Lian Wang

Background: Cardiovascular–kidney–metabolic (CKM) syndrome integrates metabolic dysfunction, kidney disease, and cardiovascular disease. In stage 4 CKM syndrome with acute decompensated heart failure (ADHF), prognosis may be influenced by dysglycaemia, triglyceride-related metabolic disturbance, systemic inflammation, and adiposity-related risk, yet risk stratification remains challenging. We evaluated whether the C-reactive protein–triglyceride–glucose index (CTI), a routinely available inflammatory-metabolic marker, refines risk stratification beyond diabetes status and related inflammatory-metabolic biomarkers in patients with stage 4 CKM syndrome and ADHF. Methods: This single-centre retrospective cohort included 2,000 eligible patients hospitalized for ADHF with CKM stage 4. CTI was calculated as 0.412 × ln[CRP (mg/L)] + ln[TG (mg/dL) × FPG (mg/dL) / 2]. High CTI was defined using the cohort-specific upper-tertile threshold (CTI ≥ 9.50). Patients were categorized as non-DM + low CTI, non-DM + high CTI, DM + low CTI, or DM + high CTI. Outcomes were all-cause mortality and major adverse cardiac and cerebrovascular events (MACCEs). Results: During a median follow-up of 532 days, 366 deaths (18.3%) and 551 MACCEs (27.6%) occurred. Compared with non-DM + low CTI, non-DM + high CTI was associated with higher risks of all-cause mortality (HR 1.54, 95% CI 1.15–2.06) and MACCEs (HR 1.37, 95% CI 1.08–1.75). DM + low CTI was not significantly associated with either outcome, whereas DM + high CTI had the highest risks of all-cause mortality (HR 1.95, 95% CI 1.47–2.58) and MACCEs (HR 1.91, 95% CI 1.51–2.41). CTI showed approximately linear associations with both outcomes, without significant interaction by diabetes status. Adding CTI to the clinical model plus diabetes status yielded modest improvements in discrimination (ΔC-index = 0.018 for mortality and 0.016 for MACCEs), exceeding those of the evaluated biomarker models. Sensitivity analyses generally supported the primary findings. Conclusion: In patients with stage 4 CKM syndrome hospitalized for ADHF, elevated CTI was associated with higher risks of all-cause mortality and MACCEs, with the greatest risk in patients with both diabetes and high CTI. CTI may be a candidate adjunctive marker for risk refinement; external validation is required before clinical implementation.

The C-reactive protein–triglyceride–glucose index (CTI) is a composite marker integrating systemic inflammation and insulin resistance. Althoug

The C-reactive protein-to-albumin ratio (CAR) is an emerging biomarker linked to cardiovascular disease. However, its role in predicting outcomes among acute decompensated heart failure (ADHF) patients, particularly when stratified by glycemic status, remains poorly defined. This retrospective study included 1,494 consecutive ADHF patients admitted between 2018 and 2023, with the primary endpoint being major adverse cardiac and cerebrovascular events (MACCEs). Patients were stratified into low- and high-CAR groups using an optimal cutoff of 0.29, derived from maximally selected rank statistics. To assess the relationship between CAR and MACCEs in different glucose metabolism states, multivariable Cox proportional hazards models, restricted cubic splines (RCS), and Kaplan-Meier survival curves were used. During a median follow-up of 528 days, 565 patients (37.8%) experienced MACCEs. After adjusting for potential confounders, higher CAR levels were significantly associated with an increased risk of MACCEs (Model 3: hazard ratio [HR]: 1.45, 95% confidence interval [CI]: 1.19-1.77, p < 0.001). When stratified by glycemic status, CAR as a robust predictor in diabetic patients (Model 3 HR: 1.91, 95% CI: 1.41-2.58, p < 0.001), whereas no significant associations were observed in prediabetic or normoglycemic individuals (all p > 0.05). In conclusion, CAR demonstrates independent prognostic value in ADHF patients with concomitant diabetes, highlighting its potential as a stratification tool for personalized risk assessment and therapeutic optimization in this high-risk population.

Angiographic microvascular resistance (AMR) serves as an effective metric for assessing coronary microvascular status. The aim of this study was to investigate the predictive value of AMR for left ventricular thrombus (LVT) in ST-segment elevation myocardial infarction. This study enrolled 401 consecutive patients with anterior STEMI who underwent primary percutaneous coronary intervention (PPCI) between May 2019 and July 2023. AMR was measured immediately after PPCI via coronary angiography. LVT was identified during hospitalization through cardiac magnetic resonance imaging (CMR) or transthoracic echocardiography (TTE). Major adverse cardiac and cerebrovascular events (MACCEs) were recorded over 36 months follow-up. The predictive value of AMR was evaluated by logistic regression and receiver operating characteristic (ROC) analysis. Kaplan-Meier analysis was performed to estimate event-free rates for MACCEs. LVT was identified in 38 out of 401 anterior STEMI patients (9.5%). After adjusting for confounders through multivariable analysis, AMR was found to be an independent predictor of LVT (odds ratio [OR] 1.240 per 0.1 mmHg·s/cm, 95% confidence interval [CI]: 1.131-1.359, P < 0.001). ROC analysis demonstrated an area under the curve (AUC) of 0.742. For LVT, AMR provided modest incremental predictive value over established risk factors (continuous net reclassification improvement, 0.826 [95% CI: 0.523-1.129]; P < 0.001). Furthermore, Kaplan-Meier analysis revealed MACCEs for anterior STEMI patients with AMR ≥ 2.82 (log-rank P < 0.001). AMR is an independent predictor of LVT in anterior STEMI, providing incremental predictive value beyond traditional risk factors, and may be utilized to identify patients at risk for LVT.

Background: In some patients with nonischemic cardiomyopathy (NICM), left ventricular (LV) function improves with medical assistance, resulting in left ventricular reverse remodeling (LVRR). However, predictors of LVRR are not fully understood. The left atrium (LA) has been reported as a prognostic predictor in patients with heart failure (HF). The present study aimed to evaluate clinical predictors of LVRR related to LA function on cardiac magnetic resonance (CMR). Methods: A total of 103 patients with reduced left ventricular ejection fraction (LVEF) were enrolled in this retrospective study between September 2015 and July 2021. CMR parameters, including strain data, were measured in all patients. Echocardiographic data obtained approximately 2 years after enrollment were analyzed to assess LVRR. Results: LVRR occurred in 46 patients (44.7%) during follow-up. The value of LA conduit strain was higher in the LVRR group than in the non-LVRR group (6.6 [interquartile range (IQR): 5.6–9.3]% versus 5.0 [IQR: 3.0-6.2]%; p < 0.001). The multivariate logistic regression analysis showed that LA conduit strain was an independent predictor of LVRR (odds ratio [OR]: 1.216, 95% confidence interval [CI]: 1.050–1.408; p = 0.009). The area under the receiver operating characteristic (ROC) curve of the LA conduit strain was 0.746, and the cutoff value was 6.2%. The Kaplan‒Meier analysis revealed that the incidence of adverse cardiac events was significantly lower in patients with LA conduit strain > 6.2% compared to those with ⩽6.2%. (log-rank test, p = 0.019). Conclusions: LA conduit strain derived from CMR is an independent predictor of LVRR in patients with NICM.

Background: Fibrosis-5 (FIB-5) index is a marker of liver fibrosis and has been shown to have a good prognostic value for patients with acute heart failure (AHF), and C-reactive protein (CRP) has inflammatory properties and predicts adverse prognosis in patients with HF. However, the long-term prognostic value of FIB-5 index combined with CRP in patients with acute decompensated HF (ADHF) is yet unclear. Methods: This retrospective study included 1153 patients with ADHF hospitalized from January 2018 to May 2022.The FIB-5 index was calculated as (albumin [g/L]×0.3 + PLT count [10⁹/L]×0.05)−(ALP [U/L]×0.014 + AST to ALT ratio×6 + 14). Patients were stratified into the following four groups according to the median value of FIB-5 index (=-2.11) and CRP (= 4.5): Group 1 had a high FIB-5 index (FIB-5 index >-2.11) and a low CRP (CRP ≤ 4.5); Group 2 had both low FIB-5 index and low CRP; Group 3 had both high FIB-5 index and high CRP; Group 4 had a low FIB-5 index (FIB-5 index ≤-2.11) and a high CRP (CRP > 4.5). The endpoint was major adverse cardiac and cerebral events (MACCEs). Multivariate Cox analysis was used to evaluate the association of the combination with the development of MACCEs. Net reclassification improvement (NRI) and integrated discrimination improvement (IDI) analysis were used to compare the accuracy of the combination with a single prognostic factor for predicting the risk of MACCEs. Results: During the mean follow-up period of 584 ± 12 days, 488 (42.3%) patients had MACCEs. Kaplan–Meier analysis revealed that the incidence of MACCEs was different in the four groups (P < 0.001). After adjusting for the confounding factors, the hazard ratio (HR) for MACCEs in Group 4 (low FIB-5 index + high CRP) was the highest (Model 1, HR = 2.04, 95%CI 1.58–2.65, P < 0.001; Model 2, HR = 1.67, 95%CI 1.28–2.18, P < 0.001; Model 3, HR = 1.66, 95%CI: 1.27–2.17, P < 0.001). Additionally, the combination of FIB-5 index and CRP enabled more accurate prediction of MACCEs than FIB-5 index alone (NRI, 0.314,95%CI 0.199–0.429; P < 0.001; IDI, 0.023; 95% CI 0.015–0.032; P < 0.001). Conclusions: In patients with ADHF, the combination of the FIB-5 index and CRP may be useful in risk stratification in the future.

LMNA gene encodes lamin A/C protein which participates in the construction of nuclear lamina, the mutations of LMNA result in a wide variety of diseases known as laminopathies. LMNA-related dilated cardiomyopathy(LMNA-DCM) is one of the more common laminopathy which characterized by progressive heart failure and arrhythmia. However, the mutation features of LMNA-DCM are yet to be elucidated. Herein we described a dilated cardiomyopathy family carrying novel variant c.467G > C(p.Arg156Pro) of LMNA as heterozygous pathogenic variant identified by whole-exome sequencing. With the help of Alphafold2, we predicted mutant protein structure and found an interrupted α-helix region in lamin A/C. In the analysis of 49 confirmed pathogenic missense of laminopathies, Chi-square test showed the DCM phenotype was related to the α-helix region mutation (p < 0.017). After screening the differentially expressed genes (DEGs) in both mice models and human patients in Gene Expression Omnibus database, we found the variation of α-helix-coding region in LMNA caused abnormal transcriptomic features in cell migration, collagen-containing extracellular matrix, and PI3K-Akt signaling pathway. Subsequently we constructed (TF)-mRNA-microRNA (miRNA) regulatory network and identified 7 key genes (FMOD, CYP1B1, CA3, F2RL1, HAPLIN1, SNAP91, and KANSL1) as potential biomarkers or therapeutic targets in LMNA-DCM patients.