Li Luo, Lian Wang, Xian Yu, Qiuyue Yang, Xian Ming, Hongbo Xiong, Dongsheng Li, Xisheng Yan
{"title":"C-reactive protein-triglyceride glucose index for the detection of the severity of coronary artery disease in different glucose metabolic states in patients with H-type hypertension.","authors":"Li Luo, Lian Wang, Xian Yu, Qiuyue Yang, Xian Ming, Hongbo Xiong, Dongsheng Li, Xisheng Yan","doi":"10.1186/s12933-026-03318-6","DOIUrl":"10.1186/s12933-026-03318-6","url":null,"abstract":"<p><strong>Background: </strong>The C-reactive protein-triglyceride glucose index (CTI) is a novel composite biomarker that integrates inflammation and insulin resistance. However, its association with the severity of coronary artery disease (CAD) in patients with H-type hypertension under different glucose metabolism statuses remains unclear.</p><p><strong>Methods: </strong>This retrospective study enrolled 1392 hypertensive patients who underwent coronary angiography. CTI was calculated as 0.412 × ln(CRP[mg/L]) + ln(TG[mg/dL] × FPG [mg/dL]/2). Patients were divided into three groups according to CTI tertiles: T1 group (6.748 ≤ CTI < 8.674), T2 group (8.674 ≤ CTI < 9.549), and T3 group (9.549 ≤ CTI ≤ 12.713). Based on the Gensini score derived from coronary angiography, the study cohort was divided into three groups according to the severity of stenosis: low stenosis, medium stenosis, and high stenosis. Logistic regression, restricted cubic spline (RCS) analysis, and receiver operating characteristic (ROC) curve analysis were used to investigate the association between CTI and CAD severity across different glucose metabolism statuses and H‑type hypertension subgroups. Incremental utility of CTI was evaluated using receiver operating characteristic (ROC) curves, net reclassification improvement (NRI), integrated discrimination improvement (IDI), and decision curve analysis (DCA).</p><p><strong>Results: </strong>The results show that CTI is significantly associated with CAD severity in hypertensive patients. After adjusting for risk factors, CTI remained significantly associated with multi-vessel CAD (OR = 2.155, 95%CI 1.839-2.455) and moderate-to-severe coronary stenosis (OR = 1.818, 95% CI 1.603-2.062). RCS analysis revealed a linear dose-response relationship between CTI and CAD severity (P for non-linearity > 0.05). Notably, we observed significant interaction between CTI and H-type hypertension on CAD severity (P = 0.033). Under different glycemic statuses, high CTI levels were associated with CAD severity; however, no association between CTI and moderate‑to‑severe coronary stenosis was observed in patients with diabetes mellitus (DM). In the DM subgroup of patients with H-type hypertension, after adjustment for risk factors, patients in the T3 group had a 6.475-fold increased risk of multi-vessel CAD compared with those in the T1 group (95% CI 1.693-24.773, P = 0.006). ROC analysis demonstrated that, across different glucose metabolism subgroups, CTI showed the highest discriminative ability for multi‑vessel CAD in patients with H‑type hypertension and comorbid DM (AUC = 0.712, 95% CI 0.619-0.804, P < 0.001).</p><p><strong>Conclusion: </strong>CTI is an independently associated factor for coronary stenosis severity in patients with hypertension, particularly in those with H‑type hypertension and comorbid diabetes. This simple and cost‑effective composite biomarker holds promise as a practical tool for early risk stratification and for guidin","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"25 1","pages":""},"PeriodicalIF":15.6,"publicationDate":"2026-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A three-metabolite microbiota-associated signature for early risk stratification of gestational diabetes mellitus.","authors":"Shuo Ma, Chen Zhang, Yuming Yao, Meiling Zhou, Ai Chen, Yaya Chen, Yinhao Chen, Jiwei Wang, Gulinaizhaer Abudushalamu, Shijie Cai, Fengfeng Zhao, Dawen Chen, Xiao Li, Yue Zheng, Juxiang Fan, Xun Gao, Yonghui Liu, Weimin Fan, Feng Zhu, Jin Yang, Miao Miao, Xiaobo Fan, Guoqiu Wu","doi":"10.1186/s12933-026-03278-x","DOIUrl":"10.1186/s12933-026-03278-x","url":null,"abstract":"<p><strong>Background: </strong>Gestational diabetes mellitus (GDM) is associated with adverse pregnancy outcomes and long-term metabolic and cardiovascular risk. However, oral glucose tolerance testing at 24-28 gestational weeks limits early risk stratification. Gut microbiota-associated metabolites may reflect early metabolic abnormalities, including those relevant to cardiometabolic health, but robust early-pregnancy biomarkers remain limited.</p><p><strong>Methods: </strong>We conducted a multicenter nested case-control and prospective study involving 2,693 pregnant women. Untargeted metabolomics and metagenomics were integrated to identify GDM-associated metabolites and gut microbial alterations. Three consistently dysregulated metabolites, 3-hydroxydecanoic acid, γ-Glu-Leu, and propionic acid, were quantified by targeted LC-MS/MS. Candidate algorithms were compared using repeated 10-fold cross-validation, and a final generalized linear model was externally and prospectively validated.</p><p><strong>Results: </strong>Women who later developed GDM showed an adverse early-pregnancy metabolic profile, including higher BMI, triglycerides, and platelet count. Untargeted metabolomics identified 14 persistently altered metabolites enriched in energy, oxidative stress, and amino acid metabolism pathways. Metagenomics revealed taxonomic restructuring and coordinated microbiota-metabolite associations. The three-metabolite model achieved AUCs of 0.838 (95% CI, 0.791-0.885) in training, 0.840 (95% CI, 0.769-0.911) in internal validation, 0.955 (95% CI, 0.925-0.985) and 0.917 (95% CI, 0.875-0.958) in two external cohorts, and 0.969 (95% CI, 0.937-1.000) in the prospective cohort.</p><p><strong>Conclusion: </strong>Early microbiota-associated metabolic dysregulation is detectable before routine GDM diagnosis. This compact three-metabolite panel may support early GDM risk stratification and provides metabolic evidence relevant to broader cardiometabolic risk assessment in pregnancy.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"25 1","pages":""},"PeriodicalIF":15.6,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13450031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148688431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Predicting all-cause and cardiovascular mortality in hypertensive patients by combining the CHG index and its obesity indicators: a prospective cohort study with survival prediction model.","authors":"Yuting Zhang, Tao Sun, Qingyuan Xue, Bei Liu","doi":"10.1186/s12933-026-03281-2","DOIUrl":"10.1186/s12933-026-03281-2","url":null,"abstract":"<p><strong>Background: </strong>Hypertension is closely related to the development and mortality of cardiovascular disease (CVD), insulin resistance (IR) plays a key role in hypertension-related metabolic dysfunction, but there is no universally accepted IR marker for hypertensive populations. Recently, the cholesterol-HDL-glucose (CHG) index and its obesity indicators (CHG-BMl, CHG-WC, and CHG-WHtR) have emerged as reliable IR markers. In this research, we aimed to assess their associations with all-cause and cardiovascular mortality among hypertensive patients with machine learning analysis.</p><p><strong>Methods: </strong>Data from 4661 hypertensive participants in the the China Health and Retirement Longitudinal Study (CHARLS) were analysed. Survival machine learning models (Cox, Cox-LASSO, Survival XGBoost) were applied. Model discrimination was assessed by Harrell's C-index and time-dependent ROC (tdAUC) at 3, 5, 7 years. Incremental predictive value was evaluated using continuous net reclassification index (NRI), integrated discrimination improvement (IDI), and decision curve analysis (DCA). Competing-risk (Fine-Gray) regression was performed for cardiovascular mortality.</p><p><strong>Results: </strong>The CHG index and its obesity indicators were independent predictors of both all-cause and cardiovascular mortality among hypertensive patients. The CHG-WHtR showed strong associations with both all-cause (HR = 2.060, 95% CI: 1.852-2.292, P < 0.001) and cardiovascular mortality (HR = 2.020, 95% CI 1.816-2.247, P < 0.001) per 1-SD increase. The test C-index of Cox-LASSO was 0.920 (95% CI 0.878-0.962), with tdAUC ranging 0.851-0.916 across 3, 5 and 7 years. Adding CHG indices substantially improved reclassification (continuous NRI ranging: 0.349-0.496, IDI ranging: 0.024-0.040). L-shaped relationships were observed with both all-cause (non-linear P < 0.001) and cardiovascular mortality (non-linear P < 0.001). The combination of the CHG index or its obesity indicators into predictive models substantially improved the prediction performance for mortality outcomes.</p><p><strong>Conclusions: </strong>The CHG index and its obesity indicators are significant predictors of all-cause and cardiovascular mortality in hypertensive patients, and CHG-WHtR exhibits better prognostic performance in terms of mortality risk. The inclusion of obesity indicators enhances risk stratification and may benefit from tailored interventions among hypertension population.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"25 1","pages":""},"PeriodicalIF":15.6,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13551966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"STIM1-mediated Treg instability in HFpEF: a new immunological target emerges?","authors":"Anna Planavila, Albert Blasco-Roset","doi":"10.1186/s12933-026-03317-7","DOIUrl":"10.1186/s12933-026-03317-7","url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) accounts for nearly half of all heart failure cases and remains a major unmet clinical challenge. Increasing evidence supports the view of HFpEF as a systemic inflammatory syndrome driven by aging and cardiometabolic comorbidities, including obesity, hypertension, and chronic kidney disease. Within this framework, regulatory T cells (Tregs), which are essential for maintaining immune tolerance and limiting excessive inflammation, have emerged as important modulators of disease progression. However, the mechanisms underlying Treg dysfunction in HFpEF have remained poorly understood. In this issue, Srinivas et al. identify stromal interaction molecule 1 (STIM1)-dependent calcium signaling as a critical regulator of Treg instability in HFpEF. The authors show that patients with HFpEF exhibit reduced circulating Treg numbers, increased STIM1 expression, and activation of endoplasmic reticulum stress, apoptotic, and inflammatory pathways. Using a cardiometabolic murine model and Treg-specific STIM1 knockout mice, they establish a causal role for Treg-intrinsic STIM1 signaling in disease development. These findings position STIM1 as a molecular link between cardiometabolic stress, immune dysregulation, and cardiac remodeling. They further support the concept that immune-cell plasticity is a major determinant of HFpEF pathogenesis and suggest that preserving Treg stability may represent a novel therapeutic strategy. Although important questions remain regarding disease timing, clinical translation, and sex-specific effects, this work advances our understanding of HFpEF as an immune-mediated disorder and identifies STIM1-dependent calcium signaling as a promising therapeutic target.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"25 1","pages":""},"PeriodicalIF":15.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13428441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148653194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kun Liu, Kazuki Osuka, Mengying Xu, Rhea Takhar, Neda Mohammadi, Adam Trevett, Jinyan Zhong, Ching-Wen Chang, Nan Wang, Xinyu Hu, Ruirui Dong, Shunan Zhang, YoonYoung Choi, Thamali Ayagama, Mingyu Li, Linna Zhou, Che-Mai Chang, Wan-Chen Huang, Wei-Chiao Chang, Neil Herring, Annika Winbo, Guoliang Hao, Jie Zhang, Dan Li
{"title":"Compartment-specific cAMP dysfunction in diabetic cardiomyopathy in hiPSC-derived cardiomyocytes: therapeutic potential of fibroblast growth factor 1.","authors":"Kun Liu, Kazuki Osuka, Mengying Xu, Rhea Takhar, Neda Mohammadi, Adam Trevett, Jinyan Zhong, Ching-Wen Chang, Nan Wang, Xinyu Hu, Ruirui Dong, Shunan Zhang, YoonYoung Choi, Thamali Ayagama, Mingyu Li, Linna Zhou, Che-Mai Chang, Wan-Chen Huang, Wei-Chiao Chang, Neil Herring, Annika Winbo, Guoliang Hao, Jie Zhang, Dan Li","doi":"10.1186/s12933-026-03288-9","DOIUrl":"10.1186/s12933-026-03288-9","url":null,"abstract":"<p><strong>Background: </strong>Diabetic cardiomyopathy (DCM) represents a distinct form of heart failure occurring independently of coronary artery disease, yet effective treatments remain limited. While cAMP signaling alterations have been reported in diabetic hearts, the compartment-specific consequences across distinct subcellular pools remain poorly understood. We investigated cytosolic and mitochondrial cAMP microdomain dysfunction in DCM, focusing on ADCY2 and PDE4DIP as potential regulators, and evaluated fibroblast growth factor 1 (FGF1) as a therapeutic intervention using integrated two-dimensional (2D) and three-dimensional (3D) human induced pluripotent stem cell (hiPSC)-derived cardiac models.</p><p><strong>Methods: </strong>Healthy hiPSC-derived cardiomyocytes were exposed to a diabetic-like environment (high glucose, endothelin-1 and cortisol) in 2D and 3D culture. Two-dimensional studies included bulk RNA sequencing, FRET-based cAMP measurements in cytosolic and mitochondrial outer membrane compartments, and microelectrode array electrophysiology. Three-dimensional cardiac microtissues were assessed by optical mapping to characterize spatial calcium dynamics and conduction properties.</p><p><strong>Results: </strong>DCM exhibited compartment-specific cAMP dysregulation associated with ADCY2 downregulation and PDE4DIP upregulation. Cytosolic compartments showed preserved baseline cAMP but attenuated forskolin responsiveness, while the mitochondrial outer membrane displayed both reduced baseline cAMP and impaired stimulated responses. Transcriptomic analysis revealed transcriptional signatures consistent with metabolic remodeling, including upregulated fatty acid oxidation machinery, Complex I dysfunction, and elevated phospholamban and CASQ2 expression. 3D optical mapping demonstrated reduced calcium transient amplitude, prolonged transient duration, and severely impaired calcium propagation velocity. FGF1 treatment normalized PDE4DIP expression and restored cAMP dynamics in 2D cultures and partially improved calcium transient amplitude in 3D microtissues, though conduction defects persisted.</p><p><strong>Conclusions: </strong>Compartment-specific impairment of cAMP microdomains is associated with DCM pathogenesis. Integrated 2D-3D assessment reveals that FGF1 improves cAMP signaling but does not fully reverse metabolic, electrophysiological, or structural abnormalities, highlighting the need for combination therapies targeting both cAMP pathway integrity and conduction restoration.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"25 1","pages":""},"PeriodicalIF":15.6,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13712054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149262801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epicardial adipose tissue volume and nephropathy in people living with type 2 diabetes: the Kidn-EAT study.","authors":"Anaïs Andrieu, Sopio Tatulashvili, Siwar Hammami, Mohamed Lamine Mariko, Imen Rezgani, Lucie Allard, Meriem Sal, Ines Barka, Mohamed Zerguine, Sébastien Homs, Pierre-Yves Brillet, Emmanuelle Fabre, Coralie Bloch-Queyrat, Hélène Bihan, Emmanuel Cosson","doi":"10.1186/s12933-026-03311-z","DOIUrl":"10.1186/s12933-026-03311-z","url":null,"abstract":"<p><strong>Introduction: </strong>Epicardial adipose tissue (EAT), a visceral adipose tissue located between the pericardium and the myocardium, has been linked to cardiac issues. The present study aimed to evaluate the association between EAT volume and the presence of nephropathy and its components, i.e. albuminuria/creatininuria ratio (ACR) and estimated glomerular filtration rate (eGFR) classes, in patients living with type 2 diabetes (PwT2D).</p><p><strong>Materials and methods: </strong>The present study is a cross-sectional analysis of a retrospective cohort of 700 PwT2D who had a computed tomography scan to measure both their coronary artery calcium score and EAT volume (proprietary prototype, GE HealthCare), and available data for both eGFR and ACR.</p><p><strong>Results: </strong>A total of 700 PwT2D (332 women) were included, of whom 295 patients had nephropathy (42.1%), including 87 (12.4%) with eGFR < 60 ml/min/1.73m<sup>2</sup> and 258 (36.9%) with ACR ≥ 3 mg/mmol. Mean age (± standard deviation) was 60.3 ± 10.4 years old and 44.8% had obesity. EAT volume was higher in patients with nephropathy compared to those without (respectively, 103.6 ± 39.8 versus 93.8 ± 36.8 cm<sup>3</sup>, p = 0.001). EAT volume differed across eGFR classes (≥ 60 versus < 60 mL/min/1.73m<sup>2</sup>): respectively 96.6 ± 38.1 and 107.7 ± 39.2 (p = 0.012) and ACR classes (< 3; between 3 and 29.9; ≥ 30 mg/mmol): respectively 94.7 ± 36.9, 106.0 ± 40.2, and 95.7 ± 39.8 cm<sup>3</sup> (p = 0.004). EAT volume was weakly correlated to eGFR (r = -0.146; p < 0.001) and to ACR (r = 0.124; p = 0.001). After adjustment for major confounding factors, each 10 cm<sup>3</sup> increase of EAT volume was associated with a 5.8% increase in the odds of nephropathy (OR = 1.058 [95% CI 1.007-1.112], p = 0.026) and a 5.9% increase in the odds of ACR ≥ 3 mg/mmol (OR = 1.059 [95% CI 1.008-1.114], p = 0.024), but not with eGFR < 60 mL/min/1.73m<sup>2</sup> (OR = 1.047 [95% CI 0.975-1.123], p = 0.204).</p><p><strong>Conclusion: </strong>EAT volume was associated with nephropathy and especially with increased ACR in PwT2D. This association may be partly explained by metabolic and inflammatory mechanisms, potentially driven by EAT and/or other associated ectopic fat depots in PwT2D.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"25 1","pages":""},"PeriodicalIF":15.6,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13711880/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149262771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elena Fortin, Olle Melander, Giulia Ferrannini, Per Näsman, Anna Norhammar, Lars Rydén, Stina Smetana, Malin Svensson, Linda Mellbin
{"title":"Effect of empagliflozin on copeptin levels in patients with recent acute coronary syndrome and newly detected dysglycaemia: a post-hoc analysis of the SOCOGAMI randomized controlled trial.","authors":"Elena Fortin, Olle Melander, Giulia Ferrannini, Per Näsman, Anna Norhammar, Lars Rydén, Stina Smetana, Malin Svensson, Linda Mellbin","doi":"10.1186/s12933-026-03312-y","DOIUrl":"10.1186/s12933-026-03312-y","url":null,"abstract":"<p><strong>Background: </strong>Copeptin, a surrogate marker for vasopressin secretion, is associated with cardiovascular disease, insulin resistance and dysglycaemia. The cardioprotective effects of sodium-glucose cotransporter 2 inhibitors (SGLT2i) may involve vasopressin modulation through fluid redistribution, but whether this effect persists long-term in high-cardiovascular-risk patients with newly detected dysglycaemia remains unknown.</p><p><strong>Methods: </strong>In this post-hoc analysis of the SOCOGAMI double-blind, placebo-controlled trial, 42 patients (mean age 67.5 years, 19% females) with impaired glucose tolerance or newly detected type 2 diabetes following an ACS and no heart failure were randomized to empagliflozin 25 mg/day (n = 20) or placebo (n = 22) for 7 months. Copeptin was measured during oral glucose tolerance tests (OGTT) at baseline, after 7 months on-treatment, and 3 months after treatment withdrawal. Treatment effects were assessed by repeated-measures ANOVA with treatment × time interaction and linear mixed-effects models.</p><p><strong>Results: </strong>Haematocrit, but not copeptin, showed a significant between-group difference at 7 months (p = 0.03 and p = 0.63, respectively). Both markers returned toward baseline after treatment withdrawal, but the overall treatment × time interaction was not significant for either (p = 0.72 and p = 0.64 respectively). Results were unchanged after accounting for a baseline imbalance in diuretic use (35% vs. 14%). Copeptin was not associated with the glucose-lowering effect of empagliflozin and no differential copeptin response during the OGTT across groups or visits was observed. In exploratory analyses, copeptin correlated with arterial pulse wave velocity at baseline (rs = 0.40, unadjusted p = 0.03).</p><p><strong>Conclusions: </strong>In this post-hoc analysis, empagliflozin treatment was not associated with statistically significant sustained vasopressin secretion in post-ACS patients with newly detected dysglycaemia and preserved cardiac function. Due to the limited power and the absence of early on-treatment sampling these findings cannot exclude AVP modulation and warrant confirmation in adequately powered studies.</p><p><strong>Trial registration: </strong>EudraCT number 2015-004571-73.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"25 1","pages":""},"PeriodicalIF":15.6,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Franck Phan, Fabrizio Andreelli, Thomas Broussaud, Samia Boussouar, Anne-Caroline Jeannin, Suzanne Laroche, Anne Toulgoat, Antonio Gallo, Olivier Bourron, Alban Redheuil
{"title":"Diabetic retinopathy enhances coronary artery calcium-based cardiovascular risk stratification in patients with type 2 diabetes: insights from the ACCoDiab study.","authors":"Franck Phan, Fabrizio Andreelli, Thomas Broussaud, Samia Boussouar, Anne-Caroline Jeannin, Suzanne Laroche, Anne Toulgoat, Antonio Gallo, Olivier Bourron, Alban Redheuil","doi":"10.1186/s12933-026-03314-w","DOIUrl":"10.1186/s12933-026-03314-w","url":null,"abstract":"<p><strong>Background: </strong>The coronary artery calcium (CAC) score is a validated imaging biomarker enhancing cardiovascular risk stratification in patients with type 2 diabetes mellitus (T2DM). However, residual risk persists, particularly among patients with moderate CAC scores. Diabetic retinopathy (DR), a microvascular complication of diabetes, may reflect systemic vascular vulnerability and provide additional prognostic information.</p><p><strong>Methods: </strong>This observational cohort study was conducted as part of the primary prevention ACCoDiab study. 424 patients with T2DM (175 females and 249 males, with a mean age of 61 years) and no history of cardiovascular events underwent CAC scoring and clinical assessments, including DR screening. Patients were monitored for seven years or until the first cardiovascular events, including nonfatal myocardial infarction, ischemic stroke, hospitalization for heart failure, peripheral artery disease revascularization, and cardiovascular death. Cox regression, Kaplan-Meier survival analysis, receiver operating characteristic (ROC) curves, and net reclassification improvement (NRI) were used to evaluate the added prognostic value of DR to CAC scoring and to develop a simple integrated cardiovascular risk score.</p><p><strong>Results: </strong>Fifty patients (11.8%) had incident cardiovascular events. DR was significantly more prevalent among those who experienced events (58% vs. 25%, p < 0.001). Both CAC score and DR were independently associated with cardiovascular events. When incorporating DR into the CAC-based risk model, the predictive power was significantly enhanced AUC 75 [0.69-0.82] vs. 68 [0.61-0.75], p = 0.01). Further improvement was observed after adjusting for traditional risk factors (AUC 79 [0.73-0.86] vs. 73 [0.66-0.81], p = 0.04). The presence of DR reclassified a significant proportion of patients into higher-risk categories, particularly those with low and moderate CAC scores. Additionally, the severity of DR was also found to provide incremental prognostic information but did not provide significant additional stratification beyond the binary presence of DR.</p><p><strong>Conclusion: </strong>The combination of diabetic retinopathy and CAC score significantly enhances cardiovascular risk stratification in T2DM patients, beyond traditional risk factors, highlighting that both microvascular and macrovascular factors should be considered in comprehensive cardiovascular risk assessment. This approach, integrated to clinical routine, may help identify patients for earlier intervention and more personalized treatment strategies. Trial registration NCT03920683.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"25 1","pages":""},"PeriodicalIF":15.6,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13685371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149236984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Longitudinal inflammatory-metabolic-adiposity burden and incident heart failure across cardiovascular-kidney-metabolic stages: a prospective cohort study.","authors":"Fangyi Dai, Yong Dai","doi":"10.1186/s12933-026-03310-0","DOIUrl":"10.1186/s12933-026-03310-0","url":null,"abstract":"<p><strong>Background: </strong>Heart failure remains a major health burden among older adults. Although systemic inflammation, metabolic dysregulation, and central adiposity are individually recognized as heart failure risk factors, composite biomarkers capturing their longitudinal convergence and interaction with cardiovascular-kidney-metabolic (CKM) staging remain unexplored.</p><p><strong>Objectives: </strong>To investigate the association of longitudinal CTGW composite index (C-reactive protein × triglyceride-glucose index × waist-to-height ratio) trajectories and cumulative burden with incident heart failure, and to examine effect modification by baseline CKM stage.</p><p><strong>Methods: </strong>This prospective cohort study included 1946 participants aged 50 years and older from the English Longitudinal Study of Ageing, free of heart failure at Wave 2 (2004-2005), followed through Wave 8 (2016-2017). Group-based multi-trajectory modeling jointly classified longitudinal CRP, triglycerides, glucose, and WHtR across three waves. Cumulative CTGW burden was quantified using the trapezoidal rule. Cox proportional hazards regression with sequential adjustment and restricted cubic spline analyses were employed.</p><p><strong>Results: </strong>Over a median follow-up spanning 12 years, 113 participants (5.8%) developed incident heart failure. Three distinct trajectories were identified: low-stable (n = 697, 35.8%), moderate-metabolic (n = 943, 48.5%), and high-inflammatory (n = 306, 15.7%). In fully adjusted models, the high-inflammatory trajectory conferred the greatest risk (HR = 2.69, 95% CI 1.46-4.93, P = 0.001), followed by the moderate-metabolic trajectory (HR = 1.96, 95% CI 1.17-3.29, P = 0.011). For cumulative burden, the highest quartile was significantly associated with incident heart failure (HR = 2.35, 95% CI 1.31-4.24, P = 0.004; P for trend < 0.001), with each standard deviation increase corresponding to 19% higher risk (HR = 1.19, 95% CI 1.04-1.36, P = 0.014). A nonlinear dose-response relationship was confirmed (P for nonlinearity = 0.032), with the risk threshold identified at approximately 8.2. Stratified analyses revealed significant effect modification by CKM stage (P for interaction = 0.031), with the strongest association observed in Stage 3-4 (HR = 2.37, 95% CI 1.24-4.53, P = 0.009). Subgroup analyses demonstrated consistent effect directions across age, sex, BMI, and comorbidity strata without significant interactions.</p><p><strong>Conclusions: </strong>Longitudinal CTGW trajectories and cumulative burden are independently associated with incident heart failure in a nonlinear dose-response manner, with the association amplified across advancing CKM stages, supporting the CTGW composite index as a potential integrative biomarker for heart failure risk stratification.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"25 1","pages":""},"PeriodicalIF":15.6,"publicationDate":"2026-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Li Jiang, Yuan Li, Hua-Yan Xu, Xue-Ming Li, Ke Shi, Jin Wang, Shi-Qin Yu, Yu Jiang, Han Fang, Wei-Feng Yan, Ying-Kun Guo, Zhi-Gang Yang
{"title":"Association of the triglyceride-glucose index with subclinical left ventricular dysfunction in type 2 diabetes mellitus: mediation by myocardial energetic efficiency and resting perfusion.","authors":"Li Jiang, Yuan Li, Hua-Yan Xu, Xue-Ming Li, Ke Shi, Jin Wang, Shi-Qin Yu, Yu Jiang, Han Fang, Wei-Feng Yan, Ying-Kun Guo, Zhi-Gang Yang","doi":"10.1186/s12933-026-03308-8","DOIUrl":"10.1186/s12933-026-03308-8","url":null,"abstract":"<p><strong>Background: </strong>The triglyceride-glucose(TyG) index, a surrogate marker of insulin resistance, has been linked to cardiac dysfunction; however, its underlying associated pathways in patients with type 2 diabetes mellitus(T2DM) remain unclear. This study used cardiac magnetic resonance(CMR) to explore the association of TyG index with subclinical left ventricular(LV) myocardial dysfunction and whether imaging indicators statistically mediate this relationship.</p><p><strong>Methods: </strong>In this retrospective cross-sectional study, a total of 235 T2DM patients who underwent CMR examination were included and assigned to three groups based on the tertiles of their TyG indexes as follows: low(< 8.73, n = 78), moderate(8.73-9.36, n = 79), and high TyG index(≥ 9.36, n = 78) groups. LV geometry, function, myocardial energetic efficiency index (MEEi), resting first-pass perfusion, and global peak strain in radial(GRPS), circumferential(GCPS), and longitudinal(GLPS) directions were measured. Univariate and multivariate linear regression models and exploratory mediation analysis were used to analyze the associations of TyG index on LV global strain.</p><p><strong>Results: </strong>Compared with the low and moderate TyG index groups, the high TyG index group had significantly higher LV remodeling index, lower LV global function index, lower MEEi, impaired resting myocardial perfusion, and reduced LV global peak strain (all p ≤ 0.002). Multivariate analysis showed that TyG index remained independently associated with reduced LV strain after adjusting for confounders (GRPS β = -0.261; GCPS β = 0.271; GLPS β = 0.381; all p < 0.001). And MEEi and upslope were also independently associated with reduced LV GRPS and GLPS (all p < 0.05). Further mediation analysis revealed the statistically mediated proportions of the association between the TyG index and LV global strain were 8.2-8.6% for MEEi and 4.3% to 12.5% for upslope. In model comparison analyses, the TyG index demonstrated substantially better model fit than either component alone across all strain directions (all Akaike Information Criterion difference > 150).</p><p><strong>Conclusions: </strong>In patients with T2DM, a higher TyG index is independently associated with decreased LV global strain, and this relationship is statistically mediated by reduced MEEi and impaired resting perfusion upslope. These findings generate hypotheses regarding myocardial energetics and resting perfusion as potential pathways associated with diabetic myocardial dysfunction that warrant prospective investigation.</p>","PeriodicalId":9374,"journal":{"name":"Cardiovascular Diabetology","volume":"25 1","pages":""},"PeriodicalIF":15.6,"publicationDate":"2026-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13435890/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148668429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}