Cardiovascular Diabetology最新文献

Background: Post-myocardial infarction (MI) patients remain at high risk of mortality and recurrent cardiovascular events. Metabolic disorders in patients after MI are closely related to high residual cardiovascular risk. The cholesterol, high-density lipoprotein, and glucose (CHG) index, calculated as Ln {[TC (mg/dL) × FBG (mg/dL)]/[2 × HDL-C (mg/dL)]}, is a recently proposed composite metabolic index. This study aimed to investigate the association between the CHG index and adverse outcomes in MI populations.

Methods: This study included two cohorts: 16,959 individuals with a history of MI from the UK Biobank and 6,253 post-MI patients with coronary artery disease from Fuwai Hospital. The primary endpoints in the UK Biobank cohort were all-cause mortality and cardiovascular mortality. In the Fuwai Hospital cohort, the primary endpoint was major adverse cardiovascular events (MACE, including all-cause mortality, non-fatal MI, and ischemia-mediated revascularization) and hard endpoint (including cardiovascular mortality and non-fatal MI). Cox proportional hazards models, Kaplan-Meier curves, and restricted cubic splines (RCS) were used to evaluate the associations between the CHG index and the endpoints. Time-dependent receiver operating characteristic (ROC) curves were employed to assess the predictive performance.

Results: In the UK Biobank cohort (median follow-up of 13.4 years), after multivariate adjustment, compared to the Q1 of the CHG index, Q4 showed significantly increased risks of all-cause mortality (HR: 1.39, 95% CI: 1.33-1.41) and cardiovascular mortality (HR: 1.42, 95% CI: 1.14-1.74). In the Fuwai Hospital cohort (median follow-up of 3.1 years), the CHG Q4 group also demonstrated a significantly elevated risk of MACE (HR: 1.37, 95% CI: 1.17-1.61) and hard endpoint (HR: 1.87, 95% CI: 1.24-2.81). Kaplan-Meier curves showed significant separation in cumulative event rates across CHG quartiles in both cohorts (log-rank P < 0.05). RCS analyses demonstrated positive linear associations between CHG and all outcomes in both cohorts. Time-dependent ROC curves showed that the CHG index consistently outperformed the TyG index model in predicting adverse outcomes (all FDR-adjusted P < 0.05).

Conclusions: In two large independent cohorts of individuals with prior MI, the CHG index was independently associated with risks of adverse events. While its independent discriminative power is modest, the index serves as a valuable adjunctive tool that enhances risk reclassification, warranting further validation in prospective clinical settings to confirm its utility in secondary prevention.

Background: Sodium-glucose cotransporter-2 inhibitors (SGLT2i) lower blood pressure (BP) and provide cardiovascular protection. In animal models, SGLT2i blunt sodium-induced BP elevation, but this effect remains unexplored in humans. We investigated whether SGLT2i reduce the salt sensitivity of BP in patients with type 2 diabetes (T2D) and explored the underlying mechanisms.

Methods: In an open-label, non-randomized study, 26 patients with T2D (14 on treatment with SGLT2i, 12 controls) completed two sequential 7-day dietary phases consisting of a very-low-sodium background diet with the addition of either high sodium (HS, + 4,800 mg/day) or low sodium (LS, + 1,200 mg/day). Changes in twenty-four hour ambulatory BP monitoring (24-hour ABPM), postprandial natriuresis and diuresis, plasma renin and aldosterone concentrations, glycosuria, and hydration were assessed.

Results: The median change in systolic BP between HS and LS diets was greater in controls (median [IQR] Δ24-h SBP: +5.6 [2.0, 20.3] mmHg, p = 0.005), than in the SGLT2i group (Δ24-h SBP: -1.2 [-3.6, 4.2] mmHg, p = 0.594; p = 0.007 between groups). Diastolic BP changes showed similar patterns (Δ24-h DBP: +4.6 [1.3, 9.8] mmHg vs. -1.2 [-3.1, 1.4] mmHg; p = 0.002 between groups). SGLT2i-treated participants showed enhanced postprandial natriuresis during both HS (median [IQR]: 55.0 [28.3, 126.6] µEq/min vs. -0.7 [-148.6, 109.0] µEq/min; p = 0.049) and the LS diet (18.4 [1.3, 42.2] µEq/min vs. -14.5 [-30.2, 15.7] µEq/min; p = 0.046), and postprandial diuresis during the HS diet (median [IQR]: 0.52 [0.10, 1.18] ml/min vs. -0.21 [-0.58, 0.45] ml/min p = 0.041). In response to the LS diet, renin and aldosterone levels increased markedly in controls but not in SGLT2i-treated patients. Hydration and glycosuria were unchanged and unrelated to natriuretic responses.

Conclusions: In T2D, treatment with SGLT2 inhibitors is associated with a reduced BP response to high sodium intake, accompanied by enhanced postprandial sodium and water excretion, along with attenuated neurohormonal activation. These findings identify physiological associations that may contribute to the BP-lowering and cardiovascular protective effects of SGLT2 inhibition.

Trial registration: NCT06007157 (registered on 18/08/2023).

International guidelines define standards of care for type 2 diabetes (T2D), obesity, cardiovascular disease (CVD), metabolic dysfunction-associated steatotic liver disease (MASLD) and chronic kidney disease (CKD). Yet implementation at the national level remains inconsistent, leading to persistent gaps between evidence-based recommendations and real-world practice. Key barriers include linguistic and cultural adaptation, limited communication to clinicians, and siloed regulatory and reimbursement processes. Addressing these challenges requires coordinated strategies, such as concise translations, digital platforms and decision-support tools, integration into medical education, and structured monitoring and evaluation frameworks with feedback and incentives. Equitable and sustainable access further depends on coordination between medical societies, governmental authorities, payers, and patient representatives. Evidence from existing initiatives shows that systematic, context-sensitive approaches can measurably improve care. Building on these lessons, this Commentary recommends priorities for national implementation to ensure that guidelines move more effectively from publication to practice and realise their full potential to improve patient outcomes.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is burdened by significant all-cause and cardiovascular mortality, yet simple and effective predictive indices for long-term outcomes are currently lacking. In this study, we investigated the prognostic value of the triglyceride glucose-a body shape index (TyG-ABSI), a novel composite of insulin resistance and visceral adiposity, for mortality in MASLD.

Methods: This prospective cohort study included 7515 adults with MASLD from the National Health and Nutrition Examination Survey (NHANES, 1999-2018). MASLD was defined as a Fatty Liver Index ≥ 60 accompanied by at least one cardiometabolic risk factors. The primary outcomes were all-cause mortality (ACM) and cardiovascular mortality (CVM). Kaplan-Meier survival curves, multivariable Cox regression, restricted cubic splines (RCS), and receiver operating characteristic (ROC) analyses were employed to evaluate the predictive value of TyG-ABSI. Additionally, subgroup, sensitivity, and mediation analyses were conducted to verify robustness and explore underlying mechanisms.

Results: During a median follow-up of 138 months, 1368 all-cause and 376 cardiovascular deaths were recorded. TyG-ABSI demonstrated improved predictive accuracy compared to TyG, TyG-BMI, TyG-WC, and TyG-WHtR, as evidenced by higher AUC values and significant Net Reclassification Improvement（NRI). In fully adjusted models, participants in the highest TyG-ABSI quartile faced significantly elevated risks of ACM (HR 1.49, 95% CI 1.03-2.14) and CVM (HR 2.32, 95% CI 1.02-5.30) relative to the lowest quartile. RCS analysis indicated a linear dose-response relationship, and the associations remained robust across subgroup and sensitivity analyses. Mediation analysis revealed that accelerated biological aging significantly mediated mortality risks, with KDM and HD explaining 24.75% and 32.15% of ACM, and 34.89% and 46.53% of CVM, respectively.

Conclusions: TyG-ABSI serves as a robust, independent predictor of mortality in patients with MASLD, outperforming traditional TyG-related metrics. The association is significantly associated with the pathway of accelerated biological aging, highlighting the utility of TyG-ABSI for enhanced risk stratification in clinical practice.

Background: Insulin resistance (IR) serves as a core pathophysiological factor among patients with metabolic dysfunction-associated steatotic liver disease (MASLD) and has an adverse impact on prognosis. As a reliable indicator of IR, the estimated glucose disposal rate (eGDR) is associated with cardiometabolic risk and mortality. However, the prognostic significance of eGDR in MASLD remains unclear. This study aims to examine the association between eGDR and cause-specific mortality in patients with MASLD.

Methods: Totally 6,847 patients with MASLD were included from the National Health and Nutrition Examination Survey (NHANES) 1999-2018. Patients were divided into four groups based on eGDR quartiles. The study outcomes were all-cause, cardiovascular and diabetes mortality. Restricted cubic splines (RCS) and the Cox proportional hazard model were used to evaluate the associations between eGDR and outcomes. Receiver operating characteristic (ROC) analyses were conducted to show its predictive ability for outcomes. Subgroup analyses were conducted to evaluate the robustness of performance.

Results: During the median follow-up of 8.8 years, 19.6% patients (n = 1,345) experienced death, with 6.5% (n = 443) cardiovascular mortality, and 1.3% (n = 89) diabetes mortality. After adjusting for confounders, higher eGDR level was significantly associated with lower risk of all-cause mortality (HR = 0.94, 95% CI: 0.92-0.97, P < 0.001), cardiovascular mortality (HR = 0.90, 95% CI:0.85-0.95, P < 0.001), and diabetes mortality (HR = 0.70, 95% CI: 0.62-0.80, P < 0.001). ROC analyses showed that the eGDR had a significant but modest predictive performance for all-cause mortality (AUC = 0.606) and cardiovascular mortality (AUC = 0.631), with a moderate performance for diabetes mortality (AUC = 0.729). Among different subgroups, the association between the eGDR and the risk of cause-specific mortality was similar to the main results.

Conclusion: Higher eGDR levels are independently associated with reduced risks of all-cause, cardiovascular, and diabetes mortality among patients with MASLD, highlighting the prognostic relevance of insulin resistance in this population. The modest discriminative performance of eGDR further supports its role in cardiometabolic risk stratification.

Background: Epicardial adipose tissue (EAT) transformation in heart failure with reduced ejection fraction (HFrEF) is poorly understood, which limits its potential as a therapeutic target and prognostic factor. The aim of our study was to characterize EAT in patients with HFrEF at the histological, computed tomography (CT) imaging and radiomic level to better understand its transformation in HFrEF.

Methods: We enrolled 70 patients with HFrEF who were scheduled for implantation of a left ventricular assist device (LVAD) or orthotopic heart transplantation (OHT). Fifty non-heart failure (HF) subjects served as controls. All participants underwent contrast- or non-contrast-enhanced chest CT imaging for EAT analysis. Left ventricular myocardial cones with overlying EAT were obtained from LVAD patients during surgery, from explanted OHT hearts, and from 20 unused healthy donor hearts for histological analysis.

Results: While total EAT volume did not differ between non-HF and HFrEF subjects, its density assessed in CT images, was higher in HFrEF. Moreover, periventricular EAT exhibited density gradient, with the densest voxels immediately adjacent to the myocardium (over up to 1 mm). This density gradient was extended to almost 3 mm in LV EAT in HFrEF patients. Histological analysis showed that adipocytes also exhibited a characteristic cell size gradient, with smaller cells adjacent to the myocardium, more pronounced than in non-HF subjects; moreover, median LV EAT adipocyte size was smaller in HFrEF vs. non-HF patients. However, EAT fibrosis and blood vessel density did not differ between non-HF and HFrEF subjects. Both histological analysis and radiomic analysis of CT images revealed that EAT was more heterogeneous in HFrEF than in non-HF subjects. These changes were most pronounced in LV EAT, but other EAT depots (RV and periatrial) were also affected.

Conclusions: LV EAT in HFrEF contains smaller adipocytes and has higher density in CT images, exhibits pronounced cell size/density gradient and is more heterogeneous than in non-HF subjects. Thus LV EAT undergoes complex remodeling in HFrEF. Further studies are needed to elucidate the mechanisms driving this remodeling, determine whether it can be therapeutically targeted, and assess which parameters may have prognostic value in patients with HFrEF.