烟酸与framingham评分关系

The Framingham risk score (FRS) has been used to assess the risk of a cardiovascular event and to identify patients for risk factor modifications. Therefore, the purpose of this study was to evaluate the relationship of the FRS with dietary intake and inflammatory biomarkers. We conducted a cross-sectional study of 180 men (49.2 ± 10.2 years) with MS. Serum levels of high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), and adiponectin were examined. Participants were asked to complete the food frequency questionnaire (FFQ) using the previous 1 year as a reference point. The absolute cardiovascular disease (CVD) risk percentage over 10 years was calculated to estimate the FRS, which was classified as low risk (< 10%), intermediate risk (10-20%), and high risk (> 20%). Mean intake of polyunsaturated fatty acids was lower in subjects who had > 20% FRS than in subjects who had < 10% FRS (3.7 ± 1.9 g/day vs. 4.7 ± 1.9 g/day; P < 0.05). Significant differences in the Index of Nutritional Quality of protein, phosphorus, iron, vitamin A, vitamin B(1), niacin, vitamin B(6), and vitamin C were observed between the > 20% FRS group and the < 10% FRS group (P < 0.05). IL-6 concentrations were significantly lower in subjects with a < 10% FRS than in subjects who were 10-20% FRS or > 20% FRS (0.91 ± 0.26 vs. 1.48 ± 033 vs. 2.72 ± 0.57 pg/mL, respectively; P < 0.05). IL-6 and dietary intake of polyunsaturated fatty acids together explained 6.6% of the variation in FRS levels in a stepwise multiple regression model. Our results provide some evidence that dietary intake in the higher CVD risk group was inferior to that in the lower risk group and that dietary fat intake and IL-6 were associated with FRS and MS in Korean men.

Lipoprotein (a) [Lp(a)] has a strong association with coronary disease (CHD). We evaluated the implications of implementing a niacin strategy in persons above low risk by the Framingham risk score (FRS). Patients referred to a university lipid management program from January 2004 to June 2010 had an Lp(a) level measured at initial evaluation. Factors associated with an increase in Lp(a) and predictors of a high risk Lp(a) (≥50 mg/dL) were assessed. FRS and Lp(a) levels were used to assess eligibility for niacin with an Lp(a) ≥50 mg/dL. A total of 692 patients (57% male, mean age 52 ± 14 years) had a mean Lp(a) of 32 ± 40 mg/dL. In a multiple logistic regression model, African-American race, female gender, presence of CHD, and lower triglyceride levels were significant predictors of high risk Lp(a). Ten percent were determined to be intermediate and 44% high risk by FRS. A total of 9% of intermediate- and 26% of high-risk patients had an Lp(a) ≥50 mg/dL, and 84% were not taking niacin. A total of 19% of moderate- and high-risk patients were eligible for initiation of niacin based upon values ≥50 mg/dL. If niacin were also used for an high-density lipoprotein cholesterol levels ≤40 mg/dL, only 5.1% additional patients would require niacin. High-risk levels of Lp(a) are associated with female gender, African- American race, and CHD. 19% of moderate and high risk patients would be candidates for treatment with niacin if the indication is a cutpoint Lp(a) ≥50 mg/dL.

High-density lipoprotein (HDL) cholesterol is a heterogeneous group of lipoproteins exhibiting a variety of properties like prostacyclin production stimulation, decrease in platelet aggregation, endothelial cell apoptosis inhibition, and low-density lipoprotein oxidation blockade. Epidemiologic studies have shown an inverse relation between HDL cholesterol levels and cardiovascular risk. Low HDL cholesterol is associated with increased risk for myocardial infarction, stroke, sudden death, peripheral artery disease, and postangioplasty restenosis. In contrast, high HDL levels are associated with longevity and protection against atherosclerotic disease development. Given the evolving epidemic of obesity, diabetes mellitus, and metabolic syndrome, the prevalence of low HDL will continue to rise. In the United States, low HDL is present in 35% of men, 15% of women, and approximately 63% of patients with coronary artery disease. Data extracted from the Framingham study highlight that 1-mg increase in HDL levels decreases by 2% to 3% the risk of cardiovascular disease. There is no doubt regarding clinical importance about isolated low HDL, but relatively few clinicians consider a direct therapeutic intervention of this dyslipidemia. In this sense, lifestyle measures should be the first-line strategy to manage low HDL levels. On the other hand, pharmacologic options include niacin, fibrates, and statins. Fibrates appear to reduce risk preferentially in patients with low HDL with metabolic syndrome, whereas statins reduce risk across all levels of HDL. Torcetrapib, a cholesteryl esters transfer protein inhibitor, represented a hope to raise this lipoprotein; however, all clinical trials on this drug had ceased after ILLUMINATE, RADIANCE and ERASE trials had recorded an increase in mortality, rates of myocardial infarction, angina, and heart failure. In the near future, drugs as beta-glucans, Apo-A1 mimetic peptides, and ACAT inhibitors, are the new promises to treat this condition.

The Cardiovascular Risk Identification and Treatment Center was established in 1997, adopting a collaborative-care clinic model for the purpose of improving the management of high-risk patients with dyslipidemia. This was a retrospective analysis of 417 high-risk patients with > or =1 year of follow-up laboratory data. Analysis included changes in total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), non-HDL, triglycerides, and total cholesterol to HDL ratio; lipoprotein goal achievement; Framingham risk score; liver function; and cardiovascular events. At baseline, 66% of patients had coronary heart disease (CHD) or equivalent risk, 45% were not receiving dyslipidemia therapy, and 29% were on statin monotherapy. After 3 years in the program, 56% were receiving combination therapy, 41% were on monotherapy, and 2% were not on therapy. The 3 most common treatment regimens were statin plus niacin (36%), statin alone (22%), and niacin alone (14%). All lipoproteins improved from baseline (p <0.001). Overall, 62% to 74% of patients reached singular lipid goals and 35% achieved combined lipid goals. Patients with Framingham 10-year CHD risk of >20% were reduced from 6% to <1%. Only 29 patients (7.0%) had a cardiovascular event, including 5 (1.0%) who experienced a myocardial infarction. Aspartate aminotransferase/alanine transferase elevation >3 times normal occurred in 1% of patients. In conclusion, a collaborative-care practice model adopting individualized, aggressive pharmacologic and nonpharmacologic treatment strategies is highly effective in achieving lipid goals, is sustainable, and is safe. Furthermore, this approach yields reduced projected 10-year CHD risk. A low rate of cardiovascular events was observed.

Reduction in total cholesterol (TC) and LDL-cholesterol (LDL-C) forms one of the principal objectives of most cardiovascular secondary prevention strategies. Many patients being treated with statins, however, have significant residual dyslipidaemia, with many having suboptimal HDL-cholesterol (HDL-C) levels. The addition of nicotinic acid to a statin has been shown to improve this profile, although clinical outcome evidence is currently lacking. This study set out to model the impact of nicotinic acid therapy on cardiovascular risk in these patients, based on Framingham risk assessments on a cohort of patients drawn from UK general practitioner records. Cardiovascular risk profiles were extracted from a research database of 602,222 patients from 98 UK general practices. 23 262 statin-treated patients with established cardiovascular disease or diabetes were identified and their 4-year Framingham risk was estimated. Patients who had either TC or HDL-C outside the desirable range then had their lipid profile adjusted in accordance with the likely performance of nicotinic acid, and the Framingham risk was then re-assessed. Baseline 4-year coronary risk in the group as a whole was 11.5% (95%CI: 11.4-11.6). After adjustment of the lipid profile, this was reduced to 9.7% (95%CI: 9.6-9.8), a reduction in risk of 15.9% (95%CI: 15.1-16.6). When modelling was limited to those with diabetes or an abnormal treated lipid profile, the magnitude of change was increased to 23-29% depending on sex and subgroup. Risk factor modelling suggests that raising HDL-C levels using nicotinic acid in statin-treated patients is likely to yield significant incremental clinical benefits. The results of clinical trials currently under way are awaited with interest.

Although reduction of LDL-C levels is a priority in the treatment of dyslipidemia, not all coronary events are prevented despite aggressive LDL-C lowering, and risk reduction can be improved by treating additional lipid abnormalities. The Framingham Study was the first to demonstrate the inverse relationship between HDL-C and risk of coronary heart disease (CHD). This relationship was present at all levels of LDL-C, whereas the highest risk was associated with low HDL-C and high LDL-C. THE ANTIATHEROGENIC ACTIONS OF HDL-CHOLESTEROL: The antiatherogenic actions of HDL-C are complex. HDL-C plays a major role in reverse cholesterol transport, mobilizing cholesterol from the periphery to the liver. In addition, cardioprotective effects of HDL-C include endothelial protection, anti-inflammatory activity, as well as antioxidant and antithrombotic effects. In addition to lowering LDL-C, statins increase HDL-C by 5 to 15% by increasing apolipoprotein A-I synthesis. Fibrate therapy results in an increase in HDL-C of 10 to 25 % by activating PPAR- , which stimulates hepatic apolipoprotein A-I gene expression. Niacin is the most effective agent used for increasing HDL-C, causing increase of 15 to 35%. The side effects of niacin therapy, which is largely mediated by prostaglandins, may be minimized by the use of prolonged-release formulation of nicotinic acid. Combination therapy with HDL-raising agents, such as nicotinic acid and statin, markedly increases HDL-C, lowers LDL-C and improves the lipoproteins subclass distribution. New therapeutic modalities in the treatment of low HDL-C and lowering LDL-C, either in combination or as a monotherapy, may provide additional benefits in reducing CHD risk.

Although circumstantial evidence supports raising high-density lipoprotein cholesterol (HDLC) in patients with low levels of HDLC, the scarcity of event-based trials has led to uncertainty with regard to the benefit of high-density lipoprotein (HDL)-raising therapy. Based on the National Cholesterol Education Program guidelines, therapy for dyslipidemia is focused initially on targeting low-density lipoprotein cholesterol (LDLC), and in patients with hypertriglyceridemia, secondarily on targeting non-HDLC. When HDLC remains low, the decision to target HDLC depends on the assessment of risk of cardiovascular events. We often consider drug therapy specifically to raise HDLC in high-risk patients, such as those with established atherosclerotic vascular disease, type 2 diabetes, or a Framingham risk score of 20% or above. The majority of high-risk patients require drug therapy, usually a statin, to achieve aggressive LDLC and non-HDLC goals, and thus many patients with low HDLC are candidates for statin therapy. However, a second drug is often required to achieve substantial HDL raising. Although no formal goals for HDLC exist, reasonable goals are HDLC greater than 40 mg/dL in men and greater than 50 mg/dL in women. We often add either niacin or a fibrate to a statin in high-risk patients with low HDLC levels. Targeting HDLC with pharmacologic therapy is a more difficult decision in moderate-risk patients, in whom therapy must be highly individualized.

Low serum levels of high density lipoprotein cholesterol (HDL-C) is an established risk factor for coronary heart disease (CHD). Among a variety of lipid modifying drugs, the best single drug therapy to increase HDL-C levels, especially among high risk, isolated low HDL-C (ILHDL-C) cases is yet to be identified. The objectives of the present study were to evaluate the best pharmacological measure among atorvastatin, fenofibrate and niacin aimed to raise HDL-C and its effect in decreasing the estimated Framingham-10-year CHD risk percentage (CHD-RP) among high risk ILHDL-C cases in north India. Two hundred CHD equivalent (CHD-RP≥20), ILHDL-C cases were randomly assigned for treatment either with atorvastatin 10 mg/day (n=70), micronized fenofibrate 160 mg/day (n=65) or niacin-extended release (ER) 750 mg/day (n=65). After 6 wk of treatment, the dosages of drugs were doubled and the patients were finally assessed after 12 wk for their lipid values. Baseline characteristics were similar in the three groups. Niacin therapy 750 mg and 1.5 g/day resulted in a significant rise in HDL-C by 8.10 ± 3.19 and 12.41 ± 4.39 per cent (P<0.001), respectively. Fenofibrate 160 and 320 mg/day also resulted in a significant rise in HDL-C by 3.85 ± 3.48 and 6.24 ± 4.43 per cent (P<0.001), respectively, while atorvastatin 10 and 20 mg/day resulted in a non-significant increase in HDL-C by 0.13 ± 2.92 per cent and 0.51 ± 2.63 per cent, respectively. By increasing HDL-C values, niacin was found to be most effective in reduction of 10-year CHD-RP (P<0.001), followed by fenofibrate (P=0.010), while atorvastatin had no effect. Our findings indicate that niacin rather than fibrates or statins seems to provide a safe and effective therapy for increasing HDL-C, thus reducing the cumulative CHD risk among ILHDL-C cases.

The use of statins in patients with high risk for cardiovascular disease (CVD) has resulted in a 30-40% decrease in clinical events in the last couple of decades. However, despite of a marked reduction (up to 60%) in LDL-C, about 30% of patients continue to have CVD events. This high residual risk in statin-treated patients initiated the search for new ways to reduce CVD risk. HDL is the next logical target. Epidemiological and cross-sectional studies identified low HDL-C level as an independent risk for CVD. Based on the Framingham Heart Study data, HDL-C <35 mg/dl was established an independent risk factor and HDL-C >60 mg/dl as protective.(3) Presently the cut point is <40 mg/dl for men and <50 mg/dl for women.

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is an independent risk factor for atherosclerosis (AS), but the mechanism is different from classical AS risk factors. Nicotinamide phosphoribosyltransferase (NAMPT) is involved in the pathophysiology of AS via multiple pathways, and its expression is closely related to hypoxia. The association of NAMPT with hypoxia and the risk of cardiovascular morbidity in the patients of OSAHS remains to be defined. Therefore, we carried out this study to investigate the association of NAMPT with hypoxia and the risk of early cardiovascular disease [based on the Framingham risk score (FRS)] in patients with OSAHS. A total of 82 patients diagnosed with OSAHS were enrolled in this cross-sectional survey design, along with 18 healthy controls who were age- and gender-matched. The general characteristic parameters including height and weight as well as biochemical parameters including blood glucose and lipid were collected from the subjects. The Framingham vascular risk score calculates the risk of developing vascular disease based on the above indicators. Polysomnography was performed in patients with OSAHS, and blood oxygen saturation and apnea-hypopnea index (AHI) were collected, and patients were grouped by disease extent by AHI. The serum NAMPT level of the research subjects was detected using an enzyme-linked immunosorbent assay. Spearman correlation analysis and multiple linear regression to explore the independent correlations of hypoxia on serum NAMPT activity in OSAHS patients. Serum NAMPT level in patients with OSAHS increased with the severity of the disease. Correlation analysis showed that NAMPT was significantly positively correlated with FRS in patients with OSAHS (r=0.829, P<0.05). Multiple linear regression analysis with FRS as the outcome measure showed that NAMPT activity and minimum blood oxygen saturation were independent associated with the risk of developing cardiovascular disease (β=0.03, P=0.000; β=-0.13, P=0.034). Univariate and multivariate regression analyses revealed that hypoxia was significantly associated with NAMPT levels in OSAHS patients, and the oxygen desaturation index (ODI) was independent associated with the expression of NAMPT activity (β=4.09, P=0.000). In patients with OSAHS, hypoxia is independently associated with NAMPT. NAMPT increases the risk of cardiovascular morbidity in this population may be influenced by hypoxia.

The 2 principal approaches to management of dyslipidemias are lifestyle intervention and lipid-modifying drug therapy. Recent revisions to the American Heart Association's dietary guidelines for reducing cardiovascular disease emphasize an overall healthy eating pattern and maintenance of appropriate body weight, together with achieving a desirable blood pressure and a desirable lipoprotein profile. New National Cholesterol Education Program treatment guidelines include a scoring system for calculating coronary heart disease (CHD) risk that is adapted from the Framingham Heart Study, as well as a category of CHD risk equivalents (e.g., diabetes) that will encourage more aggressive therapeutic intervention for individuals at high short-term risk for CHD, even in the absence of clinically evident coronary disease. Classes of lipid-modifying drugs include bile acid sequestrants (resins), fibrates, and statins, with each class exerting different effects on the lipid profile. Nicotinic acid (niacin) is also an approved lipid-modifying agent. The armamentarium for treating lipid disorders and atherosclerosis now includes statins that can decrease low-density lipoprotein (LDL) cholesterol levels by up to 55%, as well as a resin with improved tolerability. In patients with high levels of LDL cholesterol and triglycerides, together with low concentrations of high-density lipoprotein cholesterol, combination therapy may be effective. Moreover, researchers are currently investigating the development of drugs directed at molecular targets, including cholesterol esterification and accumulation in macrophage foam cells (e.g., inhibiting acyl-coenzyme A : cholesterol acyltransferase), degradation of atherosclerotic plaque (e.g., decreasing the expression of matrix metalloproteinases), and reverse cholesterol transport (e.g., stimulating ATP-binding cassette transporter A1).

: Currently, there are significant data to support a link between lipoprotein(a) [Lp(a)] levels and cardiovascular risk. However, there has not been a clinical trial examining the effects of Lp(a) reduction on cardiovascular risk in a primary prevention population. Until such a trial is conducted, current consensus supports using an Lp(a) percentile greater than 75% for race and gender as a risk stratification tool to target more aggressive low-density lipoprotein cholesterol (LDL-C) or apolipoprotein B (apoB) goals. Therefore, Lp(a) measurements should be considered in the following patients: individuals with early-onset vascular disease determined by clinical presentation or subclinical imaging, intermediate and high Framingham risk patients with a family history of premature coronary disease, and low Framingham risk patients with a family history and low high-density lipoprotein cholesterol (HDL-C) levels. Once LDL-C goals are met, Lp(a) levels may be taken into account in selecting secondary agents to reach more aggressive secondary goals, including non-HDL-C and apoB. To achieve Lp(a) reduction, one evidence-based approach is to initiate therapy with low-dose aspirin and extended-release niacin, titrated from 0.5 g up to 2 g over several weeks. If higher doses of niacin are desired, crystalline niacin allows for titration to a dosage as high as 2 g three times a day; however, the flushing side effect usually is quite prominent. Although hormone replacement therapy (HRT) has been shown to lower Lp(a), there are no indications for using HRT for primary or secondary prevention; therefore, we do not advocate initiating it solely for Lp(a) reduction. LDL apheresis is an option to lower LDL-C levels in patients with homozygous familial hypercholesterolemia who are not responsive to medical therapy. Although it does lower Lp(a), there is no treatment indication for this. A recent study supports the cholesterol absorption inhibitor ezetimibe's ability to lower Lp(a), a finding that deserves further investigation as it has not been previously reported in multiple ezetimibe trials. Additionally, the apoB messenger RNA antisense therapy mipomersen currently is in phase 3 trials and may serve as a potential inhibitor of Lp(a) production. Ultimately, more trial evidence is needed to determine whether lowering Lp(a) actually reduces cardiovascular risk, although this may be difficult to isolate without a specific Lp(a)-lowering therapy.

We planned to carry out a pilot study to evaluate the efficacy and safety as an antihypercholesterolemic agent of a brand dietary supplement made of Monascus purpureus titrated extract, octacosanols and niacin on 111 Caucasian patients with low cardiovascular disease risk (<20% by Framingham algorithms), comparing them with the antihypercholesterolemic effect of a low dosage of Pravastatin on 20 subjects with similar risk profile. In our study, the tested dietary supplement determined a significant decrease of Total Cholesterol (TC), Low Density Lipoprotein Cholesterol (LDL-C), and Triglycerides (TG) in moderately hypercholesterolemic subjects without clinically relevant change in liver and muscular toxicity markers. The reduction of LDL-C reached the 20%, and it is similar to that obtained with a well-known effective statin like Pravastatin. Further long-term and double blind evaluation have to be carried out before to infer the observed results, however it appears that the studied dietary supplements could be a safe and efficacious antihypercholesterolemic agent for patients at low risk for cardiovascular diseases.

The purpose of the present study was to explore the role of gender in the relation of high-sensitivity C-reactive protein (hsCRP), white blood cell (WBC) count, and serum uric acid (UA) to the risk of future cardiovascular disease (CVD) events. In total, 404 workers were recruited to obtain the measurements of serum markers for CVD risk. Demographic data, nutrition, exercise, smoking, and alcohol consumption were assessed through a questionnaire. The Framingham Risk Score (FRS) was adopted to estimate the risk of future CVD events. Multiple linear regression models were used to determine CVD risk markers in relation to the FRS by gender. The hsCRP was not significantly correlated with the FRS for all workers after adjusting for covariates, including demographic data and health-related lifestyle. WBC count was positively correlated with FRS for all workers, but WBC count did not show an interaction with gender with respect to the FRS. Serum UA showed an interaction with gender on the FRS, and UA positively correlated with the FRS in males though not in females. With respect to CVD prevention, the WBC count can be used to monitor the risk for all workers. Due to a gender difference shown in the relationship between serum UA and the FRS, serum UA can be a monitor of the risk of future CVD events in male workers only.

BACKGROUND AND AIMS Little is known about differences of cardiometabolic risk factors (CMRF) and the function of Framingham Risk Score (FRS) within severe obesity, thus we aimed to study not only CMRF and FRS, but to determine significant differences between BMI ranges within severe obesity. METHODS AND RESULTS In this baseline analysis of the Traditional Brazilian Diet (DieTBra) Trial, several CMRF were assessed in 150 adult patients in two BMI ranges: 35.0-44.9 kg/m2 (n = 76) and ≥45 kg/m2 (n = 74). Body composition was evaluated by multifrequency bioelectrical impedance analysis to measure the percent of body fat, visceral fat area and waist circumference. Pearson's Chi-squared, Fisher's Exact, Student's t-test, and Mann-Whitney's test were used in the statistical analysis with a 5% significance level. Hypertension, C-reactive protein, systolic and diastolic blood pressure and positive family history for heart diseases were more prevalent in BMI ≥45.0 kg/m2 (p < 0.05). Mean values of waist circumference, body fat %, visceral fat area, and systolic blood pressure were significantly higher in patients with BMI ≥45.0 kg/m2. Regarding the function of FRS, 40.0% of the patients were at high risk. No differences were found for diabetes, lifestyle, lipid parameters, and FRS within different BMI ranges, except for dyslipidemia, significantly higher among participants with BMI 35.0-44.9 kg/m2. CONCLUSION BMI >45 kg/m2 was associated with higher prevalence of hypertension, systolic and diastolic blood pressure, C-reactive protein, waist circumference, body fat % and family history of heart diseases, enhancing the risk for the occurrence of cardiovascular diseases.

BACKGROUND In the current study we aimed to evaluate the gender-specific associations between metabolic and psychological risk factors of cardiovascular disease (CVD) and Framingham Risk Score (FRS) in patients with metabolic syndrome. METHODS In a cross-sectional study of 256 patients with metabolic syndrome (157 men, 99 women), the cardiovascular disease risk was evaluated using the FRS scoring system by a pre-defined computerized algorithm. Psychological distress was also assessed by general health questionnaire (GHQ)-12. Evaluation of the biochemical parameters including fasting serum glucose (FSG), lipid profile, liver enzymes and adiponectin concentrations were also performed using the enzymatic methods. RESULTS The prevalence of low, intermediate and high risk of CVD in men was significantly higher than women (P < 0.05). Both genders in high risk of CVD had significantly higher age, systolic blood pressure (SBP) and FSG concentrations compared with male and females in intermediate and low risk of CVD (P < 0.05). In multiple logistic regression, being single was in the highest relationship with high psychological distress values compared with married or divorced/separated marital status. Moreover, high SBP and low high density lipoprotein (HDL) concentrations were also potent determinants of high psychological distress (P < 0.05). CONCLUSIONS In the current study, the prevalence of CVD risk factors were higher in men compared with women. Moreover, higher age, SBP and FSG were potent determinants of FRS in both genders. Marital status and serum HDL were in relation with psychological distress among patients with metabolic syndrome.

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Background B vitamins play a crucial role in the balance and metabolism of energy. Energy metabolism mainly benefits from the B-complex vitamins. Specifically, decarboxylation, transamination, acylation, oxidation, and reduction of substrates that are ultimately employed in energy intake require thiamin, riboflavin, niacin, and vitamin B6. Vitamin deficiency could lead to chronic disease occurrence. Objectives To assess the impact of energy-releasing B-vitamins intake (B1, B2, B3, and B6) on selected indices of obesity and cardiac function. Methods A cross-sectional study was performed on 491 apparently healthy adults (18-64 years old) between January and May 2019 at Hashemite University, Jordan. Anthropometric measurements were taken, lipid profiles were analyzed, and indices of obesity and cardiac function were calculated. The typical dietary intake of B1, B2, B3, and B6 vitamins was calculated. Results Conicity index (CI) and abdominal volume index (AVI) scores significantly decreased with the increased adjusted vitamin B1 and B6 intake. Also, body roundness index (BRI), weight-adjusted-waist index (WWI), lipid accumulation product (LAP), and atherogenic index of plasma (AIP) scores were decreased with the increase of adjusted B6 intake ( p<0.05). The total sample showed a significant inverse weak correlation between energy-adjusted intake of B1 and AVI (r= -0.156, p=0.001) and BRI (r= 0.111, p=0.014). Similar correlations were detected among male participants between energy-adjusted B1 intake and BAI, AVI, and BRI. Female participants had a significant weak inverse correlation between BAI and energy-adjusted B2 (r= -0.180, p=0.029) and B6 intake (r= -0.212, p=0.010). Only B1, the vitamin, significantly explained 2.43 and 1.24% of changes observed in the AVI and BRI scores, respectively ( p<0.05). Conclusions Increasing the consumption of B1, B2, and B6 may significantly lower values of indices of obesity and cardiac function regardless of sex differences. Thus reducing the occurrence of obesity and related coronary heart diseases.

BACKGROUND Low circulating concentrations of B vitamins are linked to various chronic and neurodegenerative diseases. Notably, pyridoxal 5´-phosphate (B6) deficiency is linked to altered inflammatory responses and cellular immune function, both critical in multiple sclerosis (MS). Nevertheless, most MS research has focused on folate (B9) and vitamin B12, leaving other B vitamins understudied. OBJECTIVE This secondary analysis investigated B-vitamin serum concentrations and related metabolites across MS phenotypes (primary progressive MS, relapsing-remitting MS and secondary progressive MS) and disease severity levels. Additionally, the impact of endurance exercise on B-vitamin concentrations was investigated. METHODS 106 individuals with MS participated in a randomized controlled trial, including different endurance exercise conditions. Serum B-vitamin concentrations were analyzed in 99 participants before and after three-weeks of intervention. Prior to analysis, participants were dichotomized to one of two disability groups based on their Expanded Disability Status Scale (EDSS) score: EDSS≥4.5 (n=47, EDSS: 5.86±0.56) and EDSS<4 (n=52, EDSS: 3.59±0.83). RESULTS Higher EDSS scores were associated with lower pyridoxal 5'-phosphate (B6) concentrations (rs=-0.32, 95%CI [-0.49, -0.12], p=.011), with the EDSS≥4.5 group also showing lower baseline pyridoxal 5'-phosphate (B6) concentrations (β=-0.18, 95%CI [-0.30, -0.07], p=.007) compared to the EDSS<4 group. Significant time x EDSS group interactions were evident for pyridoxal 5'-phosphate (B6) (β=0.05, 95%CI [0.02, 0.08], p=.011), pyridoxal (B6) (β=0.05, 95% CI [0.02, 0.09], p=.005) and riboflavin (B2) (β=0.06, 95%CI [0.02, 0.09], p=.008), showing increases in these vitamers in the EDSS≥4.5 group post-exercise. N1-methylnicotinamide (B3) (β=-0.11, 95%CI [-0.15, -0.06], p<.001) decreased in both groups over time. CONCLUSION Disease severity was associated with distinct B-vitamin profiles in individuals with MS, while endurance exercise appeared to modify specific B-vitamin concentrations. This trial was registered at clinicaltrials.gov as NCT04356248.

Pregnant women are at higher risk of vitamin D deficiency due to increased nutritional requirements and limited dietary sources. Fish is the major source of vitamin D, but its availability varies by region. This study aims to assess the availability of vitamin D-rich fish and develop food-based recommendations (FBRs) for pregnant women in East Lombok, Indonesia. This comparative cross-sectional study was conducted in East Lombok, Indonesia, which is part of Action Against Stunting cohort of pregnant women. Twenty-five village markets in the area were scored based on availability of vitamin D-rich fish and number of fish sellers in each market and were categorized into high availability (HD) for the highest quartile and low availability (LD) for the lowest quartile. QGIS software was used to identify each of respondents' houses using 2.4km buffer zones to either HD or LD markets. Dietary intake data was collected from 24-hour dietary recalls and linear programming (LP) analysis using Optifood was used to identify problem nutrient and dietary inadequacy. No significant difference in vitamin D intake was found between HD and LD areas (p=0.633). While both groups' FBRs ensure adequacy of iron, zinc, vitamins A, B1, B2, B3, B6, and B12, calcium remain as dietary inadequacy in the LD group, suggesting that availability play a role in ensuring dietary adequacy. Future studies to develop nutrient-dense foods and improved fish availability mapping which consider non-static position of market (mobile vendor) are recommended.

Strategies to address the nutritional needs of adolescent girls and young women often focus on supplementation. In this study, an action‐research approach involving a nutrition education and entrepreneurship intervention was carried out among adolescent girls and young women in poor neighborhoods of Medellín, Colombia. The intervention group significantly increased its intake of several nutrients, including energy, protein, total fat, saturated fat, monounsaturated fat, polyunsaturated fat, cholesterol, dietary fiber, calcium, zinc, and vitamins A, B2, B3, B9, and C. A significant increase was observed in the intake of the Global Diet Quality Score (GDQS) healthy food groups (other fruits, other vegetables, legumes, high‐fat dairy products), accompanied by a decrease in the consumption of some unhealthy food groups (sweets and ice creams). A multivariate regression controlling for age, socioeconomic status, occupation, Household Hunger Scale, mean probability of adequacy, physical activity, and body self‐perception showed that the nutrition intervention improved the total GDQS by 33% in the intervention group—a substantial improvement notwithstanding the study group's precarious social and economic conditions. We conclude that nutrition education and entrepreneurship models based on this approach may improve the dietary profile of this population and reduce future pressures from nutrition‐related chronic diseases.

BACKGROUND Obesity and micronutrient deficiencies contribute to the risk of cardiometabolic diseases such are type 2 diabetes mellitus and Cardiovascular Disease (CVD). OBJECTIVE We examined the frequency of concomitant deficit of Magnesium (Mg) and vitamin D in obese patients and evaluated the connection of these combined deficiencies with indicators of cardiometabolic risk in non-diabetic subjects. METHODS Non-diabetic middle aged adults (n = 80; mean age 36 ± 4 years, 52% women) were recruited based on weight/adiposity parameters [i.e. Body Mass Index (BMI) and body fat percentage (FAT%)]. Cardiometabolic risk indicators [insulin resistance (Homeostatic Model Assessment for Insulin Resistance (HOMA-IR)) and CVD risk (Framingham risk score for predicting 10-year CVD)], Mg status (i.e. total serum Mg concentration (TMg), Chronic Latent Mg Deficiency (CLMD) - 0.75-0.85 mmol/L), vitamin D status (i.e. serum concentration of 25-hydroxyvitamin D (25(OH)D), vitamin D deficiency <50 nmol/l) were assessed. RESULTS Among obese subjects 36% presented a combination of vitamin D deficiency and CLMD. In all studied patients, 25(OH)D and TMg levels both, individually and combined, showed a negative linear correlation with HOMA-IR and CVD risk. In subjects with CLMD (TMg <0.85 mmol/L), a negative linear coefficient was found between 25(OH)D and, HOMA-IR and CVD risk, compared with subjects with normal TMg status (TMg ≥0.85 mmol/L). CONCLUSION CLMD and vitamin D deficiency may commonly be present in obese non-diabetic subjects. Individually and combined, both deficiencies predispose non-diabetic patients to increased risk of cardiometabolic diseases. Maintaining normal Mg status may improve the beneficial effects of vitamin D on cardiometabolic risk indicators.

Evidence of the effects of water-soluble vitamins (e.g., B vitamins, vitamin C, and total folate) on cognitive function in patients with neurodegenerative diseases is mixed. Furthermore, the relationships among homocysteine (Hcy) metabolism, water-soluble vitamins, and cognitive impairment remain unclear. Therefore, we aimed to investigate the role of the levels of water-soluble vitamins [e.g., vitamins B1, B2, B3, B5, B6, 5-methyltetrahydrofolate (5mTHF), B12, and C and total folate] and Hcy in dementia progression in patients with neurodegenerative diseases. In this retrospective cohort study, we enrolled 280 healthy controls and 646 patients with a neurodegenerative disease. Patients were classified into a Parkinson’s disease (PD) group (n = 312), Alzheimer’s disease (AD) group (n = 219), or other dementia group (n = 115) according to pathological features. The other dementia group comprised 25 patients with frontotemporal dementia, 38 with Lewy body dementia, 34 with vascular dementia, and 18 with semantic dementia. Serum vitamins (i.e., B1, B2, B3, B5, VB6, 5mTHF, and C) were measured via liquid chromatography-mass spectrometry/mass spectrometry. Total Hcy, vitamin B12 and total folate levels were measured using commercial electrochemiluminescence immunoassays. The serum levels of vitamins B1, B2, B5, B6, 5mTHF, and C were lower in all patient groups than in the control group. The logistic regression results revealed that lower levels of serum vitamins B2, B6, 5mTHF, and B12 were associated with a higher risk of dementia in PD patients, and higher Hcy levels and lower serum vitamin B6 and 5mTHF levels were associated with a higher risk of AD-related cognitive impairment. In addition, the level of vitamins was positively correlated with neuropsychological assessment scores and negatively correlated with Hcy level and stage of dementia. The levels of several water-soluble vitamins are lower in dementia patients. Moreover, lower levels of water-soluble vitamins and higher levels of Hcy increased odds ratios for having neurodegenerative diseases or cognitive impairment. These findings suggest that estimating water-soluble vitamin levels in older adults may be valuable given that they may help improve cognitive function.

There is growing evidence that higher intermuscular fat (IMF) is associated with worse processing speed, measured by the digit symbol substitution test (DSST) in older adults. However, the underlying biological mechanisms are not well understood. Considering that both muscle and the brain are metabolically active organs, we sought to identify metabolites that may explain the IMF-DSST association. We assessed 613 plasma metabolites in 2388 participants from the Health, Aging, and Body Composition Study (mean age ± SD 74.7 ± 2.9 years, 50% men, 63% white), using liquid chromatography-mass spectrometry. We confirmed that higher IMF was associated with worse DSST scores (standardized beta (95% CI) − 0.08 (− 0.12, − 0.03), p < 0.001). Sixty-six metabolites were significantly associated with both IMF and DSST. Four of the 66 metabolites attenuated the association by ≥ 10%: higher levels of adrenic acid (polyunsaturated fatty acid), and lower levels of C20:5 lysophosphatidylcholine (lysophospholipid), 1-methylnicotinamide (vitamin B3-related myokine), and maslinic acid (triterpene) were associated with higher IMF and worse DSST. Together, they explained 41% of the IMF-DSST association. Pathway enrichment analyses identified two significant shared pathways: unsaturated fatty acid metabolism and the citrate (TCA) cycle. This study provides hypothesis-generating evidence that a set of circulating metabolites related to unsaturated fatty acids, energy metabolism, and myokines may partially explain the inverse association of IMF with processing speed. The findings, if further confirmed by independent studies, advance our understanding of molecular pathways underlying muscle-brain crosstalk. Whether the identified metabolites are early predictors of future decline in processing speed should be further investigated.

Abstract Evidence suggests that probiotics and nicotinic acid (vitamin B3) may improve symptoms and outcomes of Parkinson’s disease through gut microbiome modulation. This study aimed to determine whether a 12-week placebo-controlled randomized clinical trial would result in changes in constipation, drug efficacy, neuroendocrine levels, and quality of life in people diagnosed with Parkinson’s disease. Forty-eight participants were randomly assigned to one of three groups: (1) probiotics + nicotinic acid, (2) probiotics + placebo, or (3) dual placebo for 12 weeks. Constipation, depression, anxiety, quality of life, mood, symptoms, and nutrition were assessed at baseline, midpoint, and the end of the trial. Blood and stool samples were collected for blood chemistry and gut microbiome analysis using next-generation sequencing (16S rRNA genes, Illumina MiSeq). Statistical significance was set at p < 0.05. The results showed improvements in constipation problems, Movement Disorder Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), Parkinson’s Disease Questionnaire-39 (PDQ-39), quality-of-life scores, and communication issues in probiotics and nicotinic acid groups compared with the placebo group. Blood chemistry remained within normal reference ranges. Supplementation did not change assessments of anxiety, depression, or mood. Gut microbiome analyses showed significant differences in alpha and beta diversity, as well as distinct microbiome compositions related to different interventions, disease status, anxiety, and depression. Several differences became more pronounced after 12 weeks compared with 6 weeks of intervention. Nicotinic acid appeared to have a stabilizing effect on the gut microbiome. The findings suggest that supplementation for twelve weeks may benefit constipation symptoms, gut microbiome, and quality of life measures.

Framingham risk score (FRS) is an important cardiovascular risk assessment tool, based on objective measurements of blood pressure and lipid profile, among other factors. However, in large population surveys, these measures are not always available, which limits their use. Evaluate the performance of the FRS predictive results using subjective measures. Cross-sectional study of 1,414 male rotating shift workers in an iron ore extraction company. The original FRS was calculated using objective systolic and diastolic blood pressure measurements, total cholesterol (TC), and HDL cholesterol. The modified FRS was calculated using subjective measurements of blood pressure and lipid profile, based on self-reported medical diagnosis and use of medications for these conditions. Three adaptations were proposed: (1) FRS-SAH, which considers only self-reported hypertension; (2) FRS-DLP, based solely on self-reported dyslipidemia; and (3) FRS-SAH and DLP, which integrates both self-reported factors. Agreement between the two scores was assessed using the kappa coefficient and the Bland-Altman analysis. The accuracy of the scores in predicting cardiovascular risk was compared using the ROC curve and the area under the curve (AUC). The scatter plot showed a strong correlation (r = 0.9036, p < 0.001) between adapted FRS-SAH and original FRS. The ROC curve showed an AUC with results above 0.85 for all models, confirming the effectiveness of the adapted scale. Bland-Altman indicated good precision between the measurements. Binary logistic regression analysis showed that all the factors associated with CVD-risk by the original FRS were similar to those associated with the adapted FRS. Among the adaptations, the FRS-SAH demonstrated the highest correlation and predictive accuracy. The adapted FRS proved to be effective in estimating CVD-risk, showing high correlation, sensitivity, specificity, and accuracy compared to the original FRS. Adaptive FRS based on self-reported hypertension, showed the best performance, making it a reliable alternative for contexts where direct measurements are not feasible.

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Background The American Heart Association's framework “ideal cardiovascular health” (CVH) focuses on modifiable risk factors to reduce cardiovascular disease (CVD). Metabolomics provides important pathobiological insights into risk factors and CVD development. We hypothesized that metabolomic signatures associate with CVH status, and that metabolites, at least partially, mediate the association of CVH score with atrial fibrillation (AF) and heart failure (HF). Methods and Results We studied 3056 adults in the FHS (Framingham Heart Study) cohort to evaluate CVH score and incident outcomes of AF and HF. Metabolomics data were available in 2059 participants; mediation analysis was performed to evaluate the mediation of metabolites in the association of CVH score and incident AF and HF. In the smaller cohort (mean age, 54 years; 53% women), CVH score was associated with 144 metabolites, with 64 metabolites shared across key cardiometabolic components (body mass index, blood pressure, and fasting blood glucose) of the CVH score. In mediation analyses, 3 metabolites (glycerol, cholesterol ester 16:1, and phosphatidylcholine 32:1) mediated the association of CVH score with incident AF. Seven metabolites (glycerol, isocitrate, asparagine, glutamine, indole‐3‐proprionate, phosphatidylcholine C36:4, and lysophosphatidylcholine 18:2), partly mediated the association between CVH score and incident HF in multivariable‐adjusted models. Conclusions Most metabolites that associated with CVH score were shared the most among 3 cardiometabolic components. Three main pathways: (1) alanine, glutamine, and glutamate metabolism; (2) citric acid cycle metabolism; and (3) glycerolipid metabolism mediated CVH score with HF. Metabolomics provides insights into how ideal CVH status contributes to the development of AF and HF.

Background This cohort study was conducted to examine the association between modifiable risk factors, including hypertension, smoking, physical activity, diabetes, cholesterol, and high-density lipoprotein with Framingham risk score in the prediction of 10-year-risk of cardiovascular diseases (CVD) between men and women in an Arab community of Southwest Iran, Hoveyzeh. Materials and methods A total of 8,526 people aged 35–70 participated in this cohort study. Framingham was used to estimate the 10-year risk of CVD. Also, the linear regression models were used to assess the relationship between modifiable risk factors and the 10-year risk of CVD. Finally, the area under the receiver operating characteristic curve (AUC) was used to measure the ability of modifiable risk factors to predict the 10-year risk of CVD. Results Our results of linear regression models showed that hypertension, smoking, PA, diabetes, cholesterol, and HDL were independently associated with the CVD risk in men and women. Also, AUC analysis showed that hypertension and diabetes have the largest AUC in men 0.841; 0.778 and in women 0.776; 0.715, respectively. However, physical activity had the highest AUC just in women 0.717. Conclusion Hypertension and diabetes in both gender and physical activity in women are the most important determinant for the prediction of CVD risk in Hoveyzeh. Our cohort study may be useful for adopting strategies to reduce CVD progression through lifestyle changes.

Background Arterial stiffness played an important role in the development of cardiovascular disease (CVD) events. The aim of this study was to verify the relative importance of arterial stiffness for different CVD risk scores in a large sample of Chinese women. Methods We measured arterial velocity pulse index (AVI) and CVD risk scores in 2220 female participants (mean age 57 years). Framingham Risk Score (FRS), and the prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR) were used to estimate CVD risk, respectively. The relationships between AVI and risk scores were investigated by linear regressions and restricted cubic spline (RCS) analysis. To determine the relative importance of AVI in predicting CVD risk scores, random forest analysis was used. Results There was a significant positive correlation between AVI and FRS, China-PAR in all subgroup groups stratified by age, blood pressure and BMI. AVI showed higher importance in predicting CVD risk scores in FRS model, compared with these traditional risk factors. In China-PAR model, although AVI was not as predictive as SBP, it had better predictive power than many known risk factors such as lipids. Furthermore, AVI had significant J-shaped associations both with FRS and China-PAR scores. Conclusions AVI was significantly associated with CVD risk score. In FRS and China-PAR model, AVI showed relatively high importance in predicting CVD risk scores. These findings may support the use of arterial stiffness measurements in CVD risk assessment.

Purpose: The new non-invasive arterial stiffness indices, arterial velocity pulse index (AVI) and arterial pressure volume index (API) are known to be associated with cardiovascular disease risk. The present study aimed to examine the “dose-response” associations between AVI, API and Framingham cardiovascular disease risk score (FCVRS). Methods: This survey included individuals with arterial stiffness indices collected at age 18 years and older. We used Pearson’s correlation coefficients and multivariate linear analyses to evaluate associations of AVI and API to other variables. The associations between FCVRS and AVI, API were analyzed by restrictive cubic spline. Results: 4311 people were included in the full study population, including 2091 males and 2220 females. In restricted cubic spline regression models, AVI or API had significant U-shaped associations with FCVRS, with the lowest risk score of cardiovascular disease was 8 units or 18 units, respectively. After AVI increased to 12 units, FCVRS increased rapidly until AVI was 27 units, and the FCVRS increased relatively flat afterward. For API, results were similar. When API increased to 23 units, the FCVRS increased rapidly, and after API was 52 units, FCVRS increased relatively flat. Conclusions: AVI or API had U-shaped associations with FCVRS. The associations may provide a new perspective for early treatment or lifestyle modifications to prevent cardiovascular diseases.

Background Elevated total cholesterol (TC), low‐density lipoprotein cholesterol (LDL‐C), triglycerides, and non‐high‐density lipoprotein cholesterol (non‐HDL‐C) and low high‐density lipoprotein cholesterol (HDL‐C) concentrations correlate with atherosclerotic cardiovascular disease (ASCVD) and mortality. Therefore, understanding how lipid trajectories throughout adulthood impact ASCVD and mortality risk is essential. Methods and Results We investigated 3875 Framingham Offspring participants (54% women, mean age 48 years) attending ≥1 examination between 1979 and 2014. We evaluated longitudinal correlates of each lipid subtype using mixed‐effects models. Next, we clustered individuals into trajectories through group‐based modeling. Thereafter, we assessed the prospective association of lipid trajectories with ASCVD and mortality. Male sex, greater body mass index, and smoking correlated with higher TC, LDL‐C, triglycerides, non‐HDL‐C, and lower HDL‐C concentrations. We identified 5 TC, HDL‐C, and LDL‐C trajectories, and 4 triglycerides and non‐HDL‐C trajectories. Upon follow‐up (median 8.2 years; 199 ASCVD events; 256 deaths), elevated TC (>240 mg/dL), LDL‐C (>155 mg/dL), or non‐HDL‐C (>180 mg/dL) concentrations conferred >2.25‐fold ASCVD and mortality risk compared with concentrations <165 mg/dL, <90 mg/dL, and <115 mg/dL, respectively ([TC hazard ratio (HR)ASCVD=4.17, 95% CI 1.94–8.99; TC HR death=2.47, 95% CI 1.28–4.76] [LDL‐C HRASCVD=5.09, 95% CI 1.54–16.85; LDL‐C HR death=4.04, 95% CI 1.84–8.89] [non‐HDL‐C HRASCVD=4.60, 95% CI 1.98–10.70; LDL‐C HR death=3.74, 95% CI 2.03–6.88]). Consistent HDL‐C concentrations <40 mg/dL were associated with greater ASCVD and mortality risk than concentrations >70 mg/dL (HRASCVD=3.81, 95% CI 2.04–7.15; HR death=2.88, 95% CI 1.70–4.89). Triglycerides trajectories were unassociated with outcomes. Conclusions Using a longitudinal modeling technique, we demonstrated that unfavorable lipid trajectories over 35 years confer higher ASCVD and mortality risk later in life.

. The Framingham Risk Score (FRS) assesses coronary heart disease (CHD) risk and predicts acute coronary events. Metabolic markers like LDL cholesterol, fasting blood glucose, uric acid, triglycerides, and TG/HDL ratio play critical roles in atherosclerosis and cardiovascular risk. Elevated LDL cholesterol, fasting blood glucose, and uric acid contribute to plaque formation, inflammation, and vascular damage, while high triglycerides and low HDL cholesterol exacerbate atherogenesis. This study explores the relationship between these markers and FRS to enhance CHD risk prediction and support targeted cardiovascular interventions. This study analyzed LDL cholesterol, fasting blood glucose, uric acid, triglycerides, and TG/HDL ratio with Framingham Risk Score in 85 participants, excluding those with incomplete data or chronic illnesses. The analysis found significant correlations between metabolic parameters and the 10-year myocardial infarction risk. LDL cholesterol, triglycerides, and uric acid showed moderate positive associations with cardiovascular outcomes, while the triglyceride-to-HDL ratio and fasting blood glucose had weaker but significant correlations. These findings highlight lipid profiles and metabolic markers as key contributors to cardiovascular risk. This study highlights significant correlations between LDL cholesterol, fasting blood glucose, uric acid, triglycerides, and the triglyceride/HDL ratio with 10-year cardiovascular risk. These findings emphasize the importance of lipid profiles, glycemic control, and metabolic markers in predicting coronary outcomes and guiding targeted preventive interventions for improved cardiovascular risk management.

BACKGROUND The association between uric acid to high-density lipoprotein cholesterol ratio (UHR) and abdominal aortic calcification (AAC) is not fully understood. This study aimed to explore the potential association between UHR and AAC in adults older than 40 years. METHODS In this cross-sectional study, data were collected from the 2013 to 2014 National Health and Nutrition Examination Survey (NHANES). UHR equals uric acid (mg/dL) divided by high-density lipoprotein cholesterol (mg/dL). We used weighted multiple logistic regression or linear regression analysis to investigate the association between UHR and AAC. We conducted subgroup and interaction analyses to investigate whether these associations varied by different confounders. Receiver operating characteristic curve studies were used to compare the diagnostic power of the Framingham scoring model with the Framingham and UHR models for AAC and severe abdominal aortic calcification (SAAC). Sensitivity analyses to determine the robustness of the UHR and AAC association results. RESULTS The final evaluation covered 2294 participants older than 40 years (mean age: 59.01 years; 52.57% female). A 1-unit rise in the log-UHR led to a 0.80 increase in the AAC scores (β [95% CI]: 0.80 [0.46, 1.13]) and a 90% higher risk of AAC (odds ratio [OR] [95% CI]: 1.90 [1.42, 2.54]), and the risk of SAAC increased by 95% (OR [95% CI]:1.95 [1.37, 2.77]). Subgroup analyses showed that the association between log-UHR and AAC scores with SAAC varied by sex. CONCLUSIONS This study identified a positive association between UHR and AAC risk, whereas the association of UHR with AAC scores and SAAC was significant only in the female subgroup.

BACKGROUND The association between the serum uric acid-to-high-density lipoprotein cholesterol ratio (UHR) and cardiovascular disease (CVD) risk in Asian populations with metabolic dysfunction-associated steatotic liver disease (MASLD) remains insufficiently elucidated. AIM To investigate the relevance and dose-responsive relationship between UHR and 10-year CVD risk among Asian MASLD patients. METHODS In this retrospective analysis, 3901 MASLD patients were enrolled based on established screening criteria. As measured by the Framingham risk score, participants were stratified according to their 10-year CVD risk. The association between UHR and CVD risk was evaluated using binary logistic regression, while dose-response patterns were explored through restricted cubic spline (RCS) modeling. The discriminatory capability of UHR, in comparison with conventional biomarkers, was further examined by receiver operating characteristic curve analysis. RESULTS Multivariable-adjusted analyses revealed that elevated UHR levels were significantly associated with an increased likelihood of intermediate-to-high CVD risk. RCS modeling demonstrated a linear dose-response relationship between UHR and the Framingham risk score (P for nonlinearity = 0.114). Sex-stratified RCS analyses further indicated that this linear association persisted among males (P for nonlinearity = 0.167) but was not statistically significant in females (P for nonlinearity = 0.476). Further stratified analyses revealed that the association was particularly pronounced among younger individuals (< 50 years), males, and those with central obesity, whereas it was attenuated in older adults (≥ 50 years) and females. Receiver operating characteristic analysis demonstrated that UHR outperformed individual biomarkers in predicting 10-year CVD risk, showing an area under the curve of 0.655 (95% confidence interval: 0.635-0.674). CONCLUSION UHR functioned as an independent predictor of 10-year CVD risk in Asian patients with MASLD, demonstrating a linear dose-response association and superior discriminative performance relative to conventional biomarkers, especially among younger individuals, males, and those with central obesity.

Background: Studies exploring the relationship between serum uric acid (sUA) and cardiovascular risk in the Nigerian population remain sparse. The study aimed to assess the association between sUA levels and two measures of cardiovascular risk, namely the Framingham 10-year Cardiovascular Risk Score (FRS) and the Atherogenic Index of Plasma (AIP). Methods: This retrospective study used data from clinical records of new, previously unregistered patients presenting at a private cardiac hospital over one year from November 2022 to October 2023. In total, 428 patients presented newly to the hospital in that period. The records of 138 patients were included in the project after various exclusions were made including for incomplete anthropometric and laboratory data. Statistical tests of association were used to determine the significance of the relationship between sUA levels and the measures of cardiovascular risk. Two-tailed p <0.05 was deemed statistically significant. Results: Hyperuricemia was more prevalent in individuals with central obesity, i.e., waist circumference ≥94cm in males or 80cm in females (93.4% vs 6.6%; p=0.03). Serum uric acid also positively correlated with FRS (correlation coefficient: 0.190; p<0.05) and serum triglyceride levels and AIP (correlation coefficient: 0.259 and 0.294, respectively; p<0.001 for both). After multivariate analyses, uric acid was significantly and independently associated with high FRS and AIP after adjusting for age, smoking and diabetes history, blood pressure, total and high-density lipoprotein cholesterol, serum triglycerides and waist circumference (p<0.001). Conclusion: The results emphasize the emergence of sUA as a pertinent cardiovascular risk factor in clinical settings. More research is needed to deduce the relationship, if any, between cardiovascular risk reduction and pharmacological reduction of sUA levels.

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BACKGROUND AND AIMS Serum uric acid (SUA) is involved in the development of cardiovascular disease (CVD). However, information on the dose-response relationship between SUA and CVD is limited in the Chinese population. This study aimed to investigate the potential nonlinear dose-response association of SUA with CVD risk in a Chinese population and to explore the effect of sex on these associations. METHODS AND RESULTS Cross-sectional data, from 6252 Chinese adults aged 30-74 years who participated in the China Health and Nutrition Survey 2009, were stratified by SUA deciles. The 10-year risk of CVD was determined using the Framingham risk score. A restricted cubic spline (RCS) was incorporated into the logistic models to assess the nonlinear relationship between SUA and CVD. Among the participants, 65%, 20%, and 15% had low, moderate, and high 10-year CVD risks, respectively. Compared with the reference SUA strata of 225 to <249 μmol/L, CVD risk was significantly increased at SUA ≥294 μmol/L, with adjusted ORs ranging from 2.39 (1.33-4.33) to 4.25 (2.37-7.65). An increasingly higher nonsignificant CVD risk was found at SUA <225 μmol/L and showed a nonlinear U-shaped association. In the fitted RCS model, an approximate U-shaped association between SUA and CVD risk scores was found in women, but this significant nonlinear relationship was not found in men. CONCLUSION This study showed that both lower and higher SUA levels were associated with a higher 10-year CVD risk among Chinese adults, forming a U-shaped relationship, and this pattern was particularly pronounced for women.

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Non-alcoholic fatty liver disease (NAFLD) and serum uric acid (SUA) levels are risk factors for developing cardiovascular disease (CVD). Additionally, previous studies have suggested that high SUA levels increase the risk of having NAFLD. However, no study has investigated the relationship between SUA and CVD risk in NAFLD. This study analyzed the relationship between SUA and CVD in NAFLD. Data for this study used the 2016–2018 Korean National Health and Nutrition Examination Survey, which represents the Korean population. A total of 11,160 NAFLD patients were included. Participants with hepatic steatosis index ≥ 30 were considered to have NAFLD. Ten-year CVD risk was estimated using an integer-based Framingham risk score. Estimated 10-year CVD risk ≥ 20% was considered high risk. Multiple logistic regression was conducted to calculate the odds ratios (ORs) associated with SUA level and CVD risk. High CVD risk OR increases by 1.31 (95% CI 1.26–1.37) times per 1 mg/dL of SUA. After adjustment, SUA still had an increased risk (OR 1.44; 95% CI 1.38–1.51) of CVD. Compared with the lowest SUA quartile group, the highest quartile group showed a significantly higher risk of having CVD before (OR 2.76; 95% CI 2.34–3.25) and after (OR 4.01; 95% CI 3.37–4.78) adjustment. SUA is independently associated with CVS risk in NAFLD.

Background: Previous studies have demonstrated an association between hyperuricemia and cardiovascular disease (CVD). The Framingham study confirmed that patients with high atherosclerotic risks (HARs) had worse prognoses. However, after adjusting for confounding factors, the association between serum uric acid (SUA) and all-cause mortality and cardiovascular mortality remains unclear, especially for HAR patients. Objective: The aim of this study was to reveal the relationship of SUA with all-cause and cardiovascular mortality in HAR patients. Methods: This multicenter cohort study enrolled 3,047 participants, and the follow-up was 68.85 ± 11.37 months. Factors related to cardiovascular and all-cause mortality were tested by multivariate Cox regression analysis. Restricted cubic splines (RCSs) with knots were used to explore the shape of the dose–response relationship with SUA and the hazard ratio (HR) of all-cause and CVD mortality. SUA transformed by RCS was added to the Cox regression model as an independent variable, and all-cause and CVD mortality scores were calculated. Survival receiver operating characteristic curves were produced using a regression model predicting the score. Results: SUA demonstrated a “U-shaped” relationship with all-cause and cardiovascular mortality. SUA predicted all-cause and CVD mortality, with cutoff values of values of >370.5 μmol/L for males and >327.65 μmol/L for females and <180.5 μmol/L for males and <165.7 μmol/L for females, respectively. The survival ROC curve indicated that SUA is able to predict all-cause and CVD mortality, with areas under the curve of 0.702 and 0.711, respectively. The HRs of all-cause mortality (male and female) with hyperuricemia and hypouricemia were 2.08 and 2.01 and 2.04 and 1.98, respectively, and the HRs of CVD mortality (male and female) were 2.09 and 1.79, and 2.02 and 1.89, respectively. Conclusion: Abnormal SUA levels were significant and independent risk factors for all-cause and CVD mortality. Hyperuricemia and hypouricemia increased mortality in both males and females. Routine SUA evaluation and intensive management are needed for HAR patients. Clinical Trial Registration: www.ClinicalTrials.gov, identifier: NCT03616769.

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Objective Advanced glycation end-products (AGEs) may contribute to the pathogenesis of atherosclerotic cardiovascular disease (ASCVD), potentially influencing its development and progression differently at various life stages. This study aimed to elucidate the associations between AGEs and the risk of ASCVD across different age groups. Methods In this cross-sectional study, 1,240 subjects were enrolled and divided into three groups (Group Ⅰ, 20–39 years old, n = 468; Group Ⅱ, 40–59 years old, n = 471; Group Ⅲ, 60–79 years old, n = 301). Skin AGEs were measured by skin autofluorescence (SAF). ASCVD risk was assessed by a validated Framingham risk score calculator. Other proven ASCVD risk factors were also measured, including glycosylated hemoglobin, uric acid, lipid profile, homocysteine, and cystatin C. Results An increasing trend in skin AGEs was observed from Group Ⅰ to Group Ⅲ. Skin AGEs were significantly associated with ASCVD risk in all subjects (OR 1.029, 95% CI 1.003–1.056, P = 0.018), independent of some of the proven cardiovascular risk factors. This association was particularly significant in individuals aged 40–59 and 60–79 (OR = 1.047, 95% CI: 1.025–1.069; OR = 1.022, 95% CI: 1.002–1.042; both P < 0.05). ROC analysis showed that skin AGEs predicted the diagnosis of medium or high ASCVD risk in the pooled group, Group Ⅱ, and Group Ⅲ. Conclusion Our study substantiates that skin AGEs play an important role as an independent risk factor for ASCVD, highlighting their significance beyond traditional risk assessment models, particularly in middle-aged and older populations.

Background End-stage kidney disease (ESRD) patients on dialysis face pronounced cardiovascular and metabolic risks due to disruptions in lipoprotein(a), phosphorus, potassium, uric acid, and lipid balance. Current therapeutic options offer limited capacity to address these multifaceted abnormalities. Niacin is unique in this regard, as it not only lowers lipoprotein(a) but also influences phosphorus and uric acid metabolism. This study evaluates the efficacy of niacin therapy in improving these biochemical markers, thereby addressing an important therapeutic gap in this vulnerable population. Methods In a randomized, controlled trial, 50 hemodialysis patients were divided into two groups of twenty-five each. The control group continued standard care, while the niacin group received 500 mg/day niacin alongside standard therapy. Patients were followed for 3 months. Results Systolic and diastolic blood pressure were stabilized by niacin administration, in contrast to the control group, where both parameters rose significantly. Phosphorus decreased significantly in the niacin group (5.59 to 4.85 mg/dL, P = 0.0077), while increasing in controls. PTH levels decreased by 60% with niacin but rose by 41.6% in controls (P = 0.001). Potassium levels fell by 27% in the niacin group, whereas they rose by 23.9% in controls. Sodium remained stable with niacin but declined in controls. Uric acid levels rose sharply in controls but remained stable with niacin. Niacin significantly improved lipid profiles, notably reducing LDL (31.9% vs. 7.9%) and total cholesterol (13.3% vs. 3.7%). Although triglycerides and VLDL rose in both groups, these variations were not of statistical significance. Importantly, Lp(a) levels decreased by 11.4% in the niacin group. Conclusion Niacin (500 mg/day) offers significant cardiovascular and metabolic benefits for hemodialysis patients, supporting its role as an adjunctive therapy in managing ESRD-associated risks. Clinical trial registration https://clinicaltrials.gov/, NCT06406140

BACKGROUND AND AIMS Both elevated serum uric acid (SUA) and peripheral endothelial dysfunction (PED) are associated independently with cardiovascular disease (CVD). However, the association between SUA and PED is yet to be established. We hypothesized that high normal range of SUA is associated with PED. METHODS We performed a retrospective cross-sectional analysis of patients who were referred to Mayo Clinic between 2006 and 2014 for routine cardiovascular evaluation and who underwent evaluation of Reactive Hyperemia Peripheral Arterial Tonometry (index <2 consistent with PED). A high UA was defined as ≥5 mg/dL, in keeping with previous studies evaluating the link between SUA and CVD outcomes. RESULTS One hundred forty patients were included (mean age 50.7 ± 12.9 years, 86 (61.4%) female). Twenty four patients (17.1%) had pre-existing CVD (8 (9.3%) in females). Thirty patients (21.6%) had a Framingham score > 10% (8 (9.4%) in females). Fifty eight (41.4%) had PED and 77 (55.0%) had an elevated SUA. SUA levels were higher in patients with PED compared to those without (5.5 ± 1.4 vs 4.8 ± 1.2 mg/dL; p = 0.004). In an univariate analysis, elevated SUA levels were associated with PED (Odds Ratio (OR): 2.7; 95% confidence interval [CI] 1.33-5.48; p = 0.005). In a multivariate analysis adjusting for age, sex, presence of obstructive CVD and Framingham score>10, elevated SUA levels were associated with PED (OR 2.45; 95% CI 1.08-5.52; p = 0.031). After stratifying by sex, this association persisted in females only. CONCLUSIONS High normal SUA levels are associated with PED in women who are otherwise at low risk for CVD. Thus, SUA is a promising circulating biomarker that could be used to assist in risk stratification in female patients with chest pain and/or those undergoing evaluation of CVD risk.

Serum uric acid level is a risk factor for cardiovascular disease (CVD). However, whether it is an independent risk factor or not remains controversial. We analyzed the association between serum uric acid level and cardiovascular risk. In total, 973 nonhypertensive and nondiabetic participants in the I-Lan Longitudinal Aging Study were eligible for this study. Subjects were divided into tertiles according to uric acid levels. The 10-year cardiovascular risk was calculated using Framingham risk score (FRS). Study subjects in the highest tertile of serum uric acid level were older, more likely to be male, and had higher systolic blood pressure, body mass index, carotid artery intima–media thickness and serum triglyceride, high-sensitivity C-reactive protein, and low-density lipoprotein cholesterol levels and lower serum high-density lipoprotein cholesterol levels (all p < 0.05). Subjects in the highest tertile had significantly higher FRS (p < 0.001). After adjusting for other risk factors, serum uric acid level remained associated significantly with the FRS (p < 0.05). In binary logistic regression analysis, the serum uric acid level was an independent predictive factor for high (≥20%) FRS (odds ratio 1.33, 95% confidence interval 1.10–1.68). These findings warrant attention to this cardiovascular risk factor in apparently healthy adults.

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Background Serum uric acid (SUA) is an important predictor of cardiovascular events and mortality. The ABCG2 rs2231142 variant (TT genotype) is associated with hyperuricemia (HUA), but the relationship between ABCG2 gene polymorphisms and coronary artery disease (CAD) risk is poorly elucidated. We investigated the association between ABCG2 rs2231142 genetic variants and the Framingham Risk Score for Cardiovascular Disease (FRS-CVD) in a Taiwanese population. Methods This cross-sectional study enrolled 139,508 Taiwanese participants aged 30–70 years based on data from the Taiwan Biobank (TWB) database that was obtained from questionnaires, laboratory investigations, anthropometry, and Affymetrix TWB genome-wide single-nucleotide polymorphism (SNP) chip data analysis. The association between ABCG2 rs2231142 and FRS-CVD risk was evaluated using logistic regression analysis. Results Compared to those with the GG genotype, participants with the ABCG2 rs2231142 TT genotype had a significantly lower systolic blood pressure, smoking rate, body mass index, triglyceride level, waist circumference, waist–hip ratio, and body fat percentage, but had higher high-density lipoprotein cholesterol level. Despite the same FRS-CVD score, participants with TT genotypes had higher SUA. Even with the same SUA, TT carriers had a lower FRS-CVD than GT and GG carriers. Participants with the TT genotype had significantly lower CVD risk, particularly female participants with HUA and BMI <27 (OR: 0.760, 95 % CI: 0.587–0.985; p = 0.0381) group. Conclusion The ABCG2 rs2231142 TT genotype is associated with a lower FRS-CVD, particularly in non-obese hyperuricemic female individuals. The complicated interplay among genetic variations, metabolic profile, and CVD risk provides insights for precision health.

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Background: Data are limited on the prevalence, distribution, and extent of subclinical atherosclerosis (SCA) in populations with primary hypertension and an in-depth evaluation is required to explore the impact of elevated serum uric acid (SUA) levels on the systemic extent of SCA. Methods: A total of 1,534 individuals with blood pressure-controlled primary hypertension registered from January 1, 2015 to May 31, 2018 were included. The systemic extent and risk factors of SCA in the carotid, coronary, thoracic, and renal territories were investigated by Doppler ultrasound and computed tomography. Results: SCA was present in 85.9% of patients. The proportion of focal, intermediate and generalized SCA was 17.9, 21.3, and 46.6%. Plaques were most common in the thoracic aorta (74%), followed by the coronary (55.3%), carotid (51.6%), and renal (45.8%) arteries, respectively. Participants were stratified into quartiles based on gender-specific SUA levels. Compared with patients in the first quartile, the Odds Ratio (OR) [95% confidence interval] for SCA in the second, third and fourth quartile were 1.647 (1.011–2.680), 3.013 (1.770–5.124), and 5.081 (3.203–10.496), respectively. Patients with elevated SUA levels at high 10-year Framingham risk had a higher likelihood of a more severe risk of SCA (95.8%). However, extensive SCA was also present in a substantial number of low 10-year-Framingham risk patients at the higher quartiles of SUA (53.8%). Conclusions: SCA was highly prevalent in the hypertension population and the thoracic aorta was the most frequently affected vascular site. Elevated SUA concentration was significantly associated with the prevalence and severity of SCA regardless of territories.

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Human serum uric acid concentration (SUA) is a complex trait. A recent meta-analysis of multiple genome-wide association studies (GWAS) identified 28 loci associated with SUA jointly explaining only 7.7% of the SUA variance, with 3.4% explained by two major loci (SLC2A9 and ABCG2). Here we examined whether gene–gene interactions had any roles in regulating SUA using two large GWAS cohorts included in the meta-analysis [the Atherosclerosis Risk in Communities study cohort (ARIC) and the Framingham Heart Study cohort (FHS)]. We found abundant genome-wide significant local interactions in ARIC in the 4p16.1 region located mostly in an intergenic area near SLC2A9 that were not driven by linkage disequilibrium and were replicated in FHS. Taking the forward selection approach, we constructed a model of five SNPs with marginal effects and three epistatic SNP pairs in ARIC—three marginal SNPs were located within SLC2A9 and the remaining SNPs were all located in the nearby intergenic area. The full model explained 1.5% more SUA variance than that explained by the lead SNP alone, but only 0.3% was contributed by the marginal and epistatic effects of the SNPs in the intergenic area. Functional analysis revealed strong evidence that the epistatically interacting SNPs in the intergenic area were unusually enriched at enhancers active in ENCODE hepatic (HepG2, P = 4.7E−05) and precursor red blood (K562, P = 5.0E−06) cells, putatively regulating transcription of WDR1 and SLC2A9. These results suggest that exploring epistatic interactions is valuable in uncovering the complex functional mechanisms underlying the 4p16.1 region.

BACKGROUND The prevalence of coronary heart disease (CHD) is higher in patients with depression than in the general population. Recently, multiple novel biomarkers have been proposed to predict CHD risk, and these factors have been reported to be altered in patients with depression. AIM To explore whether these new biomarkers are associated with an increased risk of CHD in patients with depression. METHODS We recruited 279 healthy controls and 164 sex- and age-matched patients with depression and collected their clinical characteristics and laboratory values of novel cardiovascular biomarkers. The Framingham CHD risk score was used to assess the CHD risk of all individuals, and the cardiovascular markers related to the CHD risk in patients with depression were analyzed. RESULTS Patients with depression had an increased CHD risk of 5.3% (95% confidence interval: 4.470-6.103) and altered novel cardiovascular biomarkers compared to healthy controls, which included lower levels of thyroid stimulating hormone, albumin, total bilirubin, total cholesterol, high-density lipoprotein cholesterol, and higher levels of triglyceride (TG) and uric acid. Further regression analysis showed that illness duration, family history of depression, serum TG, and urea acid levels were significantly correlated with the Framingham risk score in patients with depression. CONCLUSION Patients with depression had a higher CHD risk and that their illness duration, family history of depression, serum TG, and uric acid levels could play important roles in predicting CHD risk. Moreover, elevated CHD risk in patients with depression was not only related to physiological changes caused by depression but also to their genetic susceptibility.

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BACKGROUND Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout. METHODS Genome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant single nucleotide polymorphisms (SNPs) were replicated in white (n=11 024) and black (n=3843) individuals who took part in the study of Atherosclerosis Risk in Communities (ARIC). The SNPs that reached genome-wide significant association with uric acid in either the Framingham cohort (p<5.0 x 10(-8)) or the Rotterdam cohort (p<1.0 x 10(-7)) were evaluated with gout. The results obtained in white participants were combined using meta-analysis. FINDINGS Three loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric acid. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7.0 x 10(-168) and 2.9 x 10(-18) for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2.5 x 10(-60) and 9.8 x 10(-4)), and rs1165205 in SLC17A3 (p=3.3 x 10(-26) and 0.33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0.59 per T allele, 95% CI 0.52-0.68, p=7.0 x 10(-14)), rs2231142 (1.74, 1.51-1.99, p=3.3 x 10(-15)), and rs1165205 (0.85, 0.77-0.94, p=0.002). In black participants of the ARIC study, rs2231142 was direction-consistent with gout (1.71, 1.06-2.77, p=0.028). An additive genetic risk score of high-risk alleles at the three loci showed graded associations with uric acid (272-351 mumol/L in the Framingham cohort, 269-386 mumol/L in the Rotterdam cohort, and 303-426 mumol/L in white participants of the ARIC study) and gout (frequency 2-13% in the Framingham cohort, 2-8% in the Rotterdam cohort, and 1-18% in white participants in the ARIC study). INTERPRETATION We identified three genetic loci associated with uric acid concentration and gout. A score based on genes with a putative role in renal urate handling showed a substantial risk for gout.

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BACKGROUND Microalbuminuria has been linked to cardiovascular (CV) risk in patients with diabetes or hypertension, and in an unselected general population; serum uric acid (UA) is emerging as a novel risk factor for CV disease. The aim of our study was to evaluate the prevalence of excess microalbuminuria and its relation to established CV risk factors and serum UA in healthy subjects. METHODS We screened 900 healthy blood donors (age range, 20-65 years; 747 men, 153 women), and measured total, HDL and LDL cholesterol, blood glucose, serum and urinary creatinine, serum UA, blood pressure (BP) and microalbuminuria (urinary albumin/creatinine ratio, ACR). The Framingham risk score was also calculated. RESULTS After excluding 52 participants, we found that in 848 participants (702 men, 146 women) the overall prevalence of excess ACR, using a 30 mg/g creatinine cutoff, was 9.3% (9.7% of men, 7.5% of women, p=0.16); adopting a gender-dependent cutoff, we found that the overall prevalence was 13.6% (15.1% of men, 6.2% of women, p<0.01). ACR was highly correlated to diastolic (r=0.88, p<0.001) and systolic (r=0.74, p<0.001) BP, and also--though not as strongly--to serum UA (r=0.38, p<0.001). In a stepwise multiple regression model, systolic and diastolic BP, total cholesterol, serum creatinine and UA were segregated as independent predictors of microalbuminuria (model R=0.91, R square=0.83). Correlation of serum UA to ACR remained significant, albeit attenuated (r=0.09, p=0.02), after adjustment for serum creatinine, total cholesterol, systolic and diastolic BP. CONCLUSIONS The results of our study show ACR to be abnormal in a significant proportion of seemingly healthy subjects, and serum UA to be an independent predictor of microalbuminuria.

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Objective To investigate the relationship between hyperuricemia and coronary heart disease (CHD) risk based on the Framingham risk score (FRS) in a middle-aged and elderly Chinese population. Methods This cross-sectional study enrolled patients undergoing routine check-ups at Xiangya Hospital between October 2013 and November 2014. Hyperuricemia was defined as uric acid ≥416 mmol/l for males and ≥360 mmol/l for females. A 10-year CHD risk was calculated from FRS. A multivariable logistic analysis model was used to evaluate associations. Results Of the 6347 patients, 3415 (53.8%) were male, 1543 (24.3%) had a CHD risk ≥10% (i.e. intermediate and high risk) and the prevalence of hyperuricemia was 18.1% (n = 1148). After adjusting for potential confounding factors, the 10-year CHD risk was increased in patients with hyperuricemia compared with those without hyperuricemia by 0.28 times in the total population (odds ratio [OR] 1.28; 95% confidence interval [CI] 1.09, 1.48), by 0.25 times in the male population (OR 1.25; 95% CI 1.06, 1.47) and by 2.76 times in the female population (OR 3.76; 95% CI 2.08, 6.79). Conclusion Hyperuricemia was positively associated with a 10-year risk of CHD suggesting that it might be an independent CHD risk factor in middle-aged and elderly individuals.

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Background and objective Given the enormous public health burden posed by acute ischemic stroke (AIS), it becomes imperative to identify associated risk factors such as serum uric acid (SUA) and lipid profile that can be tangibly assessed. This could potentially provide useful markers for disease risk or progression, facilitating timely diagnosis and management of AIS. This study aimed to evaluate the SUA and lipid levels in patients with AIS. Method This cross-sectional study enrolled 66 AIS patients aged >18 years, from both genders. After a thorough medical history and clinical examination, each patient was subjected to SUA analysis and lipid profiling using an auto-analyzer with dedicated reagents. Results were statistically analyzed using Chi square test, and p-value ≤0.05 indicated statistical significance. Results and interpretation The study cohort showed a mean age of 61.17 ± 14.01 years and male to female (M:F) ratio of 1.7:1, with mean blood levels of SUA, triglyceride, and high-density lipoprotein (HDL) reaching 5.68 ± 1.71 g/dL, 205.42 ± 105.08 g/dL, and 29.80 ± 8.45 g/dL, respectively. Most patients suffered from hypertension (81.82%), diabetes (77.27%), and alcoholism (24.24%). Cerebrovascular Doppler findings revealed the combined presence of plaque and stenosis (24.24%). Male AIS patients showed a significantly greater association with alcohol and smoking/nicotine use (p<0.001). Gender showed no significant association with SUA, lipid profile, hypertension, and diabetes (p>0.05). Conclusion AIS is associated with hyperuricemia and dyslipidemia, with no significant gender differences.

The life expectancy and the risk of developing cardiovascular diseases in patients with inborn errors of immunity are systematically increasing. The aim of the study was to assess cardiovascular risk factors and to evaluate the heart in echocardiography in patients with primary antibody deficiency (PAD). Cardiac echography and selected cardiovascular risk factors, including body mass index, sedentary lifestyle, nicotine, glucose, C-reactive protein, lipid profile, uric acid level, certain chronic diseases, and glucocorticoid use, were analyzed in 94 patients >18 years of age with PAD. Of the patients,25.5% had a cardiovascular disease (mostly hypertension, 18%), 10.5% smoked, 17% were overweight, 14% were obese, and 15% were underweight. Abnormal blood pressure was found in 6.5% of the patients. Lipid metabolism disorders were found in 72.5% of in the studied cohort, increased total cholesterol (45.5%), non-high-density lipoprotein (HDL) (51%), low-density lipoprotein (LDL) (47%), and triglycerides (32%) were observed. Furthermore, 28.5% had a decrease in HDL and 9.5% had a history of hyperuricemia. The average number of risk factors was 5 ± 3 for the entire population and 4 ± 2 for those under 40 years of age. Elevated uric acid levels were found de novo in 4% of participants. In particular, 74.5% of the patients had never undergone an echocardiogram with a successful completion rate of 87% among those tested. Among them, 30% showed parameters within normal limits, primarily regurgitation (92.5%). New pathologies were identified in 28% of patients. Prevention in patients with PAD, aimed at reducing cardiovascular risk, should be a priority.

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BackgroundLesch-Nyhan disease is a rare X-linked neurodevelopemental metabolic disorder caused by a wide variety of mutations in the HPRT1 gene leading to a deficiency of the purine recycling enzyme hypoxanthine-guanine phosphoribosyltransferase (HGprt). The residual HGprt activity correlates with the various phenotypes of Lesch-Nyhan (LN) patients and in particular with the different degree of neurobehavioral disturbances. The prevalence of this disease is considered to be underestimated due to large heterogeneity of its clinical symptoms and the difficulty of diagnosing of the less severe forms of the disease. We therefore searched for metabolic changes that would facilitate an early diagnosis and give potential clues on the disease pathogenesis and potential therapeutic approaches.MethodsLesch-Nyhan patients were diagnosed using HGprt enzymatic assay in red blood cells and identification of the causal HPRT1 gene mutations. These patients were subsequently classified into the three main phenotypic subgroups ranging from patients with only hyperuricemia to individuals presenting motor dysfunction, cognitive disability and self-injurious behavior. Metabolites from the three classes of patients were analyzed and quantified by High Performance Ionic Chromatography and biomarkers of HGprt deficiency were then validated by statistical analyses.ResultsA cohort of 139 patients, from 112 families, diagnosed using HGprt enzymatic assay in red blood cells, was studied. 98 displayed LN full phenotype (86 families) and 41 (26 families) had attenuated clinical phenotypes. Genotype/phenotype correlations show that LN full phenotype was correlated to genetic alterations resulting in null enzyme function, while variant phenotypes are often associated with missense mutations allowing some residual HGprt activity. Analysis of metabolites extracted from red blood cells from 56 LN patients revealed strong variations specific to HGprt deficiency for six metabolites (AICAR mono- and tri-phosphate, nicotinamide, nicotinic acid, ATP and Succinyl-AMP) as compared to controls including hyperuricemic patients without HGprt deficiency.ConclusionsA highly significant correlation between six metabolites and the HGprt deficiency was established, each of them providing an easily measurable marker of the disease. Their combination strongly increases the probability of an early and reliable diagnosis for HGprt deficiency.

The lifespan of schizophrenia (SCZ) patients is considered 25 years shorter compared to the general population, primarily due to cardiovascular (CV) disease. This study aims to assess the CV profile of the SCZ inpatients from Psychiatry Clinic I and II of Cluj-Napoca between 2018-2019. Methods: The following indicators were documented from interview and laboratory data: arterial hypertension (AHT), smoking, dyslipidemia, obesity, metabolic syndrome (MS), medication adherence (MA), Framingham score (FS), and CV diagnosis (CVd). The sample was separated into two groups based on FS and CV diagnosis: high-risk/CVd and medium/low-risk. Results: 50 SCZ patients were included in the study. 58% had AHT and 10% were prediagnosed, 90% had lipids perturbations of which 26.7% were prediagnosed, 66 % met the criteria for MS from which one prediagnosis, 12% had a CVd and the average FS was 12.7% corresponding to intermediate risk category. MA subjects had a lower risk to be in the high risk/CVd group (OR=1/0.22, p=0.02) and no association was found for the gender-CV risk categories (p=0.08). Conclusion: 1. The known CV risk factors are underdiagnosed in SCZ patients 2. SCZ might attenuate the gender CV risk stratification; and 3. MA might decrease the CV risk in SCZ.

Context Data on cardiovascular risk (CVR) score among HIV-infected patients in sub-Saharan Africa are scarce. Our first objective was to compare the CVR score of Framingham utilizing BMI and lipids at baseline, and secondary to assess evolution of CVR score over time at Month 30 in the Temprano trial. Methods HIV-infected adults with CD4 <800/mm3 without criteria for initiating ART were included and followed for 30 months in the Temprano trial, which assessed the benefits and risks of early antiretroviral treatment (ART) vs deferred ART. CVR score was estimated at baseline and Month-30 using Framingham equations with either BMI or lipids and classified as high (>20%), moderate (10–20%), and low risk (<10%). At baseline, we compare these two estimations utilizing the Pearson correlation test and analyze the increasing CV risk score over time by Proportional odds cumulative logit models for people attending the Month-30 (M30) visit. Results Among the 2056 patients, 78% were women, median age was 35 years, and median CD4 count was 464/mm3, 6.8% were obese, 6.3% had hypertension, 7.8% were smokers (1.8% women, 26.8% men), 19% had Total Cholesterol (TC) >5mmol/L, and 1% diabetes at baseline. At baseline the concordance between the two Framingham equations was excellent (r = 0.95; p<0.0001). Among the 1700 patients who attended M30 visit and with available data, 1.3% had a high CV risk score at baseline and 3.1% at M30 visit using Framingham equation with BMI. Adjusted odds ratio (aOR) of being at a higher CV risk score at M30 visit compared to a higher CV risk score at M0 visit was 1.35 (CI 95% 1.17–1.57). Stratified by sex, the increasing CV risk score was OR 1.73 (CI 95%: 1.30–2.29) for women and OR 1.24 (CI 95%: 1.02–1.50) for men. Early ART was not associated with an increasing CV risk score (p = 0.88). Results for the 1422 patients with Framingham equation using lipids were similar. Conclusion In a large trial evaluating early ART for HIV infection in Côte d’Ivoire, Framingham equation with BMI and lipids were highly correlated and CV risk score increases over time. Early ART was not significantly associated with this increasing CV risk score.

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Background: Cardiovascular diseases (CVD) and related deaths are on the rise. An efcient way to curb the mortalities by CVD is early detection of the atherosclerotic plaques for which carotid & femoral doppler bilateral B-mode ultrasound can be used to detect plaque in measure the IMT (intima-media thickness). In asymptomatic patients suspected to have subclinical atherosclerosis, scores like Framingham risk score (FRS) can be calculated in order to predict 10 years risk. This study focuses on Objectives: estimating the prevalence of plaque and future risk of atherosclerotic complications in asymptomatic population and measuring the intimamedia thickness (IMT) of common carotid artery and common femoral artery with its age specic distribution as an index of subclinical atherosclerosis/CVD and correlate it with lipid prole. It also calculates 10-year risk via FRS and the predictive value of CCA-IMT, CFA-IMT and the Framingham risk score (FRS) for plaque formation in an Indian population of 200 subjects who underwent ultrasonography of both carotid and femoral arteries. Screening of extracranial carotid system and femora Study design: l arterial bed with B-mode ultrasound was performed in 200 asymptomatic patients as preventive cardiac check-up and those with relevant family history. Measurements of IMT were recorded over a 1 cm segment in the far wall of the arteries; the prevalence of plaque (focal IMT > 1.5 mm) was studied. Imaging results were correlated with lipid prole. FRS was calculated for each patient. A total of 21 (10.5%) subjects ha Results: d atherosclerotic plaques. Out of which 13 (6.5%) had right carotid plaques; 11 (5.5%) had left carotid plaques; 7 (3.5%) had right femoral plaques; 6 (3%) had left femoral plaques. The mean right CIMT was 0.686 +/- 0.1687 mm (0.4-1.4mm); the mean left CIMT was 0.684 +/- 0.1640 mm (0.4-1.2 mm); the mean right CFIMT was 0.598 +/- 0.1567 mm (0.4 to 1.6mm); the mean left CFIMT was 0.573 +/- 0.1343 mm (0.4 to 1.2mm) . Signicantly higher mean right CIMT was observed in high FRS as compared to intermediate and low FRS grade. Early screening for subclinical Conclusions: atherosclerosis is feasible with doppler ultrasound and correlates with lipid prole (LDL, triglycerides and cholesterol). Both CIMT, CFIMT independently predict incident plaque burden beyond traditional risk factors and correlate with FRS.

Chronic kidney disease became a public health problem increasing healthcare burden. Our aim was to detect the relationship between cardiovascular risk, endothelial dysfunction, inflammation, and kidney function in chronic kidney disease patients and to detect the nontraditional factors affecting the decline in kidney functions. A cross-sectional study including 30 male and female patients with chronic kidney disease stages 3–5. Creatinine clearance and Framingham risk score points were calculated. Carotid intimal medial thickness was measured as well as absolute flow mediated dilatation in brachial artery. Highly sensitive C-reactive protein, parathyroid hormone, kidney function tests, and lipid profile were measured. Framingham risk score points and carotid intimal medial thickness increased significantly with decreasing creatinine clearance (p 0.0025, 0.0285) respectively. A significant correlation was found between highly sensitive C-reactive protein and Framingham risk score points but not with carotid intimal medial thickness (p 0.0043, 0.2229) respectively. An inverse correlation was found between creatinine clearance and highly sensitive C-reactive protein (p 0.0174). Absolute flow mediated dilatation in brachial artery decreases with increasing Framingham risk score points and decreasing creatinine clearance (p 0.0044, 0.0269) respectively. There is correlation between chronic kidney disease and impaired vascular function, subclinical atherosclerosis, and heightened inflammatory response. Chronic kidney disease patients are at increased risk of cardiovascular events with higher [10-]year cardiovascular risk.

Epidemiological and genetic studies have pointed to the role of cholesterol in Alzheimer’s disease (AD). We explored the interaction of a genetic risk score (GRS) of AD risk alleles with mid-life plasma lipid levels (LDL-C, HDL-C, and triglycerides) on risk for AD in the Framingham Heart Study (FHS). Mid-life (between the ages of 40–60 years old) lipid levels were obtained from individuals in the FHS Original and Offspring cohorts (157 cases and 2,882 controls) with genetic data and AD status available. Cox proportional hazards regression was performed to test the interaction between mid-life lipid levels and an AD GRS, as well as the individual contributing SNPs, on risk of incident AD adjusting for age, sex, and cohort. We found a significant interaction between a GRS of AD loci and log triglyceride levels on risk of clinical AD (p = 0.006), but no interaction of the GRS with HDL-C (p = 0.458) or LDL-C (p = 0.366). We then tested the interaction between the individual SNPs contributing to the GRS and log triglycerides. We found two SNPs that had interactions with triglycerides on AD risk that reached a p-value < 0.05 (rs11218343 and APOE ɛ4). The association between some AD SNPs and risk of AD may be modified by triglyceride levels. Furthermore, sequential testing of a GRS with a set of traits on disease followed by testing individual SNPs for interaction provides a framework for narrowing the associations that need to be tested for interaction analyses. Replication is needed to confirm these findings.

Background Recent studies have shown a lower prevalence of metabolic syndrome (MSyn) in vegetarians (VEG) despite the inconclusive evidence from others. Objective To verify the association between diet and other lifestyle characteristics and the prevalence of MSyn, cardiovascular risk factors (CRF), and Framingham Risk Score (FRS) in apparently healthy VEG and omnivorous (OMN) men. Methods In this cross-sectional study, 88 apparently healthy men ≥ 35 years, 44 VEG and 44 OMN, were assessed for anthropometric data, blood pressure, blood lipids, glucose, C-reactive protein (CRP) and FRS. To test the association between lifestyle and MSyn, Student t test, chi-square test, and multiple logistic regression model were used. A significance level of 5% was considered in all statistical analyses. Results Several CRF were significantly lower in VEG than in OMN: body mass index, systolic blood pressure, diastolic blood pressure, fasting serum total cholesterol, LDL-cholesterol, apolipoprotein b, glucose, and glycated hemoglobin (all p < 0.05). The FRS mean was lower in VEG than in OMN (2.98 ± 3.7 vs 4.82 ± 4.8, p = 0.029). The percentage of individuals with MSyn was higher among OMN than among VEG (52.3 vs.15.9%) (p < 0.001). The OMN diet was associated with MSyn (OR: 6.28 95%CI 2.11-18.71) and alterations in most MSyn components in the multiple regression model independently of caloric intake, age and physical activity. Conclusion The VEG diet was associated with lower CRF, FRS and percentage of individuals with MSyn.

Background: Dyslipidemia is a key modifiable risk factor for cardiovascular disease (CVD) and is highly prevalent among renal transplant recipients (RTRs). Traditional cardiovascular risk factors, such as hypertension, diabetes, and obesity, contribute to adverse cardiovascular outcomes. The Framingham Risk Score (FRS) is a widely used tool to estimate coronary heart disease (CHD) risk, incorporating lipid levels and other major risk factors. However, the association between dyslipidemia, traditional cardiovascular risk factors, and FRS in RTRs remains unclear. Objective: This study aimed to assess the relationship between dyslipidemia and traditional cardiovascular risk factors in RTRs and to evaluate the impact of dyslipidemia on FRS. Methodology: A cross-sectional observational study was conducted over 13 months (May 2019 – June 2020) at nephrology departments of multiple healthcare facilities in Bangladesh. A total of 105 RTRs, selected through purposive sampling, underwent clinical assessments, laboratory investigations, and FRS calculation. The prevalence of dyslipidemia was evaluated, and its associations with hypertension, diabetes, body mass index (BMI), and FRS were analyzed using SPSS version 16. Results: The majority of RTRs were male (88.6%) and aged ≤40 years (72.4%). Dyslipidemia was highly prevalent, affecting 88.0% of hypertensive patients, 100.0% of diabetics, and 100.0% of underweight and obese individuals. However, no statistically significant associations were found between dyslipidemia and hypertension (p = 0.498), diabetes (p = 0.455), or BMI (p = 0.470). Similarly, dyslipidemia did not show a significant correlation with FRS (p = 0.107), despite its high prevalence across all FRS categories. Conclusion: Dyslipidemia is highly prevalent among RTRs but is not significantly associated with traditional cardiovascular risk factors or FRS. These findings suggest that conventional cardiovascular risk models may not fully capture the complex risk profile of RTRs. Individualized lipid monitoring and tailored cardiovascular risk management strategies are essential for optimizing post-transplant care. Further studies with larger sample sizes and longitudinal designs are needed to elucidate the interplay between dyslipidemia, immunosuppressive therapy, and cardiovascular risk in RTRs.

Residual cardiovascular risk persists in patients with acute myocardial infarction (AMI) and hypertriglyceridaemia despite statin therapy. The potential benefit of acipimox, a niacin derivative, as an adjunct to statins in this context remains uncertain. This study evaluated the association between statin–acipimox combination therapy and cardiovascular outcomes in AMI patients with elevated triglyceride levels. We conducted a retrospective cohort study using the Tianjin Coronary Artery Disease Specialised Database (2010–2024). First-time AMI patients with triglycerides ≥ 1.7 mmol/L who received statins were included. Patients treated with statins plus acipimox were compared with those receiving statin monotherapy. The primary outcomes were 1-year major adverse cardiovascular and cerebrovascular events (MACCE) and net adverse clinical events (NACE). Associations were first evaluated in the original unmatched cohort and then in a 1:1 propensity score–matched cohort. Subgroup analyses were prespecified. Sensitivity analyses included progressively adjusted Cox models, IPTW-adjusted repetitions, adherence-stratified analyses, and Fine–Gray competing risk models. Among 38,190 eligible AMI patients with hypertriglyceridaemia, 624 received acipimox in addition to statins. In the original unmatched cohort, combination therapy was associated with lower 1-year risks of MACCE (adjusted hazard ratio [aHR] 0.66, 95% confidence interval [CI] 0.49–0.87) and NACE (aHR 0.64, 95% CI 0.52–0.79), with no significant differences in all-cause or cardiac mortality. After 1:1 propensity score matching (596 pairs), these benefits persisted (MACCE: aHR 0.68, 95% CI 0.51–0.90; NACE: aHR 0.64, 95% CI 0.48–0.84), again without a mortality difference. Secondary analyses demonstrated larger reductions in triglycerides, LDL-C and VLDL-C and greater increases in HDL-C with combination therapy. Subgroup analyses showed generally consistent protective associations across most clinical strata. Subgroup findings were generally consistent across most strata. Results remained robust across all sensitivity analyses. In this real-world cohort, adding acipimox to statin therapy was associated with improved cardiovascular outcomes in AMI patients with hypertriglyceridaemia, accompanied by a favourable downward trend in triglyceride-related lipid measures.

No abstract available

BACKGROUND Depressive disorder (DD) affects approximately 20 % of adolescents worldwide, but it is underdiagnosed due to the lack of objective biomarkers. Niacin skin flushing response (NSFR) is an objective and noninvasive biomarker of adult depression; however, its effectiveness has not been assessed in adolescents. METHODS This study included 198 adolescents with 50 % healthy controls (HC). Linear mixed-effects model and multiple linear regression analyses were performed to assess differences in NSFR between the DD and HC groups. Logistic regression models based on NSFR were constructed, and the area under curve (AUC) was calculated to evaluate the performance of models. Spearman correlations were calculated to assess the relationships between NSFR and disease duration and hormone levels associated with puberty. RESULTS Adolescents with DD displayed significantly attenuated and delayed NSFR compared to HC. NSFR effectively distinguished DD patients from HC with AUC values of 0.719 (sensitivity = 0.844) and 0.721 (sensitivity = 0.829) determined in the discovery and validation sets, respectively. Within the DD group, the maximum degree of NSFR was negatively correlated with the disease duration (r = -0.28, p = 0.011), and the overall degree of NSFR was positively associated with prolactin (r = 0.29, p = 0.039) and thyroxine (r = 0.29, p = 0.027) levels. LIMITATIONS Future investigations will be necessary to confirm our results in an independent sample set. CONCLUSIONS This study provides the first evidence of the utility of NSFR as an objective auxiliary diagnostic biomarker for adolescent depression. It provides new clues to understand the pathophysiology of the disease, and helps promote precise diagnosis, treatment, and prognostic evaluation of adolescent depression.

Introduction: Despite having clinical relevance, arterial stiffness is neglected and not routinely used parameter for evaluation of atherosclerosis. This study aimed to investigate the predictive role of simple non-invasive echocardiographic index of aortic stiffness aortic velocity propagation (AVP), Framingham risk score (FHS) and QRISK3 score for presence and severity of CAD. Methods: This cross-sectional comparative study included 250 patients who required conventional coronary angiogram for stable CAD. The relationship of AVP, FHS and QRISK3 score with CAD were evaluated using spearman’s correlation, logistic regression analysis and ROC curve. Results: On logistic regression analysis, AVP, FHS and QRISK3 were found significant predictors for the presence and severity of CAD. Inverse correlation between AVP and presence of CAD, number of coronary vessels involved and severity of CAD was observed with P=0.001. AVP value≤78 cm/s predicted presence of CAD with 86.4% sensitivity and 84.6% specificity (P≤0.0001, AUC=0.948) and≤39 cm/s predicted severe CAD (Syntax score>22) with 66.7% sensitivity and 97.9% specificity (P≤0.0001, AUC=0.868). FHS value>10 predicted the presence of CAD with a sensitivity of 33.9% and specificity of 91 % (P=0.01, AUC=0.644). QRISK3value>13.4 predicted presence of CAD with 57.1% sensitivity and 87% specificity (P≤0.0001, AUC=0.788). Conclusion: Arterial stiffness parameter AVP is inversely associated with the presence and severity of CAD. AVP and QRISK3 score may be used as a simple bedside tool for risk stratification of patients suspected of having atherosclerotic CAD.

Background: This study aimed to investigate the effects of niacin combined with B. animalis F1-7 on the improvement of alcoholic fatty liver disease (AFLD) in mice and its potential regulatory mechanism. Methods: A total of 75 8-week-old male C57BL/6N mice were acclimated for one week and randomly divided into five groups: control group, alcohol model group (AFLD), niacin intervention group (NA), B. animalis F1-7 intervention group (F1-7), and niacin combined with B. animalis F1-7 intervention group (NF). The experiment lasted for 8 weeks. Results: The results showed that all intervention groups could effectively reduce the serum lipid levels and inflammatory response of mice induced by alcohol to varying degrees. The immunofluorescence analysis showed that the GPR109A in the liver and intestine of the NF group was significantly enhanced compared with the other groups. Niacin combined with B. animalis F1-7 better restored the gut microbiota. Meanwhile, each intervention group could increase their levels of SCFAs. Among them, the combination group increased the levels of acetic acid and butyric acid more significantly than the other two groups. The Spearman’s correlation analysis of gut microbiota and SCFAs showed that Norank_f_Eubacterium_coprostanoligenes_group, Allobaculum, and Akkermansia were positively correlated with changes in SCFAs, while Coriobacteriaceae_UCG-002, Romboutsia, and Clostridium_sensu_stricro_1 were negatively correlated. Conclusions: Niacin combined with B. animalis F1-7 better regulated the gut microbial balance and increased the SCFAs in mice with alcoholic steatohepatitis. The mechanism was related to the activation of the target GPR109A, which regulates the key proteins involved in lipid synthesis and β-oxidation to improve lipid metabolic disorders.

BACKGROUND Multiple sclerosis (MS) may have its prognosis affected by several cardiovascular risk factors. The Framingham Score is a systematic way to measure the biological interactions of cardiovascular risk factors and has been related to MS clinical outcomes. OBJECTIVE assess whether the Framingham score is associated with an increased risk of MS disability, as stated by the risk of reaching an Expanded Disability Status Scale (EDSS) score of 6 during follow-up in multiethnic population in a middle-income country. METHODS This retrospective study evaluates the relationship between the Framingham Score and the last visit EDSS score, calculated using a logistic regression model, with further adjustments for confounding risk factors and a decision tree algorithm analysis. Data was collected from a tertiary multiple sclerosis (MS) center for patients admitted between 1994 and 2019. RESULTS Among 2036 medical records, we included 284 patients for final analysis. Patients who reached an EDSS of 6 or more had a mean Framingham score of 9.9 versus 5.8 among those who did not reach such EDSS. There was a positive Spearman correlation between the Framingham general cardiovascular risk score and the last-visit EDSS (rₛ = 0.414, p < 0.001). In logistic regression models using EDSS ≥ 6 as the outcome, higher Framingham scores were associated with greater odds of disability in unadjusted analyses, but this association was attenuated after adjustment for age. Among patients with baseline EDSS 0-2.5, the Framingham score significantly predicted a higher final EDSS. In this group, 25.3% of those with a score >1.91 reached EDSS ≥ 6, versus 3.9% with a score ≤1.91. DISCUSSION Our study reported an association between cardiovascular risk, as measured by the Framingham score, and disability in MS, measured by the last visit EDSS score, in a middle-income MS cohort with access to DMD. Such correlation is stronger and statistically significant among patients with an EDSS between 0 and 2.5. There is an association between the Framingham score and a higher final EDSS in patients with multiple sclerosis when the cardiovascular risk factors are present in the early course of the disease.

Objectives: This study is intended to reveal whether the boost in immune function in immunocompromised mice from niacin supplementation is connected to the upkeep of intestinal homeostasis and the modulation of the hydroxycarboxylic acid receptor 2 (HCAR2)/NOD-like receptor protein 3 (NLRP3) and prostaglandin endoperoxide synthase 2 (PTGS2)/prostaglandin E2 (PGE2) signaling pathways. Methods: Balb/c mice were employed in this study as a model for immunosuppression caused by cyclophosphamide (CTX) injection. Results: The study showed that niacin supplementation restored spleen and liver indices, enhanced cytokine secretion, and increased Th1/Th2 cytokine levels. Niacin effectively enhanced the phagocytic index, natural killer cell (NK cell) activity, splenic lymphocyte activity and delayed-type hypersensitivity (DTH) reaction in immunocompromised mice. Histopathological examination showed that niacin intervention alleviated injury in mice ilea. Intestinal barrier tight junction proteins were expressed at much higher levels, while the serum concentrations of diamine oxidase (DAO) and fatty acid-binding protein 2 (FABP2) were markedly lowered. Furthermore, the expression of the intestinal HCAR2/NLRP3 signaling pathway and subsequent inflammatory mediators was significantly elevated after niacin administration compared with the CTX group. Niacin supplementation improved the composition of the gut microbiota, increasing the Firmicutes/Bacteroidetes (F/B) ratio. Spearman correlation analysis showed significant correlations between cytokine-related indices and several gut microbiotas. Within a network pharmacology framework including target screening, network construction and molecular docking, PTGS2 emerged as a candidate target of niacin, suggesting its role in counteracting immunosuppression. Further experimental findings showed that niacin markedly decreased the protein expression of PTGS2 and the levels of its downstream mediators PGE2, E-prostanoid receptor type 2 (EP2) and (E-prostanoid receptor type 4 (EP4) in the ileal tissue of mice treated with CTX. Conclusions: In conclusion, niacin supplementation alleviated CTX-induced immunosuppression by maintaining intestinal homeostasis and regulating the intestinal HCAR2/NLRP3 and PTGS2/PGE2/EP2-EP4 pathways.

Objective: Attenuated niacin responses and changes in cytokine levels have been reported in schizophrenia. However, prior studies have typically focused on schizophrenia, and little is known about the association between niacin response and inflammatory imbalance in clinically high-risk psychosis (CHR). This study aimed to assess the niacin response to inflammatory imbalance for association with conversion to psychosis within 2 years. Methods: A prospective case-control study was performed to assess the niacin response and interleukin (IL)-1β, IL-2, IL-6, IL-8, IL-10, and tumor necrosis factor-α levels in 60 CHR individuals and 60 age- and sex-matched healthy controls (HC) from May 2019 to December 2021. Participants with CHR were identified using the Structured Interview for Prodromal Syndromes. The niacin-induced responses were measured using laser Doppler flowmetry. From the dose-response curves, the log-transferred concentration of methylnicotinate required to elicit a half-maximal blood flow response (LogEC50) and maximal minus minimal blood flow response (Span) values were calculated for each subject. Serum cytokine levels were measured using enzyme-linked immunosorbent assay. Individuals with CHR were then divided into converters (CHR-C, n = 15) and non-converters (CHR-NC, n = 45) to psychosis based on their 2-year follow-up clinical status. Results: The CHR group exhibited significantly higher LogEC50 (t = 3.650, P < .001) and Span (t = 2.657, P = .009) values than the HC group. The CHR-C group exhibited a significantly shorter Span (t = 4.027, P < .001) than the CHR-NC group. The LogEC50 showed a trend toward significance (t = 1.875, P = .066). None of the cytokine levels were significant. The conversion outcome can therefore be predicted by applying LogEC50 (P = .049) and Span (P < .001). The regression model with variables of LogEC50, Span, family history, and scores of positive symptoms showed good discrimination of subsequent conversion to psychosis and achieved a classification accuracy of 91.7%. The decreased LogEC50 in the CHR-C group was significantly correlated with the increased IL-1β/IL-10 ratio (Spearman ρ = -0.600, P = .018), but this correlation was nonsignificant in the CHR-NC group. Conclusions: Our findings indicate a significant association between niacin response and psychosis conversion outcomes in individuals with CHR. Compared with peripheral inflammatory cytokines, the niacin response can better predict conversion, although there may be an intersection between the two in biological mechanisms.

No abstract available

The aim of this study was to compare the predictions of Framingham cardiovascular (CV) risk score (FRS) and the American College of Cardiology/American Heart Association (ACC/AHA) risk score in an HIV outpatient clinic in the city of Vitoria, Espirito Santo, Brazil. In a cross-sectional study 341 HIV infected patients over 40 years old consecutively recruited were interviewed. Cohen's kappa coefficient was used to assess agreement between the two algorithms. 61.3% were stratified as low risk by Framingham score, compared with 54% by ACC/AHA score (Spearman correlation 0.845; p < 0.000). Only 26.1% were classified as cardiovascular high risk by Framingham compared to 46% by ACC/AHA score (Kappa = 0.745; p < 0.039). Only one out of eight patients had cardiovascular high risk by Framingham at the time of a myocardial infarction event registered up to five years before the study period. Both cardiovascular risk scores but especially Framingham underestimated high-risk patients in this HIV-infected population.

BackgroundThe Absolute cardiovascular disease (CVD) risk evaluation using multivariable CVD risk models is increasingly advocated in people with HIV, in whom existing models remain largely untested. We assessed the agreement between the general population derived Framingham CVD risk equation and the HIV-specific Data collection on Adverse effects of anti-HIV Drugs (DAD) CVD risk equation in HIV-infected adult Cameroonians.MethodsThis cross-sectional study involved 452 HIV infected adults recruited at the HIV day-care unit of the Yaoundé Central Hospital, Cameroon. The 5-year projected CVD risk was estimated for each participant using the DAD and Framingham CVD risk equations. Agreement between estimates from these equations was assessed using the spearman correlation and Cohen’s kappa coefficient.ResultsThe mean age of participants (80% females) was 44.4 ± 9.8 years. Most participants (88.5%) were on antiretroviral treatment with 93.3% of them receiving first-line regimen. The most frequent cardiovascular risk factors were abdominal obesity (43.1%) and dyslipidemia (33.8%). The median estimated 5-year CVD risk was 0.6% (25th-75th percentiles: 0.3-1.3) using the DAD equation and 0.7% (0.2-2.0) with the Framingham equation. The Spearman correlation between the two estimates was 0.93 (p < 0.001). The kappa statistic was 0.61 (95% confident interval: 0.54-0.67) for the agreement between the two equations in classifying participants across risk categories defined as low, moderate, high and very high.ConclusionMost participants had a low-to-moderate estimated CVD risk, with acceptable level of agreement between the general and HIV-specific equations in ranking CVD risk.

Introduction Nightmares and depression are prevalent issues among adolescents. This study explores the relationship between nightmares and depression, focusing on the mediating role of anxiety and the moderating effect of age Methods A total of 210 adolescents aged 13 to 24 were surveyed using the Nightmare Distress Questionnaire (NDQ-CV), Self-Rating Anxiety Scale (SAS), and Self-Rating Depression Scale (SDS). They also underwent niacin skin flushing response (NSFR) testing to explore physiological correlations. A moderated mediation model was applied to assess the relationships between nightmares, anxiety, and depression. Spearman correlation analysis was used to analyze the relationship between nightmares and NSFR Results Nightmares did not directly lead to depression, but anxiety served as a full mediator in this relationship. Age had no significant moderating effect. Additionally, a significant negative correlation between nightmares and NSFR was observed Conclusion Nightmares contribute to anxiety, which can lead to depression in adolescents, suggesting that clinicians can identify and intervene with nightmares in adolescents to minimize the onset of psychological disorders. The study also highlights a possible connection between nightmares and NSFR, suggesting further research is needed to understand the physiological mechanisms

Objective To evaluate gender-specific variations in cardiovascular disease (CVD) risk stratification and its modifiable determinants among individuals concurrently diagnosed with type 2 diabetes mellitus (T2DM) and subclinical hypothyroidism (SCH). Methods A cross-sectional observational study was conducted involving 2,357 patients with T2DM (1,120 males and 1,237 females) who were hospitalized at Wuxi Hospital of Traditional Chinese Medicine between 2018 and 2024. Participants were categorized into the SCH (n=196) and the euthyroid subgroups (n=2,161). The 10-year probability of cardiovascular events was estimated based on the Framingham Risk Score (FRS) model. Sex-specific differences in SCH prevalence and CVD risk were examined, and associations between FRS and biomarkers—namely thyroid-stimulating hormone (TSH), free thyroxine (FT4), cystatin C (CysC) and other factors—were analyzed via Spearman’s correlation analysis and multivariable linear regression. Results The prevalence of SCH in T2DM patients was 9.06% (10.02% in females vs. 6.43% in males). Male patients diagnosed with SCH exhibited an elevated FRS compared to their euthyroid counterparts (21.00 vs. 20.00, P= 0.025). Within this subgroup, a positive relationship was identified between TSH levels and FRS(r=0.374, P= 0.001), whereas FT4 showed a negative association (r=-0.342, P= 0.003). These relationships were not statistically significant among women diagnosed with SCH. Cystatin C was positively associated with FRS in both male (r=0.461, P<0.001) and female (r=0.452, P<0.001) groups. Multivariable linear regression evaluation in male patients revealed that TSH (β=3.87, P= 0.048), cystatin C (β=1.48, P= 0.03), and FT4 (β=-0.61, P= 0.011) continued to be significantly correlated with 10-year CVD risk. Additionally, male patients with SCH exhibited significantly higher smoking status, uric acid, and creatinine levels than their female counterparts (all P<0.05), indicating that sex-specific risk factors may contribute to elevated CVD risk. Conclusion This study identified higher FRS in male versus female patients with comorbid T2DM and SCH, potentially mediated by sex-specific variations in TSH, FT4, and CysC levels. These results underscore the importance of implementing sex-specific strategies for CVD risk management in this population.

No abstract available