns regarding efficacy have also been shaped disproportionately by the SPORT trial, a short, single-blinded, underpowered study that compared a low-dose statin with a heterogeneous group of supplements, including some with no proven lipid-lowering effects. Notably, the guideline update does not address several nutraceuticals supported by meta-analyses-such as plant sterols, soluble fibers, berberine, artichoke extract, and bergamot-whose efficacy and safety are well documented. A more constructive reading of the update suggests encouraging clinicians to recommend only evidence-based nutraceuticals and motivating further research. These agents should be considered as adjuncts to lifestyle interventions in low-risk individuals, not as substitutes for pharmacologic therapy when indicated.

Background and aim: Propionic acidemia (PA) is a genetic metabolic disorder caused by deficient activity of the enzyme propionyl-CoA carboxylase, resulting in accumulation of toxic metabolites during catabolism of odd-chain fatty acids and branched-chain amino acids. Most PA occurs in compound heterozygotes, typically presenting with metabolic acidosis and seizures in infancy. A milder phenotype of PA is prevalent in the Amish population due to a founder missense variant in PCCB (c.1606 A > G; p.Asn536Asp) and is frequently present as an isolated dilated cardiomyopathy in adolescence.

Methods and results: Here we report our experience with three Amish patients with genetically confirmed PA and end-stage heart failure. While one patient underwent successful heart transplantation with no complications, another developed recurrent cardiogenic shock after transplant due to metabolic decompensation. Based on this experience, a subsequent patient was treated with combined heart/liver transplantation.

Conclusions: These cases highlight unique challenges in managing patients with metabolic cardiomyopathies and emphasize the importance of a multidisciplinary approach to achieve the best possible outcomes.

Background and aim: Diabetic nephropathy (DN) represents the primary contributor to end-stage renal disease worldwide, and its prevalence continues to grow, even with improvements in therapies aimed at lowering glucose levels. The progression of DN has been associated with lipid metabolism, yet the direct involvement of particular lipid species is still not fully understood. This study employs two-sample Mendelian randomization (TSMR) to investigate the causal effects of 179 plasma lipid species on DN risk.

Methods and results: Lipid exposure genetic instruments were sourced from a genome-wide association study (GWAS) found in the GWAS Catalog, whereas data on the DN outcomes were collected from the FinnGen R12 cohort. The main analytical approach employed was inverse-variance weighted (IVW) regression. To evaluate pleiotropy and heterogeneity, tests such as MR-Egger intercept, Cochran's Q, MR-PRESSO, and leave-one-out analyses were performed. The analysis identified 13 lipid species with significant associations after sensitivity analyses. Among these, seven lipid species were risk factors for DN, including phosphatidylcholine (PC) (O-16:1_18:1, 15:0_18:2, 18:1_18:1, 18:1_20:2, 18:2_18:2) levels, phosphatidylethanolamine (PE) (18:1_18:1), and triacylglycerol (TAG) (56:4). Conversely, six lipid species demonstrated protective effects, including lysophosphatidylcholine (LPC) (20:4), lysophosphatidylethanolamine (LPE) (18:1), PC (17:0_20:4), sterol ester (SE) (27:1/15:0, 27:1/18:3), and TAG (52:6).

Conclusions: This study provides robust genetic evidence linking specific lipid species to DN risk. PC and PE species were identified as risk factors, whereas LPC, LPE, and SE exhibited protective effects. Additionally, TAG species demonstrated a bidirectional influence. These findings refine the understanding of lipid-mediated renal dysfunction in DN, highlighting lipid metabolism as a potential therapeutic target.

Background and aims: This study aimed to resolve the caffeine-hypertension paradox by investigating the association between urinary paraxanthine-to-caffeine molar ratio (PMR)-a functional biomarker of CYP1A2 metabolic capacity-and hypertension risk, while exploring mediation by serum uric acid (SUA) and white blood cells (WBC).

Methods and results: Using nationally representative NHANES data (2009-2014; n = 1611), urinary PMR was quantified via UPLC-ESI-MS/MS. Hypertension was defined per AHA/ACC 2017 guidelines. Multivariable logistic regression analyzed PMR-hypertension associations (unadjusted, age/sex-adjusted, fully adjusted). Dose-response relationships were modeled using restricted cubic spline (RCS) analysis. Causal mediation tested SUA/WBC pathways. Faster caffeine metabolism (higher PMR) demonstrated a nonlinear inverse relationship with hypertension. A critical inflection point at PMR = 3.03 revealed: slow metabolizers (PMR <3.03) had 51 % higher hypertension risk than fast metabolizers (OR = 0.49, 95 % CI: 0.40-0.60; P < 0.001). SUA and WBC collectively mediated 12 % of PMR's protective effect (SUA: 8.0 %; WBC: 4.0 %). Subgroup analyses showed effect modification by age and race (P interaction <0.05).

Conclusion: PMR serves as a novel biomarker clarifying the caffeine-hypertension paradox: fast metabolizers (PMR ≥3.03) exhibit significantly reduced hypertension risk, partially mediated by reduced SUA and inflammation. This supports personalized caffeine intake recommendations based on metabolic phenotype.

Background and aim: The joint effects of longitudinal changes in body mass index (BMI) and estimated glomerular filtration rate (eGFR), on hyperuricemia risk remain unclear. We aimed to investigate this relationship and identify high-risk trajectories for hyperuricemia prediction.

Methods and results: In this prospective community-based cohort (2018-2023), we enrolled 5329 Chinese adults ≥18 years with serial measurements of BMI, eGFR, and serum urate. Restricted cubic splines (RCS) nested in the Cox regression framework were applied to assess dose-response relationships between BMI, eGFR and hyperuricemia risk. Group-based trajectory modeling identified distinct BMI/eGFR patterns, with multivariable-adjusted Bayesian Cox proportional hazards models quantifying their associations with incident hyperuricemia. Over an average follow-up period of 3.25 years, 489 individuals developed hyperuricemia, resulting in an incidence rate of 15.05 per 100 person-years. Each unit increase in BMI during follow-up was associated with a 21 % (95 % CI: 14 %-30 %) increased risk for hyperuricemia. Similarly, each 10-unit decrease in eGFR correlated with a 12 % (95 % CI: 5 %-19 %) elevation in hyperuricemia risk. The RCS curves indicated linear associations between changes in BMI and eGFR and hyperuricemia risk (all p values < 0.001). The low eGFR trajectory showed a marginal HR of 1.52 (95 % CI: 1.02-2.37). The HRs for the high BMI trajectory group was 3.89 (95 % CI: 2.35-6.38). Notably, the influence of eGFR variability was more pronounced in men, while that of BMI was stronger in women.

Conclusions: Longitudinal patterns of rising BMI and declining eGFR synergistically predict hyperuricemia development, with clinically relevant sexual difference.

Background and aims: Little is known about the relationships between lipoprotein subclasses and the risk of cardiovascular disease (CVD) in individuals with metabolic dysfunction-associated steatotic liver disease (MASLD). We sought to elucidate the associations of lipoprotein subclasses with the risk of CVD in individuals with MASLD.

Methods and results: This study included 51,472 individuals with MASLD from the UK biobank. Concentrations of lipoprotein subclasses were quantified by nuclear magnetic resonance. Multivariable-adjusted Cox proportional hazards model was used to evaluate the associations between lipoprotein subclasses and the incidence/mortality of CVD. During median follow-ups of 13.3-13.5 years, 6208 incident CVD cases, 5206 coronary heart disease cases, 1270 stroke cases, and 559 CVD-related deaths were documented. Most very-low-density lipoprotein (VLDL) [hazard ratio (HR) range: 1.03-1.13; P <0.05], intermediate-density lipoprotein (HR range: 1.08-1.11; P <0.05), low-density lipoprotein (HR range: 1.05-1.11; P <0.05), very large high-density lipoprotein (HDL) particles and triglycerides in small HDL subclasses (HR range: 1.04-1.16; P <0.05) were positively associated with the risk of incident CVD, whereas other HDL particles and their subclasses were related to reduced risks of incident CVD (HR range: 0.86-0.95; P <0.05). Moreover, the association of VLDL particles with CVD strengthened as the diameter of VLDL decreased.

Conclusion: These findings suggest that associations between lipoprotein subclasses and the risk of CVD differed by particle diameter in individuals with MASLD. Integrating lipoprotein subclass assessment into clinical management and promoting subclass‑targeted lipid‑lowering strategies may strengthen CVD prevention in MASLD.