Cardiovascular Diabetology心血管糖尿病学
Cardiovascular Diabetology(英文缩写 CARDIOVASC DIABETOL),ISSN 1475-2840,eISSN 1475-2840,中文译名:心血管糖尿病学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
Cardiovascular Diabetology 最新收录文献
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1. Antecedent, landmark, and two-visit cumulative triglyceride-glucose index and non-traditional lipid measures in relation to incident cardiovascular disease in adults with cardiovascular-kidney-metabolic syndrome (CKM) stages 0-3: a nationwide prospective cohort study.
1. 既往、标志性及两次随访累积甘油三酯-葡萄糖指数和非传统血脂指标与心血管-肾脏-代谢综合征（CKM）0-3期成人新发心血管疾病的关系：一项全国性前瞻性队列研究PMID:日期:2026-09-23The triglyceride-glucose (TyG) index and non-traditional lipid parameters (nTLPs) are inexpensive markers of overlapping metabolic and lipoprotein burden. Their CVD-specific longitudinal associations and incremental prognostic contribution in adults with cardiovascular-kidney-metabolic (CKM) stages 0-3 remain uncertain. We conducted a 2015 landmark analysis in the China Health and Retirement Longitudinal Study. TyG was evaluated jointly with the atherogenic index of plasma (AIP), non-HDL cholesterol (non-HDL-C), Castelli risk indices I and II (CRI-I and CRI-II), and the lipoprotein combine index (LCI). We examined antecedent 2011 values, 2015 landmark values, and a two-visit time-weighted cumulative measure from 2011 to 2015. The primary analysis family comprised five cumulative dual-high versus dual-low comparisons for incident CVD. Cause-specific Cox and Fine-Gray models were fitted, with Benjamini-Hochberg correction. Secondary analyses addressed heart disease, stroke, dose response, effect modification, robustness, and censoring-aware five-year prediction. Among 4,420 participants with CKM stages 0-3 and valid post-landmark CVD follow-up, 827 developed CVD; endpoint-specific analyses included 4,411 participants with 571 heart-disease events and 4414 with 328 stroke events. For cumulative dual-high exposure, adjusted Cox HRs for CVD ranged from 1.29 (95% CI 1.09-1.52) to 1.45 (1.20-1.74), and Fine-Gray SHRs ranged from 1.28 (1.09-1.50) to 1.43 (1.19-1.72); all primary FDR q values were < 0.003. Secondary stroke estimates were generally larger. The covariate-only C-index was 0.616 and five-year IPCW AUC was 0.634 (0.608-0.659). The best expanded model, TyG plus CRI-II, yielded a C-index of 0.628 and AUC of 0.665 (0.640-0.690), corresponding to changes of 0.012 and 0.031, respectively. Higher two-visit cumulative TyG-nTLP burden was associated with incident CVD after accounting for competing death. However, incremental discrimination was small, and shared laboratory components limit claims of biological independence or synergy. These indices may provide additional information for epidemiologic risk characterization, while their incremental clinical predictive value appears limited and warrants further validation.
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2. Mild autonomous cortisol secretion (MACS) is associated with increased mortality in patients with adrenal adenomas only in the presence of type 2 diabetes: a retrospective cohort study.
2. 轻度自主皮质醇分泌（MACS）仅在合并2型糖尿病的肾上腺腺瘤患者中与死亡率增加相关：一项回顾性队列研究PMID:日期:2026-09-22Hypercortisolism and type 2 diabetes mellitus (T2D) independently contribute to an increased burden of cardiometabolic morbidity and mortality. However, data on the interaction of hypercortisolism and T2D are scarce-thus, we aimed to assess the cortisol-associated morbidity and mortality in the context of T2D and adrenal mild autonomous cortisol secretion (MACS). This is a retrospective cohort study including 668 patients with adrenal adenomas, who were visiting the endocrine outpatient clinic at the Vienna General Hospital between 01.01.2000 to 31.12.2022. Of those, 151 were diagnosed with T2D at the time of their 1 mg dexamethasone suppression test (DST), other diabetes types were excluded. MACS was defined as a post 1 mg DST cortisol of > 1.8 µg/dL in the absence of Cushing's stigmata and after biochemical exclusion of ACTH-dependency. The database was linked to the governmental death registry and patients alive after 01.12.2024 were censored. Kaplan Meier curves and cox proportional hazard models were analyzed via RStudio. Patients with T2D had a higher post 1 mg DST cortisol level and were more often diagnosed with hypertension, dyslipidemia and cardiovascular disease (CVD) compared to those without T2D. Compared to patients with non-functioning adrenal adenomas (NFAA) without T2D, MACS was strongly linked to increased mortality only in T2D (HR 2.51 [CI95% 1.41-4.48], p < 0.01) but not in those without T2D, even after adjustment for age, sex, BMI, smoking, hypertension, dyslipidemia and CVD at baseline. The T2D cohort with MACS had higher HbA1c and a 3-fold elevation in CVD prevalence compared to those without hypercortisolism. They did not differ according to age, sex or other cardiometabolic risk parameters (dyslipidemia, hypertension, BMI). Among patients with adrenal adenomas, MACS is related to increased CVD prevalence and is associated with mortality in patients with T2D. These findings highlight the need for confirmatory prospective studies incorporating larger sample sizes to further assess the importance of earlier identification and treatment of MACS in patients with T2D.
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3. Subclinical cardiac involvement during diabetic ketoacidosis at type 1 diabetes onset in youth: biomarker elevation, altered diastolic filling, and reduced global longitudinal strain: a prospective cohort study.
PMID:日期:2026-09-18Diabetic ketoacidosis (DKA) may be associated with cardiac involvement. Increased cardiac biomarkers and abnormalities in cardiac function were mainly reported in adults with type 1 diabetes (T1D). Pediatric data are lacking. This study therefore assessed cardiac biomarker alterations and echocardiographic changes, including strain analysis, in children with diabetic ketoacidosis at the onset of type 1 diabetes. In this prospective, observational, cohort study, patients < 18 years with T1D onset were consecutively enrolled at a single center from January 2024 to March 2025 and classified as DKA or non-DKA. Cardiac biomarkers (troponin I, NT-proBNP) were measured before and 24 h after therapy initiation in all patients, and additionally at 48 and 72 h in those with DKA. Echocardiography, including speckle-tracking strain analysis, was performed after 24 h in both groups and after 6 days in the DKA group. Eighty-one patients were included (60% male; median age 9.8 years [5.2-14.1]); 43 (53.1%) had DKA. Troponin I and NT-proBNP were significantly higher in the DKA group at baseline (troponin I: 5.7 [4.1-10.8] vs. 3.9 [3.9-4.6] ng/L, p < 0.001; NT-proBNP: 87.0 [41.0-231.0] vs. 40.0 [16.8-69.0] ng/L, p = 0.002) and remained elevated at 24 h. Echocardiography showed lower E/A ratios, higher peak a'-wave velocities, and a significantly reduced left ventricular global longitudinal strain (GLS) in the DKA group (- 19.2 [- 20.4 to - 18.1] vs. - 21.5 [- 23.0 to - 18.9], p = 0.029), with most values within the normal range. In multivariable analysis, lower bicarbonate (indicating greater DKA severity) was independently associated with higher troponin I and NT-proBNP, and younger age with higher NT-proBNP. In children with T1D, DKA at onset is associated with subclinical cardiac involvement, reflected by elevated cardiac biomarkers, altered diastolic filling parameters, and reduced left ventricular GLS. These findings indicate myocardial stress during the acute phase of DKA; whether they carry prognostic significance requires studies with longer-term follow-up. The study was registered in the German Clinical Trial Register (DRKS00032719).
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4. Retraction Note to: Dipeptidyl peptidase-4 (DPP-4) inhibition with linagliptin reduces western diet-induced myocardial TRAF3IP2 expression, inflammation and fibrosis in female mice.
4. 撤回声明：利格列汀抑制二肽基肽酶-4（DPP-4）可减少西方饮食诱导的雌性小鼠心肌TRAF3IP2表达、炎症及纤维化PMID:日期:2026-09-11该文献暂无摘要。
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5. Epigenetic and genetic factors modifying the association between diet quality and incident type 2 diabetes: the EPIC-Potsdam cohort.
PMID:日期:2026-09-11Benefits of healthy diets for type 2 diabetes (T2D) prevention are established. It remains unclear whether such recommendations should be tailored to specific subgroups according to their susceptibility to the disease. This study aimed to assess whether the association of diet quality with T2D risk differs across subgroups with different genetic or epigenetic susceptibility. We used data from a case-cohort within the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam cohort (random subsample with genetic data of 2204 participants, 750 verified incident T2D cases; random subsample with epigenetic data of 1065 participants, 676 verified incident T2D cases). The Alternative Healthy Eating Index (AHEI-2010), Dietary Approaches to Stop Hypertension (DASH), Dietary Inflammatory Index (DII) and the Mediterranean Diet Pyramid score (MedPyr) were used to assess diet quality. A blood DNA methylation risk score (MRS) was used to reflect epigenetic risk. Genetic risk was characterized using global polygenic risk scores (PRS) and pathway-specific polygenic risk scores (pPRS). Cox proportional hazards models were used to assess the modification of the diet quality-diabetes risk association by the risk scores. Higher adherence to the AHEI-2010 was associated with a lower risk of T2D, while higher MRS, PRS and pPRS predictably indicated higher risk in this population. We detected significant modification of the diet quality-T2D association by the MRS for AHEI-2010 (p = 0.008) and MedPyr (p < 0.0001) and DII (p = 0.010) but only the AHEI-2010 × MRS interaction was robust across all sensitivity analyses. However, we did not find evidence of interaction between diet quality and genetic risk. The associations of healthy diets with T2D could depend on the diabetes risk captured by blood DNA methylation profiles, but they do not seem to depend on the genetic predisposition for T2D. Confirmation of the effect modification by the MRS in independent populations is further required before considering clinical application.
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6. Integrative plasma proteomic network analysis identifies physical activity-associated protein modules potentially mediating type 2 diabetes risk.
6. 整合性血浆蛋白质组网络分析识别出可能介导2型糖尿病风险的体力活动相关蛋白模块PMID:日期:2026-09-09Moderate-to-vigorous physical activity (MVPA) lowers the risk of type 2 diabetes (T2D). Identifying protein modules that mediate this association may help dissect these biological underpinnings, but they remain incompletely characterized. We studied 28,842 diabetes-free UK Biobank participants with baseline plasma proteomics. Guideline-adherent MVPA was defined as ≥ 600 metabolic equivalent of task-minutes per week. We first evaluated associations of MVPA with incident T2D and 2910 plasma proteins, followed by mediation analyses of individual proteins. We then identified protein co-expression modules using multiscale embedded gene co-expression network analysis (MEGENA), tested module-level associations with MVPA, and mediation of incident T2D. Protein modules were further evaluated using module-level Mendelian randomization, whole-genome-sequencing genome-wide association studies, human pancreatic islet single-cell RNA sequencing, leave-one-out sensitivity analyses, and pathway enrichment analyses. Over a median 13.60 years (IQR: [12.82, 14.35]), 1225 participants developed incident T2D. Guideline-adherent MVPA was associated with lower T2D risk and with 650 circulating proteins, of which 451 were Bonferroni-significant mediators. MEGENA analysis identified 171 robust modules, with 67 mediating the MVPA-T2D association. Twelve terminal modules, representing the finest-resolution functions, were selected for further analysis based on their significant mediated effects and enrichment in potential individual mediators. Genetic and functional analyses highlighted two modules: CKB-IGFBP2-centric module was positively associated with MVPA (β [95% CI] 0.196 [0.168, 0.224]) and genetically associated with lower T2D risk (OR [95% CI] 0.57 [0.43, 0.77]). Conversely, RIDA-PCBD1-centric module was inversely associated with MVPA (- 0.134 [- 0.162, - 0.108]) and genetically associated with higher T2D risk (1.54 [1.13, 2.09]). Compared to individual protein analyses, these modules captured unique pathways, supporting the CKB-IGFBP2-centered and RIDA-PCBD1-centered modules as antigen-presentation-enriched and complement/apoptic-cell-clearance-enriched modules, respectively. Finally, the constituent genes of both modules were enriched in T2D-related gene changes in pancreatic β-cells, with the antigen-presentation-enriched module showing additional enrichment across α-, δ-, and ductal cells. MVPA may reduce T2D risk through two coordinated plasma protein networks rather than only through individual circulating proteins. Evaluating coordinated protein modules may provide a system-level biological framework for understanding how exercise protects against T2D.
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7. Evaluative performance of triglyceride-glucose-frailty index versus surrogate insulin resistance indices for advanced cardiovascular-kidney-metabolic syndrome, cardiometabolic multimorbidity, and mortality: the role of estimated glomerular filtration rate.
7. 甘油三酯-葡萄糖-衰弱指数与替代胰岛素抵抗指标对晚期心血管-肾脏-代谢综合征、心脏代谢多病共存及死亡率的评估效能比较：估算肾小球滤过率的作用PMID:日期:2026-09-03Cardiovascular-kidney-metabolic (CKM) syndrome and cardiometabolic multimorbidity (CMM) carry substantial mortality, yet whether a composite index integrating insulin resistance and frailty shows stronger associations with advanced CKM syndrome, CMM, and mortality than conventional metabolic markers remains unclear. This study evaluated the associations of the triglyceride-glucose-frailty index (TyG-FI) with CKM, CMM, and all-cause and cardiovascular mortality, and explored the role of baseline estimated glomerular filtration rate (eGFR). The analysis included 11,228 adults aged 20-79 years from the National Health and Nutrition Examination Survey 2001-2018. TyG-FI was calculated as the TyG index multiplied by the frailty index. Survey-weighted logistic and Cox proportional-hazards models were used to estimate odds and hazard ratios, with sequential adjustment for demographic, socioeconomic, and behavioral confounders. Restricted cubic splines examined non-linear relationships. Overall model performance was assessed using receiver operating characteristic curves with DeLong's test, time-dependent AUC, Harrell's C-index, calibration, and decision curve analysis. Exploratory mediation analyses quantified the proportion of mortality associations accounted for by baseline eGFR. Robustness was verified through multiple sensitivity and subgroup analyses. Over a median follow-up of 90 months (1,220 all-cause and 379 cardiovascular deaths), higher TyG-FI quartiles were associated with graded decreases in survival. Compared with the lowest TyG-FI quartile, the highest quartile yielded markedly elevated odds for advanced CKM syndrome (OR = 4.57, 95% CI: 3.50-5.99) and CMM (OR = 5.09, 95% CI: 2.83-9.16), and higher hazard for all-cause (HR = 3.90, 95% CI: 2.96-5.13) and cardiovascular death (HR = 5.82, 95% CI: 3.38-10.03). Among participants with CMM, the relationship remained for all-cause death (HR = 2.69, 95% CI: 1.69-4.28). The dose-response patterns were non-linear for outcomes (P for non-linearity < 0.001). TyG-FI demonstrated higher discrimination than most surrogate insulin resistance indices, and lower baseline eGFR partly accounted for 16.45% to 26.74% of the associations with mortality. Sensitivity analyses corroborated the consistency of all findings. TyG-FI, which captures both metabolic dysfunction and physiological frailty, showed stronger associations with advanced CKM syndrome, prevalent CMM, and mortality than most surrogate insulin resistance indices. In exploratory analyses, lower baseline eGFR partly accounted for a proportion of the association with mortality. TyG-FI may offer a pragmatic tool for early mortality risk stratification in individuals with high cardiometabolic risk.
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8. Reduced serum acetyl-L-carnitine is associated with hypertensive disorders in women with gestational diabetes mellitus: a multi-omics study.
PMID:日期:2026-08-26Gestational diabetes mellitus (GDM) and hypertensive disorders of pregnancy (HDP) are common metabolic complications during pregnancy. GDM is an independent risk factor for HDP, while HDP is a major contributor to maternal and perinatal morbidity and mortality. Reliable early tools for identifying women with GDM who are at risk of subsequently developing HDP remain limited. This study aimed to integrate metabolomic, lipidomic, and clinical data to identify reproducible candidate biomarkers associated with subsequently diagnosed HDP in women with GDM and to characterize the accompanying metabolic and lipidomic alterations. In this prospective exploratory biomarker study, a discovery cohort (n = 128) and a validation cohort (n = 55) were recruited. Serum samples collected at 24-28 weeks of gestation were analyzed using untargeted and targeted metabolomics. Lipidomics was performed to complement the metabolomic analysis and characterize lipid-related alterations. A combined predictive model was constructed using logistic regression, and its predictive performance was evaluated using receiver operating characteristic (ROC) analysis. Untargeted metabolomics identified lower serum acetyl-L-carnitine (ALC) in the GDMHDP group than in the GDM group, and this difference was confirmed by targeted LC-MS/MS in the validation cohort. The combined ALC-diastolic blood pressure (DBP) model achieved an area under the curve (AUC) of 0.907 in the discovery cohort and 0.886 in the validation cohort. Adding ALC to DBP improved discrimination and reclassification in both cohorts. Multi-omics analysis showed complementary and partly distinct lipid associations with ALC and DBP. Lower ALC was associated with selected ceramide and monolysocardiolipin species, as well as with lipid patterns consistent with altered fatty-acid handling, whereas DBP showed a partly distinct pattern of lipid correlations. Reduced serum ALC at 24-28 weeks of gestation was reproducibly associated with GDM complicated by HDP. Combining ALC with DBP improved discrimination between GDMHDP and uncomplicated GDM, suggesting complementary metabolic and hemodynamic information. Given the modest number of GDMHDP cases and the single-center design, these findings should be interpreted as exploratory and hypothesis-generating; they support further evaluation of ALC as a candidate metabolic marker but require confirmation in larger independent cohorts.
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9. Composite C-reactive protein-triglyceride-glucose adiposity indices and incident cardiovascular-liver-metabolic multimorbidity: a prospective cohort study.
9. 复合C-反应蛋白甘油三酯葡萄糖肥胖指数和心血管-肝脏代谢多发病率：一项前瞻性队列研究PMID:日期:2026-08-26The C-reactive protein-triglyceride-glucose index (CTI) is a comprehensive marker that reflects inflammation and insulin resistance. Cardiovascular-liver-metabolic (CLM) diseases caused by multiple factors may be related to insulin resistance, obesity, metabolism, etc. Our aim is to explore the association between the fat index derived from CTI and a newly identified surrogate-defined CLM multimorbidity (CLMM) phenotype, while also comparing the relative discriminatory performance of these indices and exploring potential biological domains. From the China Health and Retirement Longitudinal Study (CHARLS), a total of 6534 individuals with full baseline records were included in our analysis. Nine CTI-derived adiposity indices were calculated, including CTI, CTI-BMI, CTI-WC, CTI-WHtR, CTI-BRI, CTI-WWI, CTI-CVAI, CTI-ABSI, and CTI-CI. CVD was identified primarily from self-reported physician diagnoses, whereas MASLD was inferred using the lipid accumulation product (LAP) rather than imaging, histology, or clinical adjudication. Because the component conditions were ascertained using different methods and levels of diagnostic accuracy, CLMM was operationalized as a surrogate-defined composite phenotype rather than clinically confirmed CLMM. Associations as well as potential nonlinear relationships were examined using multivariable logistic regression, restricted cubic spline (RCS) modeling, and two-piece segmented regression analyses. Apparent discrimination and exploratory incremental model performance were quantified using receiver operating characteristic (ROC) curve analysis and reclassification measures, specifically the net reclassification improvement (NRI) and integrated discrimination improvement (IDI). Subgroup and sensitivity analyses were performed to assess stability. During the approximately four-year follow-up interval, 406 participants (6.2%) met the criteria for the newly identified surrogate-defined CLMM phenotype. Most CTI-derived adiposity indicators were significantly associated with elevated odds of this phenotype, although CTI-ABSI and CTI-WWI showed null associations after full adjustment. In fully adjusted models, CTI-BMI and CTI-CVAI (Q4 OR 3.46 for CTI-BMI; Q4 OR 2.37 for CTI-CVAI) showed the strongest associations (both P <0.001). RCS analyses further indicated significant nonlinear exposure-response relationships for all indices, except for CTI. CTI-BMI had the highest AUC among the evaluated CTI-derived indices (AUC = 0.638, 95% CI 0.611-0.664), although its absolute discriminatory ability was modest. However, CTI-BMI did not materially outperform BMI alone in a direct same-sample comparison (AUC = 0.638 vs 0.638; DeLong P = 0.924), and the IDI for CTI-BMI versus BMI was only 0.02%, despite a positive NRI. When CTI-BMI was added to the fully adjusted baseline model, the AUC increased only slightly from 0.617 to 0.627. Although the NRI indicated improved reclassification (NRI = 28.63%, 95% CI 18.63-38.64%), the IDI was 0.03% (95% CI 0.01-0.06%), indicating a minimal improvement in average discrimination. Compared with participants with low CTI and low BMI, those with low CTI and high BMI (OR 2.49, 95% CI 1.80-3.48) and those with high CTI and high BMI (OR 2.53, 95% CI 1.87-3.45) had similarly elevated odds of the newly identified surrogate-defined CLMM phenotype. The two effect estimates were numerically similar, and no statistically significant multiplicative or additive interaction was observed. Significant effect modification was observed for the association between CTI-BMI and this phenotype, with stronger relationships identified in men, current-smokers, and current-drinkers (all P for interaction <0.001). Sensitivity analyses were generally directionally consistent, with CTI-BMI remaining significantly associated with the surrogate-defined phenotype after additional adjustment for baseline CLM component status, despite a reduction in the effect estimate. In middle-aged and older adults, most CTI-related adiposity indices were significantly associated with the newly identified surrogate-defined CLMM phenotype, except for CTI-ABSI and CTI-WWI, which were not independently associated after full adjustment. Among them, CTI-BMI showed the strongest statistical association and the highest relative discrimination among the evaluated indices, although its absolute discrimination was modest. These findings suggest that both metabolic-inflammatory burden and obesity-related phenotypes may provide complementary information for population-level risk characterization of the surrogate-defined CLMM phenotype. Given the heterogeneous ascertainment and potential misclassification of its component conditions, these findings should not be interpreted as estimates of the risk of clinically confirmed CLMM.
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10. Disease-modifying anti-diabetic drugs (DMADDs): bridging the SIMPLE approach to disease interception.
10. 改善病情抗糖尿病药物（DMADDs）：连接疾病干预的SIMPLE方法PMID:日期:2026-08-26The traditional glucose-centric paradigm of type 2 diabetes management is being superseded by growing evidence that certain agents, sodium-glucose cotransporter-2 inhibitors (SGLT2i), glucagon-like peptide-1 receptor agonists (GLP-1RA), and pioglitazone, confer cardiovascular, renal, and hepatic benefits that extend well beyond glycemic control. Building on the previously proposed "diabetes/disease-modifying drugs (DMDs)" concept introduced through the SIMPLE framework, we propose a more mechanistically precise term: Disease-Modifying Anti-Diabetic Drugs (DMADDs). DMADDs are defined by four criteria: glucose-independent clinical benefit, durable organ-specific protection, mechanistic evidence of anti-inflammatory or anti-fibrotic activity, and sustained legacy effects or remission potential. Using these criteria, SGLT2i, GLP-1RA, and pioglitazone emerge as prototypical agents, while metformin, dipeptidyl peptidase-4 (DPP-4) inhibitors, insulin, and sulfonylureas do not meet the full threshold. We explicitly explain why metformin and DPP-4 inhibitors are excluded as DMADDs, situate the DMADD framework within the heterogeneity of type 2 diabetes and against what non-pharmacological interventions can achieve, and state the limitations of the proposal. Recent evidence reinforces this framework: the SOUL trial established cardiovascular superiority for oral semaglutide, extending disease-modifying properties beyond injectable formulations, while Phase 3 TRIUMPH data position retatrutide as an emerging triple-agonist candidate awaiting cardiovascular outcome data. The 2026 American Diabetes Association Standards of Care now recommend SGLT2i and GLP-1RA independent of baseline glycated hemoglobin (HbA1c), an institutional shift that mirrors the disease-interception logic proposed here. We argue that adopting the DMADD framework could reorient diabetes therapeutics from glycemic normalization toward early disease interception, potentially preserving β-cell function and expanding the clinical horizon toward remission. This terminology offers a unifying scaffold for future trials, regulatory classification, and clinical guidelines, redefining therapeutic success in type 2 diabetes beyond glucose control alone.