Objective Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) may convey disparate risks of metabolic consequences. Fasting plasma glucose (FPG), while an expedient screening procedure, may not adequately assess metabolic risk, particularly among youths. In order to inform a strategy for screening Chinese youth for pre-diabetes, we examined the relative value of IFG versus IGT to define metabolic risk by assessing their association with insulin resistance, beta-cell dysfunction, adverse adipokine profiles and other cardiometabolic risk factors. Research design and methods We recruited 542 subjects (age 14–28 years) from the Beijing Child and Adolescent Metabolic Syndrome study for an in-depth assessment of cardiometabolic risk factors, including a 2-hour oral glucose tolerance test, liver ultrasound and serum levels of four adipokines. Results FPG failed to identify nearly all (32/33) youths with IGT, whereas 2-hour plasma glucose (2 h PG) missed 80.8% (21/26) of subjects with IFG. Impaired beta-cell function was evident from decreased oral disposition indices in those with isolated impaired fasting glucose (iIFG) or isolated impaired glucose tolerance (iIGT) versus normal glucose tolerance (NGT) (all p<0.001), whereas reduced insulin sensitivity (Matsuda) index was most pronounced in the iIGT group (p<0.01). Moreover, alterations in adipokine levels (fibroblast growth factor 21, adiponectin and leptin/adiponectin ratio) were associated with iIGT (p<0.05) but not iIFG. Youths with iIGT had a 2-fold to 32-fold increased incidence of hypertriglyceridemia, hypertension and metabolic syndrome (MetS) compared with those with NGT. In addition, subgroup analyses of participants with normal FPG revealed that the odds of having IGT increased 3-fold to 18-fold among those with elevated TGs, hypertension, moderate-to-severe non-alcoholic fatty liver disease or MetS. Conclusions Chinese youth with iIGT exhibit a higher cardiometabolic risk profile than those with iIFG. Thus, 2 h PG is preferred over FPG to identify the pre-diabetes phenotype at greatest risk of subsequent development of cardiovascular disease. Trial registration number NCT03421444.

Malignant ventricular arrhythmias (VAs), such as ventricular tachycardia and ventricular fibrillation, are the cause of approximately half a million deaths per year in the United States, which is a common lethal event in heart disease, such as hypertension, catecholaminergic polymorphic ventricular tachycardia, takotsubo cardiomyopathy, long-QT syndrome, and progressing into advanced heart failure. A common characteristic of these heart diseases, and the subsequent development of VAs, is the overactivation of the sympathetic nervous system. Current treatments for VAs in these heart diseases, such as β-adrenergic receptor blockers and cardiac sympathetic ablation, aim at inhibiting cardiac sympathetic overactivation. However, these treatments do not translate into becoming efficacious as long-term suppressors of ventricular tachycardia/ventricular fibrillation events. As a key regulatory component in the heart, cardiac postganglionic sympathetic neurons residing in the stellate ganglia (SGs) release neurotransmitters (such as norepinephrine and NPY [neuropeptide Y]) to perform their regulatory role in dictating cardiac function. Growing evidence from animal experiments and clinical studies has demonstrated that the remodeling of the SG may be intimately involved in malignant arrhythmogenesis. This identifies the SG as a key potential therapeutic target for the treatment of malignant VAs in heart disease. Therefore, this review summarizes the role of SG in ventricular arrhythmogenesis and updates the novel targeting of SG for clinical treatment of VAs in heart disease.

To compare the accuracy of end-systolic elasticity (E _es)/arterial elasticity (E _a) ratio measured by single beat estimation, pressure–volume loop and cardiac magnetic resonance (CMR) combined volume method in patients with pulmonary artery hypertension, and to find a feasible and reliable method to quantitatively evaluate the function of right ventricle in patients with pulmonary artery hypertension. Forty-nine pulmonary artery hypertension patients enrolled between May 2017 and May 2018 in our hospital were retrospectively analyzed. Firstly, measure E _es/E _a ratio by single beat estimation, pressure–volume loop and CMR combined volume method, then, compare E _es/E _a ratio with New York Heart Association (NYHA) classification and NT-proBNP value respectively to evaluate the accuracy of the 3 methods. E _es/E _a ratio measured by single beat estimation is 2.07 ± 1.01, correlation analysis is not statistically significant when compare with NYHA classification and NT-proBNP value (P > .05). E _es/E _a ratio measured by pressure–volume loop is 2.64 ± 1.48, correlation analysis is not statistically significant when compare with NYHA classification and NT-proBNP value (P > .05). E _es/E _a ratio measured by CMR combined volume method is 0.72 ± 0.43, correlation analysis is statistically significant when compare with NYHA classification and NT-proBNP with negative correlation (P < .05). E _es/E _a ratio decrease according to the increase of NT-proBNP value and the NYHA classification. There is linear regression equation between E _es/E _a ratio measured by CMR combined volume method and log (NT-proBNP) value: Y = –0.257X + 1.45, and the linear regression equation is statistically significant (P = .001). E _es/E _a ratio measured by CMR combined volume method is a feasible and reliable method to quantitatively evaluate the function of right ventricule in patients with pulmonary artery hypertension, which might be further verified in a larger patient population.

Chronic heart failure (CHF) is characterized by heightened cardiac sympathetic activity and neuroinflammation within the stellate ganglia (SG), contributing to cardiac arrhythmogenesis. However, the upstream mediators of this neuroimmune interaction remain incompletely defined. This study investigated whether systemic neutralization of granulocyte–macrophage colony-stimulating factor (GM-CSF, an inflammatory cytokine) attenuates SG inflammation and cardiac sympathetic overactivation in a rat model of coronary artery ligation-induced CHF. Male Sprague–Dawley rats underwent myocardial infarction or sham surgery and were treated with a GM-CSF neutralizing antibody or vehicle. Cardiac sympathetic nerve activity (CSNA), heart rate variability (HRV), cytokine expression, and the electrophysiological properties of cardiac sympathetic post-ganglionic (CSP) neurons were assessed. CHF increased the levels of GM-CSF, ionized calcium-binding adaptor molecule 1 (IBA1, an activated macrophage marker) and pro-inflammatory markers (TNF-α, pro IL-1β) in the SG, enhanced neuronal Ca²⁺ currents, cell excitability, and CSNA, and impaired HRV. The GM-CSF neutralizing antibody significantly attenuated SG inflammation, partially normalized Ca²⁺ currents and neuronal firing, decreased CSNA, and improved cardiac autonomic balance. These findings identify GM-CSF as a key regulator of SG neuroinflammation and sympathetic dysregulation in CHF. Targeting this GM-CSF protein may represent a novel therapeutic strategy to mitigate autonomic imbalance and arrhythmic risk.

Background: Central obesity, as indicated by waist circumference (WC), is a major risk factor for coronary artery disease (CAD). However, the independent causal role of WC in CAD remains underexplored, particularly after adjusting for metabolic comorbidities such as hypertension and diabetes. Objectives: This study aims to evaluate the causal relationship between WC and CAD using a two-pronged approach: propensity score-matched observational analysis and Mendelian randomization (MR) analysis. Methods: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2023 were used for cross-sectional analysis, while genetic instrumental variables associated with WC were sourced from genome-wide association studies (GWAS). We performed inverse variance weighted (IVW) MR analysis and sensitivity tests including MR-Egger and leave-one-out analysis. Results: Propensity score matching showed that WC was significantly higher in the CAD group compared to controls (p < 0.001). MR analysis confirmed a causal relationship between increased WC and CAD risk, with an estimated causal effect size of 0.02884 (95% CI: 0.016, 0.041; p = 0.00000883). Sensitivity analyses validated the robustness of these findings. Conclusion: Our results provide strong genetic and observational evidence linking increased WC with a higher risk of CAD. These findings highlight the need for targeted interventions to reduce central obesity and prevent CAD, especially in populations prone to metabolic disorders.

Chronic kidney disease has long been viewed as a reason for caution when prescribing mineralocorticoid receptor antagonists (MRAs) in heart failure (HF), a doctrine rooted in the safety record of the steroidal agents: in TOPCAT, drug discontinuation for adverse events rose steeply as kidney function declined. The prespecified kidney-risk analysis of FINEARTS-HF, which reported consistent relative benefit of the non-steroidal MRA finerenone across KDIGO risk bands with a non-significant interaction on the primary endpoint, is widely read as a mandate to treat higher-risk patients more readily. We welcome this move away from reflexive under-treatment, but argue that a careful reading supports a more qualified conclusion than "worse kidneys, therefore more finerenone." Two features deserve emphasis. First, the reassuring safety signal was generated within the trial's enrolment window, which excluded patients with an eGFR below 25 mL/min/1.73 m2 or a serum potassium above 5.0 mmol/L; extending "no excess hyperkalaemia" to the very-low-eGFR patients who most concern clinicians is an extrapolation, not a demonstrated finding. Second, absolute benefit did not increase smoothly with rising kidney risk: modelled absolute reductions were not largest in the highest-risk stratum, and a non-significant interaction test does not establish that the treatment effect is identical across strata. Earlier, larger falls in albuminuria among higher-risk patients are encouraging but remain a candidate intermediate endpoint rather than proof of durable cardiorenal gains. We therefore propose a proportionate strategy: allow a higher renal-risk band to prompt consideration of finerenone in suitable patients, resist equating a uniform relative risk with uniformly maximal absolute benefit or unchanged safety at very low eGFR, and escalate potassium monitoring in parallel with renal risk, especially at or beyond the trial's boundaries. The strongest inference is that finerenone is effective and well tolerated in patients with moderately advanced CKD, normal potassium, and close follow-up; its least secure inference is that the highest-risk patients are ipso facto the safest or most deserving recipients. Future work should define optimal monitoring for patients whose eGFR drifts very low during treatment.