Pub Date : 2025-03-01DOI: 10.1016/S0939-4753(25)00105-X
{"title":"SPECIAL ISSUE ON NEW INSIGHTS INTO CARDIOVASCULAR RISK MANAGEMENT","authors":"","doi":"10.1016/S0939-4753(25)00105-X","DOIUrl":"10.1016/S0939-4753(25)00105-X","url":null,"abstract":"","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":"35 3","pages":"Article 103951"},"PeriodicalIF":3.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143511145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01DOI: 10.1016/j.numecd.2024.103792
Alessandro Maloberti , Valentina Colombo , Francesca Daus , Lorenzo De Censi , Maurizio Giuseppe Abrignani , Pier Luigi Temporelli , Giulio Binaghi , Furio Colivicchi , Massimo Grimaldi , Domenico Gabrielli , Claudio Borghi , Fabrizio Oliva
Aims
The most frequent consequence of elevated uric acid (UA) levels is the development of gout and urate kidney disease. Besides these effects, several studies have investigated the association between hyperuricemia and cardiovascular (CV) disease. High serum UA has been identified as an important determinant of all-cause and CV mortality and CV events (acute and chronic coronary syndrome, stroke and peripheral artery disease).
Despite the high number of publications on this topic, there are two questions that are still unanswered: do we need a specific CV cut-off of serum UA to better refine the CV risk? Is urate lowering treatment (ULT) able to reduce CV risk in asymptomatic patients? In this review, we will focus on these two points.
Data synthesis
Although no doubt exists that the relationship between CV events starts at lower levels than the actually used cut-off, different papers found dissimilar cut-offs. Furthermore, heterogeneity is present depending on the specific CV events evaluated and none of the found cut-off have been tested in external populations (in order to confirm its discriminatory capacity). Furthermore, only few randomized clinical trials on the role of hypouricemic agents in reducing the CV risk have been published giving heterogeneous results. The last published one (ALL-HEART) has strong limitations, that we will deeply discuss.
Conclusions
A definitive answer to the two questions is impossible with the actually published paper but, over identifying current gaps in knowledge we try to individuate how they can be overruled.
{"title":"Two still unanswered questions about uric acid and cardiovascular prevention: Is a specific uric acid cut-off needed? Is hypouricemic treatment able to reduce cardiovascular risk?","authors":"Alessandro Maloberti , Valentina Colombo , Francesca Daus , Lorenzo De Censi , Maurizio Giuseppe Abrignani , Pier Luigi Temporelli , Giulio Binaghi , Furio Colivicchi , Massimo Grimaldi , Domenico Gabrielli , Claudio Borghi , Fabrizio Oliva","doi":"10.1016/j.numecd.2024.103792","DOIUrl":"10.1016/j.numecd.2024.103792","url":null,"abstract":"<div><h3>Aims</h3><div>The most frequent consequence of elevated uric acid (UA) levels is the development of gout and urate kidney disease. Besides these effects, several studies have investigated the association between hyperuricemia and cardiovascular (CV) disease. High serum UA has been identified as an important determinant of all-cause and CV mortality and CV events (acute and chronic coronary syndrome, stroke and peripheral artery disease).</div><div>Despite the high number of publications on this topic, there are two questions that are still unanswered: do we need a specific CV cut-off of serum UA to better refine the CV risk? Is urate lowering treatment (ULT) able to reduce CV risk in asymptomatic patients? In this review, we will focus on these two points.</div></div><div><h3>Data synthesis</h3><div>Although no doubt exists that the relationship between CV events starts at lower levels than the actually used cut-off, different papers found dissimilar cut-offs. Furthermore, heterogeneity is present depending on the specific CV events evaluated and none of the found cut-off have been tested in external populations (in order to confirm its discriminatory capacity). Furthermore, only few randomized clinical trials on the role of hypouricemic agents in reducing the CV risk have been published giving heterogeneous results. The last published one (ALL-HEART) has strong limitations, that we will deeply discuss.</div></div><div><h3>Conclusions</h3><div>A definitive answer to the two questions is impossible with the actually published paper but, over identifying current gaps in knowledge we try to individuate how they can be overruled.</div></div>","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":"35 3","pages":"Article 103792"},"PeriodicalIF":3.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01DOI: 10.1016/j.numecd.2024.103787
Wenqing Nai , Li Lei , Qiuxia Zhang , Shaohua Yan , JieLing Xu , Lixia Lin , Wei Luo , Siyu Chen , Xiaocong Liu , Yanbin Gao , Shiping Cao , Jiancheng Xiu
Background and aim
The relationship between the systemic inflammatory response index (SIRI) and carotid atherosclerosis has not yet been assessed in a longitudinal investigation. Our current study aimed to investigate whether SIRI is related to an increased risk of incident carotid plaque.
Methods and results
Our study included individuals who did not have carotid atherosclerosis and had undergone yearly health check-ups at the Department of Health Management of Nanfang Hospital between 2011 and 2018 (total n = 3927). SIRI was computed by a composite value of neutrophils, monocytes, and lymphocytes. Over a median follow-up time of 4.42 years, 872 (22.21 %) participants developed carotid plaque in the entire cohort. The adjusted hazard ratio (HR) for the continuous SIRI was 1.093 (95 % CI: 1.021–1.223) in our present study. In the general population, individuals belonging to the highest quartile of SIRI had an elevated risk of carotid plaque, as compared to those within the lowest quartile (HR 1.122, 95 % CI: 1.011–1.391, P for trend = 0.041). Furthermore, this trend was even more pronounced among participants without hypertension, diabetes and hyperlipidemia in the highest SIRI quartile, who demonstrated a markedly increased risk of carotid plaque when contrasted with those in the lowest quartile (HR 1.277, 95 % CI: 1.041–1.568, P for trend = 0.006).
Conclusions
Our research findings suggest an association between increased SIRI levels and a higher incidence of carotid atherosclerosis, especially among the people without a history of hypertension, diabetes and hyperlipidemia.
背景和目的：尚未在纵向调查中评估全身炎症反应指数（SIRI）与颈动脉粥样硬化之间的关系。我们目前的研究旨在调查 SIRI 是否与颈动脉斑块发病风险增加有关：我们的研究纳入了2011年至2018年间在南方医院健康管理部接受年度健康体检的未患颈动脉粥样硬化的个体（总人数=3927）。SIRI由中性粒细胞、单核细胞和淋巴细胞的综合值计算得出。中位随访时间为4.42年，整个队列中有872人（22.21%）出现颈动脉斑块。在本研究中，连续 SIRI 的调整后危险比 (HR) 为 1.093（95 % CI：1.021-1.223）。在普通人群中，与属于最低四分位数的人相比，属于 SIRI 最高四分位数的人患颈动脉斑块的风险更高（HR 1.122，95 % CI：1.011-1.391，趋势 P = 0.041）。此外，这一趋势在 SIRI 最高四分位数中没有高血压、糖尿病和高脂血症的参与者中更为明显，与最低四分位数的参与者相比，他们患颈动脉斑块的风险明显增加（HR 1.277，95 % CI：1.041-1.568，P=0.006）：我们的研究结果表明，SIRI水平升高与颈动脉粥样硬化发病率升高之间存在关联，尤其是在无高血压、糖尿病和高脂血症病史的人群中。
{"title":"Systemic inflammation response index and carotid atherosclerosis incidence in the Chinese population: A retrospective cohort study","authors":"Wenqing Nai , Li Lei , Qiuxia Zhang , Shaohua Yan , JieLing Xu , Lixia Lin , Wei Luo , Siyu Chen , Xiaocong Liu , Yanbin Gao , Shiping Cao , Jiancheng Xiu","doi":"10.1016/j.numecd.2024.103787","DOIUrl":"10.1016/j.numecd.2024.103787","url":null,"abstract":"<div><h3>Background and aim</h3><div>The relationship between the systemic inflammatory response index (SIRI) and carotid atherosclerosis has not yet been assessed in a longitudinal investigation. Our current study aimed to investigate whether SIRI is related to an increased risk of incident carotid plaque.</div></div><div><h3>Methods and results</h3><div>Our study included individuals who did not have carotid atherosclerosis and had undergone yearly health check-ups at the Department of Health Management of Nanfang Hospital between 2011 and 2018 (total n = 3927). SIRI was computed by a composite value of neutrophils, monocytes, and lymphocytes. Over a median follow-up time of 4.42 years, 872 (22.21 %) participants developed carotid plaque in the entire cohort. The adjusted hazard ratio (HR) for the continuous SIRI was 1.093 (95 % CI: 1.021–1.223) in our present study. In the general population, individuals belonging to the highest quartile of SIRI had an elevated risk of carotid plaque, as compared to those within the lowest quartile (HR 1.122, 95 % CI: 1.011–1.391, P for trend = 0.041). Furthermore, this trend was even more pronounced among participants without hypertension, diabetes and hyperlipidemia in the highest SIRI quartile, who demonstrated a markedly increased risk of carotid plaque when contrasted with those in the lowest quartile (HR 1.277, 95 % CI: 1.041–1.568, P for trend = 0.006).</div></div><div><h3>Conclusions</h3><div>Our research findings suggest an association between increased SIRI levels and a higher incidence of carotid atherosclerosis, especially among the people without a history of hypertension, diabetes and hyperlipidemia.</div></div>","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":"35 3","pages":"Article 103787"},"PeriodicalIF":3.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01DOI: 10.1016/j.numecd.2024.103840
Guike Lai , Yipin Zhao , Cuiling Yang , Yuanyuan Zheng , Jingjing Sun , Yingjie Zhao , MingGe Ding
Background and aim
The Naples Prognostic Score (NPS) predicts outcomes in various diseases, but its impact on cardiovascular disease (CVD) is understudied. This study investigates the association between NPS and CVD prevalence and mortality among US adults.
Methods and results
This study utilized data from the Continuous National Health and Nutrition Examination Survey (NHANES) conducted between 1999 and 2016, with mortality follow-up data available through December 31, 2019. NPS was calculated using serum albumin, total cholesterol, neutrophil to lymphocyte ratio, and lymphocyte to monocyte ratio. Participants were stratified into low, moderate, and high NPS groups. Multiple logistic regression estimated odds ratios (OR) for CVD prevalence, while Cox proportional regression estimated hazard ratios (HR) for mortality. Of 39,572 participants, 20.24 % were in the low group, 69.79 % in the moderate group, and 9.96 % in the high group. After adjusting for confounders, the CVD prevalence ORs for moderate and high groups were 1.19 (95 % CI: 1.05, 1.34) and 1.78 (95 % CI: 1.53, 2.07), respectively (P for trend <0.001). Compared to the low group, the high group had adjusted HRs of 1.92 (95 % CI: 1.54, 2.41) for all-cause mortality, 1.61 (95 % CI: 1.12, 2.34) for cardiovascular mortality, and 1.83 (95 % CI: 1.11, 3.02) for cancer-related mortality (all P for trend <0.01). These associations remained significant across all subgroups.
Conclusion
NPS is an independent risk factor for CVD and is positively associated with all-cause and cardiovascular mortality in individuals with CVD.
{"title":"Association of Naples Prognostic Score with cardiovascular disease risk and its longitudinal prognostic impact on mortality in cardiovascular disease patients: Evidence from NHANES","authors":"Guike Lai , Yipin Zhao , Cuiling Yang , Yuanyuan Zheng , Jingjing Sun , Yingjie Zhao , MingGe Ding","doi":"10.1016/j.numecd.2024.103840","DOIUrl":"10.1016/j.numecd.2024.103840","url":null,"abstract":"<div><h3>Background and aim</h3><div>The Naples Prognostic Score (NPS) predicts outcomes in various diseases, but its impact on cardiovascular disease (CVD) is understudied. This study investigates the association between NPS and CVD prevalence and mortality among US adults.</div></div><div><h3>Methods and results</h3><div>This study utilized data from the Continuous National Health and Nutrition Examination Survey (NHANES) conducted between 1999 and 2016, with mortality follow-up data available through December 31, 2019. NPS was calculated using serum albumin, total cholesterol, neutrophil to lymphocyte ratio, and lymphocyte to monocyte ratio. Participants were stratified into low, moderate, and high NPS groups. Multiple logistic regression estimated odds ratios (OR) for CVD prevalence, while Cox proportional regression estimated hazard ratios (HR) for mortality. Of 39,572 participants, 20.24 % were in the low group, 69.79 % in the moderate group, and 9.96 % in the high group. After adjusting for confounders, the CVD prevalence ORs for moderate and high groups were 1.19 (95 % CI: 1.05, 1.34) and 1.78 (95 % CI: 1.53, 2.07), respectively (<em>P</em> for trend <0.001). Compared to the low group, the high group had adjusted HRs of 1.92 (95 % CI: 1.54, 2.41) for all-cause mortality, 1.61 (95 % CI: 1.12, 2.34) for cardiovascular mortality, and 1.83 (95 % CI: 1.11, 3.02) for cancer-related mortality (all <em>P</em> for trend <0.01). These associations remained significant across all subgroups.</div></div><div><h3>Conclusion</h3><div>NPS is an independent risk factor for CVD and is positively associated with all-cause and cardiovascular mortality in individuals with CVD.</div></div>","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":"35 3","pages":"Article 103840"},"PeriodicalIF":3.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01DOI: 10.1016/j.numecd.2024.103799
Xue Wang , Jinlong You , Jing Tang , Xiuqian Li , Rui Wang , Yuanyuan Li , Chun Yin , Yana Bai , Minzhen Wang , Shan Zheng
Background and aims
Whether the new standard of metabolic dysfunction-associated fatty liver disease (MAFLD) has more pronounced clinical and population screening diagnostic value than nonalcoholic fatty liver disease (NAFLD) is unclear. This study evaluated the utility of MAFLD and NAFLD for predicting major cardiovascular disease (CVD) risk.
Methods and results
A prospective cohort study approach was utilized to collect 19,399 study participants without CVD at baseline who completed follow-up from the Jinchang cohort platform during 2011–2017. According to clinical ultrasonic diagnosis results and disease diagnosis criteria, the baseline population was divided into MAFLD, NAFLD, Both-FLD and No-FLD groups. Based on the multifactorial Cox proportional risk model to analyze the relationship between three kinds of patients and CVD, the score prediction model of CVD was constructed with reference to the Framingham Risk Score (FRS) and the model was evaluated. Compared with No-FLD, the HRs and 95 % CIs for the risk of CVD development in patients with NAFLD, MAFLD, and Both-FLD were 1.54 (1.34–1.76), 1.57 (1.37–1.79), and 1.62 (1.41–1.87), in that order. The scoring model showed a range of 5.90%–84.59 % risk of CVD in the three groups. As the risk score increased, the risk of developing CVD gradually increased. Evaluation metrics of all three models in the training set and validation set showed that the models have good prediction efficacy.
Conclusion
In terms of CVD risk and prognosis, MAFLD had no advantage over NAFLD. However, Both-FLD was found to predict a higher risk of CVD and to have superior predictive efficacy.
{"title":"Is MAFLD better than NAFLD in predicting the risk of major cardiovascular diseases? Evidence from a 7-year prospective cohort study","authors":"Xue Wang , Jinlong You , Jing Tang , Xiuqian Li , Rui Wang , Yuanyuan Li , Chun Yin , Yana Bai , Minzhen Wang , Shan Zheng","doi":"10.1016/j.numecd.2024.103799","DOIUrl":"10.1016/j.numecd.2024.103799","url":null,"abstract":"<div><h3>Background and aims</h3><div>Whether the new standard of metabolic dysfunction-associated fatty liver disease (MAFLD) has more pronounced clinical and population screening diagnostic value than nonalcoholic fatty liver disease (NAFLD) is unclear. This study evaluated the utility of MAFLD and NAFLD for predicting major cardiovascular disease (CVD) risk.</div></div><div><h3>Methods and results</h3><div>A prospective cohort study approach was utilized to collect 19,399 study participants without CVD at baseline who completed follow-up from the Jinchang cohort platform during 2011–2017. According to clinical ultrasonic diagnosis results and disease diagnosis criteria, the baseline population was divided into MAFLD, NAFLD, Both-FLD and No-FLD groups. Based on the multifactorial Cox proportional risk model to analyze the relationship between three kinds of patients and CVD, the score prediction model of CVD was constructed with reference to the Framingham Risk Score (FRS) and the model was evaluated. Compared with No-FLD, the HRs and 95 % CIs for the risk of CVD development in patients with NAFLD, MAFLD, and Both-FLD were 1.54 (1.34–1.76), 1.57 (1.37–1.79), and 1.62 (1.41–1.87), in that order. The scoring model showed a range of 5.90%–84.59 % risk of CVD in the three groups. As the risk score increased, the risk of developing CVD gradually increased. Evaluation metrics of all three models in the training set and validation set showed that the models have good prediction efficacy.</div></div><div><h3>Conclusion</h3><div>In terms of CVD risk and prognosis, MAFLD had no advantage over NAFLD. However, Both-FLD was found to predict a higher risk of CVD and to have superior predictive efficacy.</div></div>","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":"35 3","pages":"Article 103799"},"PeriodicalIF":3.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01DOI: 10.1016/j.numecd.2024.103797
Rui Dong , Ting Tian , Zhenghan Luo , Dongchun Chang , Hong Xue , Sen Qu , Jia Wang , Chao Shen , Ru Zhang , Jie Wang
Background and aims
Patients with metabolic dysfunction-associated steatotic liver disease (MASLD) often manifest a combination of cardiometabolic risk factors of varying severity. The cardiometabolic phenotypes and their associations with advanced liver fibrosis and all-cause mortality among patients with MASLD warrant further investigation.
Methods and results
A total of 4209 and 1901 eligible participants were obtained from the National Health and Nutrition Examination Survey and included in the original and replication datasets, respectively. In the original dataset, three distinct and stable cardiometabolic phenotypes were identified using unsupervised cluster analyses, including mild cardiometabolic risk factor (MCMRF) phenotype, overweight combined with high diastolic blood pressure dominated (OCHBP) phenotype, and severe glucose and lipid metabolic dysfunction dominated (SGLMD) phenotype. The above phenotypes were subsequently replicated in the replication dataset, demonstrating similar characteristics. After adjusting for potential covariates, the results of logistic and Cox regression models showed that OCHBP and SGLMD phenotypes were significantly associated with higher odds of advanced liver fibrosis (OCHBP: OR = 4.37, 95 % CI: 1.54–12.35, P = 0.020; SGLMD: OR = 9.66, 95 % CI: 4.76–19.61, P = 0.002) and an increased risk of all-cause mortality (OCHBP: HR = 1.39, 95 % CI: 1.17–1.65, P < 0.001; SGLMD: HR = 2.51, 95 % CI: 1.86–3.40, P < 0.001) compared to the MCMRF phenotype. Moreover, the observed associations remained statistically significant in most subgroups, and a series of sensitivity analyses further confirmed the robustness of these findings.
Conclusion
Three heterogeneous cardiometabolic phenotypes were identified among participants with MASLD, showing significant associations with two critical outcomes. These novel phenotypes may be of great importance to precision medicine in MASLD.
{"title":"Cardiometabolic phenotype linked to fibrosis and mortality in metabolic dysfunction-associated steatotic liver disease","authors":"Rui Dong , Ting Tian , Zhenghan Luo , Dongchun Chang , Hong Xue , Sen Qu , Jia Wang , Chao Shen , Ru Zhang , Jie Wang","doi":"10.1016/j.numecd.2024.103797","DOIUrl":"10.1016/j.numecd.2024.103797","url":null,"abstract":"<div><h3>Background and aims</h3><div>Patients with metabolic dysfunction-associated steatotic liver disease (MASLD) often manifest a combination of cardiometabolic risk factors of varying severity. The cardiometabolic phenotypes and their associations with advanced liver fibrosis and all-cause mortality among patients with MASLD warrant further investigation.</div></div><div><h3>Methods and results</h3><div>A total of 4209 and 1901 eligible participants were obtained from the National Health and Nutrition Examination Survey and included in the original and replication datasets, respectively. In the original dataset, three distinct and stable cardiometabolic phenotypes were identified using unsupervised cluster analyses, including mild cardiometabolic risk factor (MCMRF) phenotype, overweight combined with high diastolic blood pressure dominated (OCHBP) phenotype, and severe glucose and lipid metabolic dysfunction dominated (SGLMD) phenotype. The above phenotypes were subsequently replicated in the replication dataset, demonstrating similar characteristics. After adjusting for potential covariates, the results of logistic and Cox regression models showed that OCHBP and SGLMD phenotypes were significantly associated with higher odds of advanced liver fibrosis (OCHBP: OR = 4.37, 95 % CI: 1.54–12.35, <em>P</em> = 0.020; SGLMD: OR = 9.66, 95 % CI: 4.76–19.61, <em>P</em> = 0.002) and an increased risk of all-cause mortality (OCHBP: HR = 1.39, 95 % CI: 1.17–1.65, <em>P</em> < 0.001; SGLMD: HR = 2.51, 95 % CI: 1.86–3.40, <em>P</em> < 0.001) compared to the MCMRF phenotype. Moreover, the observed associations remained statistically significant in most subgroups, and a series of sensitivity analyses further confirmed the robustness of these findings.</div></div><div><h3>Conclusion</h3><div>Three heterogeneous cardiometabolic phenotypes were identified among participants with MASLD, showing significant associations with two critical outcomes. These novel phenotypes may be of great importance to precision medicine in MASLD.</div></div>","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":"35 3","pages":"Article 103797"},"PeriodicalIF":3.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01DOI: 10.1016/j.numecd.2024.103796
Masanari Kuwabara , Ichiro Hisatome , Ryusuke Ae , Koki Kosami , Yuhei Aoki , Ana Andres-Hernando , Mehmet Kanbay , Miguel A. Lanaspa
Background and aims
Hyperuricemia is strongly linked to increased cardiovascular risk, including hypertension, coronary artery disease, arrythmia, and heart failure. Uric acid, as the end-product of purine metabolism, plays a critical role in cellular processes, but elevated levels can drive inflammation and oxidative stress. This review aims to emphasize the robust association between hyperuricemia and cardiovascular diseases, exploring whether uric acid-lowering therapies can mitigate cardiovascular events and improve patient outcomes.
Methods and results
A comprehensive review of PubMed sources was conducted, underscoring the significant link between high uric acid levels and cardiovascular events, particularly in patients with gout. Gender differences were observed, where premenopausal women have lower uric acid levels, likely due to hormonal effects, suggesting the potential need for gender-specific definitions in assessing cardiovascular risk. Epidemiological studies demonstrate a consistent correlation between hyperuricemia and adverse cardiovascular outcomes. However, interventional trials using xanthine oxidase inhibitors, such as allopurinol and febuxostat, have shown mixed results regarding their impact on reducing cardiovascular events. Additionally, emerging evidence suggests a "xanthine oxidase withdrawal syndrome" upon discontinuation of these therapies, highlighting the need for cautious management.
Conclusion
The strong association between elevated uric acid levels and cardiovascular diseases is well-documented. While lowering uric acid shows potential for reducing cardiovascular risk, current evidence from interventional trials remains inconclusive. Future research should focus on patient-specific therapeutic strategies, particularly for those at high cardiovascular risk with hyperuricemia and/or gout, to better define the benefits of targeted treatments.
{"title":"Hyperuricemia, A new cardiovascular risk","authors":"Masanari Kuwabara , Ichiro Hisatome , Ryusuke Ae , Koki Kosami , Yuhei Aoki , Ana Andres-Hernando , Mehmet Kanbay , Miguel A. Lanaspa","doi":"10.1016/j.numecd.2024.103796","DOIUrl":"10.1016/j.numecd.2024.103796","url":null,"abstract":"<div><h3>Background and aims</h3><div>Hyperuricemia is strongly linked to increased cardiovascular risk, including hypertension, coronary artery disease, arrythmia, and heart failure. Uric acid, as the end-product of purine metabolism, plays a critical role in cellular processes, but elevated levels can drive inflammation and oxidative stress. This review aims to emphasize the robust association between hyperuricemia and cardiovascular diseases, exploring whether uric acid-lowering therapies can mitigate cardiovascular events and improve patient outcomes.</div></div><div><h3>Methods and results</h3><div>A comprehensive review of PubMed sources was conducted, underscoring the significant link between high uric acid levels and cardiovascular events, particularly in patients with gout. Gender differences were observed, where premenopausal women have lower uric acid levels, likely due to hormonal effects, suggesting the potential need for gender-specific definitions in assessing cardiovascular risk. Epidemiological studies demonstrate a consistent correlation between hyperuricemia and adverse cardiovascular outcomes. However, interventional trials using xanthine oxidase inhibitors, such as allopurinol and febuxostat, have shown mixed results regarding their impact on reducing cardiovascular events. Additionally, emerging evidence suggests a \"xanthine oxidase withdrawal syndrome\" upon discontinuation of these therapies, highlighting the need for cautious management.</div></div><div><h3>Conclusion</h3><div>The strong association between elevated uric acid levels and cardiovascular diseases is well-documented. While lowering uric acid shows potential for reducing cardiovascular risk, current evidence from interventional trials remains inconclusive. Future research should focus on patient-specific therapeutic strategies, particularly for those at high cardiovascular risk with hyperuricemia and/or gout, to better define the benefits of targeted treatments.</div></div>","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":"35 3","pages":"Article 103796"},"PeriodicalIF":3.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143411329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-06DOI: 10.1016/j.numecd.2025.103903
Daniela C Andrade, Bruna Gaetani, Sara Moura, Simone N de Carvalho, Alessandra A Thole, Erika Cortez
Background and aim: Maternal obesity has been related to offspring predisposition to cardiometabolic disease development throughout life. Thus, this study aimed to analyze the impact of maternal obesity on cardiac progenitor cells and cardiometabolic disease of adult offspring.
Methods and results: The litter size reduction experimental model was used to induce obesity in female Swiss mice. Small Litter Dam (SLD-F1) and Normal Litter Dam (NLD-F1) were crossed with healthy male mice, and their offspring were followed up until 90 days old when they were euthanized. Adult offspring of obese dams (SLD-F2) had increased body mass, Lee Index and fat deposits. Heart analysis demonstrated cardiac hypertrophy, fibrosis, oxidative stress, increased cardiac mast cell number, decreased cellular proliferation, increased proinflammatory cytokines, and mitochondrial dynamic impairment. These cardiometabolic modifications were accompanied by reduced c-kit+ and Sca-1+ cardiac progenitor cell (CPC) populations and impaired CPC differentiation into new cardiomyocytes.
Conclusions: In conclusion, Obese mother-offspring developed cardiometabolic changes in adulthood that negatively impacted the CPC niches and, consequently, the formation of new cardiomyocytes. This process seems to be an essential mechanism involved in the pathophysiology of the disease, impairing cardiac homeostasis.
{"title":"Maternal obesity negatively impacts cardiac progenitor cell survival in heart adulthood offspring.","authors":"Daniela C Andrade, Bruna Gaetani, Sara Moura, Simone N de Carvalho, Alessandra A Thole, Erika Cortez","doi":"10.1016/j.numecd.2025.103903","DOIUrl":"https://doi.org/10.1016/j.numecd.2025.103903","url":null,"abstract":"<p><strong>Background and aim: </strong>Maternal obesity has been related to offspring predisposition to cardiometabolic disease development throughout life. Thus, this study aimed to analyze the impact of maternal obesity on cardiac progenitor cells and cardiometabolic disease of adult offspring.</p><p><strong>Methods and results: </strong>The litter size reduction experimental model was used to induce obesity in female Swiss mice. Small Litter Dam (SLD-F1) and Normal Litter Dam (NLD-F1) were crossed with healthy male mice, and their offspring were followed up until 90 days old when they were euthanized. Adult offspring of obese dams (SLD-F2) had increased body mass, Lee Index and fat deposits. Heart analysis demonstrated cardiac hypertrophy, fibrosis, oxidative stress, increased cardiac mast cell number, decreased cellular proliferation, increased proinflammatory cytokines, and mitochondrial dynamic impairment. These cardiometabolic modifications were accompanied by reduced c-kit+ and Sca-1+ cardiac progenitor cell (CPC) populations and impaired CPC differentiation into new cardiomyocytes.</p><p><strong>Conclusions: </strong>In conclusion, Obese mother-offspring developed cardiometabolic changes in adulthood that negatively impacted the CPC niches and, consequently, the formation of new cardiomyocytes. This process seems to be an essential mechanism involved in the pathophysiology of the disease, impairing cardiac homeostasis.</p>","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":" ","pages":"103903"},"PeriodicalIF":3.3,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143484565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background and aims: Excess adiposity correlate to cardiovascular diseases, inflammation, and telomere shortening, while the latter two are associated with cardiovascular risks. Whether inflammation and telomere length mediate the excess adiposity-cardiovascular relationship is unclear.
Methods and results: We performed a two-step Mendelian randomization analysis utilizing data from the latest genome-wide association studies: body mass index (BMI, n = 681,275), waist-to-hip ratio (WHR, n = 697,734) and BMI adjusted WHR (WHRadjBMI, n = 694,649), telomere length (n = 472,174), C-reactive protein (n = 204,402), interleukin-6 and interleukin-1 receptor antagonist (n = 21,758), tumor necrosis factor-α (n = 3454), hypertension (n = 463,010), coronary artery disease (n = 547,261), heart failure (n = 977,323), stroke (n = 446,696), ischemic stroke (n = 440,328), intracerebral hemorrhage (n = 343,663), aortic aneurysm (n = 356,934), transient ischemic attack (n = 360,692), peripheral vascular disease (n = 463,010), systolic and diastolic blood pressure changes (n = 757,601). We observed casual effects of excess adiposity on eight cardiovascular diseases, hypertension and blood pressure changes. Telomere length is causally associated with hypertension, blood pressure, coronary artery disease, aortic aneurysm, and intracerebral hemorrhage, mediates BMI's effect on coronary artery disease (2.41 %) and aortic aneurysm (4.97 %), and plays a suppressive role between WHR and systolic blood pressure changes (2.39 %).
Conclusion: Telomere length mediates the causal effects of excess adiposity on the risks of coronary artery disease, aortic aneurysm, and systolic blood pressure changes.
{"title":"Telomere length mediates the causal effects of excess adiposity on cardiovascular risk: A two-step Mendelian randomization study.","authors":"Yaxian Zeng, Xin Yuan, Jing Zi, Yifan Hu, Xiaoyu Wang, Guo Cheng, Jingyuan Xiong","doi":"10.1016/j.numecd.2025.103904","DOIUrl":"https://doi.org/10.1016/j.numecd.2025.103904","url":null,"abstract":"<p><strong>Background and aims: </strong>Excess adiposity correlate to cardiovascular diseases, inflammation, and telomere shortening, while the latter two are associated with cardiovascular risks. Whether inflammation and telomere length mediate the excess adiposity-cardiovascular relationship is unclear.</p><p><strong>Methods and results: </strong>We performed a two-step Mendelian randomization analysis utilizing data from the latest genome-wide association studies: body mass index (BMI, n = 681,275), waist-to-hip ratio (WHR, n = 697,734) and BMI adjusted WHR (WHR<sub>adj</sub>BMI, n = 694,649), telomere length (n = 472,174), C-reactive protein (n = 204,402), interleukin-6 and interleukin-1 receptor antagonist (n = 21,758), tumor necrosis factor-α (n = 3454), hypertension (n = 463,010), coronary artery disease (n = 547,261), heart failure (n = 977,323), stroke (n = 446,696), ischemic stroke (n = 440,328), intracerebral hemorrhage (n = 343,663), aortic aneurysm (n = 356,934), transient ischemic attack (n = 360,692), peripheral vascular disease (n = 463,010), systolic and diastolic blood pressure changes (n = 757,601). We observed casual effects of excess adiposity on eight cardiovascular diseases, hypertension and blood pressure changes. Telomere length is causally associated with hypertension, blood pressure, coronary artery disease, aortic aneurysm, and intracerebral hemorrhage, mediates BMI's effect on coronary artery disease (2.41 %) and aortic aneurysm (4.97 %), and plays a suppressive role between WHR and systolic blood pressure changes (2.39 %).</p><p><strong>Conclusion: </strong>Telomere length mediates the causal effects of excess adiposity on the risks of coronary artery disease, aortic aneurysm, and systolic blood pressure changes.</p>","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":" ","pages":"103904"},"PeriodicalIF":3.3,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143517143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background and aims: Previous studies have shown that frailty and metabolic syndrome (Mets) share common pathophysiological mechanisms. However, whether the observed association reflects causality requires clarification. We performed a bidirectional Mendelian randomization study to investigate the causal relationship between frailty, Mets, and their individual components.
Methods and results: Summary-level data from GWAS to identify genetic variants associated with frailty, Mets, and its components among individuals of European ancestry. Inverse variance weighting was utilized as the main method. Using bidirectional Mendelian randomization analysis, we found that the risk of frailty was causally associated with an increased risk of MetS (OR: 2.092, 95%CI: 1.564-2.799) and its components, including waist circumference (OR: 1.349, 95 % CI: 1.181-1.541), hypertension (OR: 1.099, 95 % CI: 1.075-1.125), triglycerides (OR: 1.297, 95 % CI: 1.179-1.428). Conversely, the risk of MetS was causally associated with an increased risk of frailty (OR: 1.048; 95 % CI: 1.024-1.073). however, when removing SNPs assocaited with BMI at the loci significance level and performed MVMR, Mets and frailty were not associated.
Conclusion: These findings suggest a bidirectional causal relationship between frailty and MetS, indicating that genetic factors contributing to frailty also increase the risk of MetS and its components, and vice versa. Furthermore, BMI-related SNPs may act as effect modifiers in the association between MetS and frailty. These insights into the shared pathophysiology of frailty and MetS have implications for the prevention and treatment strategies in elderly individuals with MetS.
{"title":"Genetic insights into the risk of frailty on metabolic syndrome and its components: Bidirectional Mendelian randomization study.","authors":"Zihang Zhang, Pan Zhang, Feng Zhang, Jinghui Zhong, Wen Sun, Houren Xiong","doi":"10.1016/j.numecd.2025.103898","DOIUrl":"https://doi.org/10.1016/j.numecd.2025.103898","url":null,"abstract":"<p><strong>Background and aims: </strong>Previous studies have shown that frailty and metabolic syndrome (Mets) share common pathophysiological mechanisms. However, whether the observed association reflects causality requires clarification. We performed a bidirectional Mendelian randomization study to investigate the causal relationship between frailty, Mets, and their individual components.</p><p><strong>Methods and results: </strong>Summary-level data from GWAS to identify genetic variants associated with frailty, Mets, and its components among individuals of European ancestry. Inverse variance weighting was utilized as the main method. Using bidirectional Mendelian randomization analysis, we found that the risk of frailty was causally associated with an increased risk of MetS (OR: 2.092, 95%CI: 1.564-2.799) and its components, including waist circumference (OR: 1.349, 95 % CI: 1.181-1.541), hypertension (OR: 1.099, 95 % CI: 1.075-1.125), triglycerides (OR: 1.297, 95 % CI: 1.179-1.428). Conversely, the risk of MetS was causally associated with an increased risk of frailty (OR: 1.048; 95 % CI: 1.024-1.073). however, when removing SNPs assocaited with BMI at the loci significance level and performed MVMR, Mets and frailty were not associated.</p><p><strong>Conclusion: </strong>These findings suggest a bidirectional causal relationship between frailty and MetS, indicating that genetic factors contributing to frailty also increase the risk of MetS and its components, and vice versa. Furthermore, BMI-related SNPs may act as effect modifiers in the association between MetS and frailty. These insights into the shared pathophysiology of frailty and MetS have implications for the prevention and treatment strategies in elderly individuals with MetS.</p>","PeriodicalId":49722,"journal":{"name":"Nutrition Metabolism and Cardiovascular Diseases","volume":" ","pages":"103898"},"PeriodicalIF":3.3,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143494518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号