Background:High-sensitivity C-reactive protein (hs-CRP) is a key inflammatory marker in atherosclerosis; however, the association between its long-term patterns and cardiovascular prognosis under statin therapy remains incompletely understood. This study characterized hs-CRP trajectories and their prognostic value for MACE in statin users, aiming to refine risk assessment and tailored therapy. Methods:We conducted a retrospective cohort study at the Center for Coronary Artery Disease, Beijing Anzhen Hospital, Capital Medical University (Beijing, China), using data from patients who received statin therapy for at least 12 months between January 2023 and December 2024. Eligible participants had three or more hs-CRP measurements and were free from major adverse cardiovascular events (MACEs) six months before enrollment. Latent class growth modeling was applied to categorize hs-CRP trajectories. The primary composite outcome included cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or rehospitalization for unstable angina. Event-free survival was compared across trajectory groups using Kaplan-Meier curves with log-rank testing. Multivariable Cox proportional hazards regression evaluated the association between hs-CRP trajectories and MACE, with adjustments for age, sex, hypertension, diabetes, baseline lipids, and statin intensity. Results:This study included 210 patients with a median follow-up of 11.9 months. Latent class growth modeling identified three distinct hs-CRP trajectories: persistently low (45.2%, <2 mg/L), moderately fluctuating (40.0%, 2-5 mg/L), and persistently high (14.8%, ≥5 mg/L). Over follow-up, 38 patients (18.1%) experienced a MACE. Kaplan-Meier analysis revealed significantly higher cumulative MACE incidence in persistently high compared to persistently low (38.7% vs. 5.3%, P<0.001), with moderately fluctuating also showing elevated risk (25.0% vs. 5.3%, P<0.001). Following multivariable adjustment, both persistently high [hazard ratio (HR) 4.21, P=0.02] and moderately fluctuating (HR 3.46, P=0.02) hs-CRP trajectories remained independent predictors of MACE in patients receiving statins. Conclusions:Statin-treated patients with rising hs-CRP levels face elevated MACE risk. Longitudinal patterns show prognostic promise but need validation in future trials.

Circadian blood pressure (BP) abnormalities, including nondipping and reverse-dipping patterns, are increasingly recognized as major determinants of cardiovascular target-organ damage, independent of clinic BP. Antihypertensive drug classes and dosing time may differentially influence nocturnal BP control and left ventricular (LV) remodeling. However, real-world data integrating these factors remain limited, particularly in Chinesepopulations. This retrospective, observational study included 500 adult patients with essential hypertension evaluated at a tertiary-care center between 2020 and 2024. All patients underwent valid 24-hour ambulatory BP monitoring (ABPM) and transthoracic echocardiography performed within six months of ABPM. Antihypertensive therapy was classified by drug class and dosing time (morning-only vs. evening/bedtime dosing of ≥ 1 agent). Circadian BP phenotypes were defined based on nocturnal systolic BP decline. LV mass index (LVMI) and LV geometric patterns were assessed according to standard echocardiographic criteria. Multivariable regression analyses were performed to evaluate associations between antihypertensive regimen, circadian BP indices, and LV remodeling. Nondipping or reverse-dipping BP patterns were present in 48.6

ABSTRACT Short‐term blood pressure variability (BPV) and circadian BP abnormalities are important cardiovascular risk predictors of mean BP levels, but their combined prognostic significance in essential hypertension remains incompletely understood. To evaluate the independent and combined prognostic value of 24‐hour BPV and circadian BP patterns for predicting major adverse cardiovascular events (MACE) in patients with essential hypertension. This retrospective cohort study included 500 adults with essential hypertension who underwent 24‐hour ambulatory BP monitoring. Short‐term BPV was assessed using the standard deviation of 24‐hour systolic BP. Circadian patterns were classified as dipper, non‐dipper, or reverse dipper based on nighttime systolic BP decline. The primary outcome was MACE, including myocardial infarction, stroke, hospitalization for heart failure, or cardiovascular death. Cox proportional hazards regression models were used to evaluate associations with outcomes. During a median follow‐up of 4.2 years, 128 patients (25.6%) experienced MACE. High BPV was associated with a significantly greater incidence of MACE than low BPV (34.2% vs. 17.1%, p < 0.001) and remained an independent predictor (adjusted HR 1.89, 95% CI 1.32–2.71, p < 0.001). Reverse dipping was also associated with increased risk. Patients with both elevated BPV and abnormal circadian patterns had the highest risk. Elevated short‐term BPV and abnormal circadian BP patterns are independent predictors of MACE in essential hypertension. Their coexistence identifies a particularly high‐risk phenotype. ABPM‐based dynamic BP assessment may improve cardiovascular risk stratification beyond mean BP levels.

Objective:Currently, there are limited data on the clinical outcomes of percutaneous coronary intervention (PCI) compared to coronary artery bypass grafting (CABG) for the treatment of chronic total occlusion (CTO). We compared the clinical outcomes of patients with CTO lesions treated by PCI versus CABG. Methods:This study included 2587 patients with coronary artery disease (CAD) with CTO from January 1, 2019 to December 31, 2021. Both short- and long-term clinical outcomes were compared in patients with CTO who received successful revascularization. The primary endpoint, defined as major adverse cardiac and cerebrovascular events (MACCE), was a composite of all-cause mortality, cerebrovascular events, and myocardial infarction. Unplanned revascularization and heart failure hospitalization were defined as secondary endpoints separately. Propensity score matching was applied to balance baseline characteristics between the two groups. Results:The PCI group had lower MACCE (0.47% vs. 2.11%) within 30 days of the index operation, but the difference did not reach statistical significance (p = 0.06). After an average follow-up of 37.2 months, no significant differences were observed between PCI and CABG in all-cause mortality (hazard ratio [HR] = 2.29, 95% CI: 0.79-6.61; p = 0.13), MACCE (HR = 2.03, 95% CI: 0.86-4.76; p = 0.10), or heart failure hospitalization rate (sub distribution HR [SHR] = 0.98, 95% CI: 0.26-3.74; p = 0.98). However, patients who underwent PCI had a higher risk of unplanned revascularization (SHR = 10.32, 95% CI: 2.42-43.95; p = 0.002). Conclusion:In patients with CAD with CTO, PCI was associated with a trend of lower short-term MACCE compared to CABG, but with a higher risk of long-term unplanned revascularization. There were no significant differences in long-term all-cause mortality, MACCE, or heart failure hospitalization rates between PCI and CABG.

Objective The objective of this experiment was to investigate the relationship between the circadian rhythm of blood pressure and left ventricular hypertrophy (LVH) in patients with hypertension. Methods A total of 500 hypertension patients with documented circadian rhythm of blood pressure were selected for this study. The researchers collected general patient data and fasting blood samples. The following parameters were measured within subgroups of hypertensive patients: age, sex ratio, BMI, fasting blood glucose, total cholesterol, triacylglycerol, HDL-C, LDL-C, duration of hypertension, antihypertensive drug usage, and statin intake. Results The results of the study showed that LVH hypertension had a significantly higher proportion of grade 3 hypertension compared to non-LVH hypertension (P < .001). Additionally, LVH hypertension displayed higher mean systolic blood pressure levels over a 24-hour period (P = .002), during daytime (P = .029), and during nighttime (P < .001). The 24-hour pulse pressure (P < .001) and pulse pressure index (P = 0.001) were also significantly higher in patients with LVH hypertension. Furthermore, the rate of blood pressure decline at night was significantly lower in the LVH hypertension group compared to the control group (P < .001). B-type natriuretic peptide (BNP) levels (P = .034) and left ventricular mass index (LVMI) (P < .001) were significantly higher in patients with LVH hypertension compared to non-LVH patients. Conclusions The findings of this study suggest a close association between hypertensive LVH and the weakening or disappearance of the circadian rhythm of blood pressure. It was also observed that the level of blood pressure classification and plasma BNP levels were increased in patients with LVH hypertension.

Numerous studies have demonstrated the protective benefits of sophoridine, a bioactive alkaloid, on cell damage. However, its primary biological properties such as interaction with plasma protein, which serves as the primary drug carrier, and its cardioprotective properties are still unknown. In the present study, we aimed to analyze the binding characteristics of sophoridine with alpha-2-macroglobulin (α2M) by spectroscopic and theoretical studies. Then, the cardioprotective effects of sophoridine on myocardial ischemia/reperfusion (MI/R) injury in vitro were investigated using H9c2 cardiomyocytes. The results reveal that one molecule of sophoridine favorably binds to one molecule of α2M dominantly through interaction with hydrophobic amino acid residues (VAL758, PHE735, PHE735, and TRP739). Also, sophoridine leads to partial changes in the structure of this carrier protein in the vicinity of TRP739 residue. Cellular assays exhibit that sophoridine recovered cell viability, membrane leakage, and apoptosis induced by MI/R injury. It was detected that sophoridine could mitigate the oxidative stress and intrinsic apoptosis pathway through regulation of Bax, Bcl-2, and caspase. ELISA analysis also exhibits that sophoridine upregulates phosphorylation of Akt and PI3K in H9c2 cells. Our findings suggest that sophoridine could show favorable plasma protein interaction and promising cardioprotection against MI/R injury mediated by the upregulation of PI3K/AKT signaling pathway.

Myocardial infarction (MI) is an event of heart attack due to the formation of plaques in the interior walls of the arteries. This study is conducted to explore the role of ubiquitin-specific peptidase 47 (USP47) in cardiac function and inflammatory immunity. MI mouse models were established, followed by an appraisal of cardiac functions, infarct size, pathological changes, and USP47 and NLRP3 levels. MI cell models were established in HL-1 cells using anoxia. Levels of cardiac function-associated proteins, USP7, interferon regulatory factor 1 (IRF1), platelet factor-4 (CXCL4), pyroptotic factors, and neutrophil extracellular traps (NETs) were determined. The bindings of IRF1 to USP47 and the CXCL4 promoter and the ubiquitination of IRF1 were analyzed. USP47 was upregulated in myocardial tissues of MI mice. USP47 inhibition alleviated cardiac functions, and decreased infarct size, pro-inflammatory cytokines, NETs, NLRP3, and pyroptosis. The ubiquitination and expression levels of IRF1 were increased by silencing USP47, and IRF1 bound to the CXCL4 promoter to promote CXCL4. Overexpression of IRF1 or CXCL4 in vitro and injection of Nigericin in vivo reversed the effect of silencing USP47 on alleviating pyroptosis and cardiac functions. Collectively, USP47 stabilized IRF1 and promoted CXCL4, further promoting pyroptosis, impairing cardiac functions, and aggravating immune inflammation through NLRP3 pathways.

The effect of percutaneous coronary intervention (PCI) of chronic total occlusion (CTO) on left ventricular dyssynchrony was unclear. Patients with one CTO vessel were included. Tissue Doppler imaging (TDI) was used to assess the left ventricular dyssynchrony index (DI) in twelve segments before and after successful CTO PCI. Multiple regression was used to identify independent correlates of DI reduction. Ninety one patients were included with the mean age of 62.04 years. 88(96.70

Background: : The in-hospital outcomes of percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) in patients with left ventricular systolic dysfunction (LVSD) and chronic total occlusion (CTO) remain unclear. Methods: : From 2014 to 2020, patients with LVSD and CTO who underwent PCI or CABG were collected. The primary endpoint was in-hospital major adverse cardiac or cerebrovascular events (MACCE), defined as the composite of all-cause mortality, cardiovascular mortality, stroke, myocardial infarction (MI), and target vessel revascularization. Inverse probability of treatment weighting (IPTW) was performed to evaluate the association between revascularization strategies and in-hospital outcomes. The hazard ratio (HR) and 95% confidence interval (CI) were calculated using the Cox proportional hazards model. Results: : Of the 773 patients who met the inclusion criteria, 543 (70.2%) underwent PCI, and 230 (29.8%) underwent CABG. The primary endpoint was observed in 25 (3.2%) patients. The incidence of in-hospital MACCE (6.5% vs . 1.8%, p < 0.001) was significantly higher in the CABG group than in the PCI group. After IPTW, the risk of inhospital MACCE was not found to be significantly different between CABG and PCI groups (HR = 1.81; 95% CI: 0.37-8.82; p = 0.460). Compared with patients who underwent PCI, those who underwent CABG exhibited a significantly higher risk of MI (HR = 6.92; 95% CI: 1.24-38.60; p = 0.027). Conclusions: : Patients with LVSD and CTO could experience better outcomes with PCI, which offers a safer alternative coronary revascularization strategy and a reduced risk of MI.

The postprocedural outcomes of coronary chronic total occlusion (CTO) revascularization in patients with left ventricular systolic dysfunction (LVSD) are still unclear. In this study, the periprocedural safety of percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) for revascularization of CTO in patients with LVSD is evaluated.In this study, patients hospitalized for coronary heart disease complicated by LVSD who underwent CTO PCI or CTO CABG between 2014 and 2020 were involved. The primary endpoint was 30-day major adverse cardiac or cerebrovascular events (MACCE), defined as the composite of all-cause mortality, cardiovascular mortality, stroke, myocardial infarction (MI), and target vessel revascularization. To evaluate the influence of the CTO revascularization strategies on 30-day outcomes, inverse probability of treatment weighting (IPTW) based on the propensity score was employed, and to identify predictors of 30-day MACCE, Cox regression was utilized.Among the 658 patients who satisfied the criteria, 440 (66.87%) underwent CTO PCI, and 218 (33.13%) underwent CTO CABG. The primary endpoint occurred in 30 (4.56%) patients, which is mainly attributed to all-cause mortality. Following IPTW adjustment, CTO CABG was found to be associated with significantly elevated risks of 30-day MACCE and MI (all P < 0.05).In this study in which patients with CTO and LVSD were examined, an increased risk of 30-day MACCE was observed in those who underwent CTO CABG. For such complex and high-risk patients, CTO PCI may represent a revascularization strategy that offers superior postprocedural safety.

Background: The optimal treatment strategy for patients with coronary chronic total occlusion (CTO) and left ventricular systolic dysfunction (LVSD) remains unclear. This study investigated the long-term outcomes of percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG), and medical therapy (MT) in this specific patient cohort. Methods and Results: This retrospective cohort study included 987 consecutive patients with CTO and LVSD who met the inclusion criteria and underwent either CTO-PCI (n=277), CTO-CABG (n=222), or CTO-MT (n=488) between 2014 and 2020. The primary outcome was all-cause mortality during follow-up. Secondary endpoints were major adverse cardiac and cerebrovascular events (MACCE) and their components, including cardiovascular mortality, myocardial infarction (MI), stroke, unplanned revascularization, and hospitalization for heart failure. During a median follow-up of 5.3 years, 232 (23.51%) patients died from any cause. In the unadjusted analysis, CTO-MT was associated with worse long-term survival prospects. After inverse probability of treatment weighting and variable adjustment, CTO-PCI and CTO-CABG demonstrated significant reductions in the long-term risks of all-cause and cardiovascular mortality. Notably, CTO-CABG was associated with the lowest long-term risks of MACCE, MI, unplanned revascularization, and hospitalization for heart failure. Conclusions: For patients with CTO and LVSD, successful CTO revascularization significantly improved long-term survival compared with CTO-MT. CTO-CABG can be regarded as the optimal treatment modality for better long-term prognosis.

Background: The risk of sudden cardiac death (SCD) after coronary revascularization in patients with left ventricular (LV) systolic dysfunction has not been characterized completely. This study aims to evaluate the incidence and time course of SCD after revascularization in such patients. The determinants of SCD within 3 months after revascularization were also assessed. Methods: A cohort study of patients with reduced ejection fraction (EF ≤40%), who underwent revascularization was performed. The incidence of SCD was estimated to account for the competing risk of deaths due to other causes. Results: 2317 patients were enrolled. With a median follow-up of 3.5 years, 162 (32.1%) of the 504 deaths were due to SCD. The risk of SCD was highest in the first 3 months after revascularization, with an incidence rate of 0.37%/month. The event rate decreased to 0.12%/month, 0.08%/month, 0.09%/month, 0.14%/month, and 0.19%/month at 3–6 months, 6–12 months, 1–3 years, 3–5 years, and 5–10 years, respectively. A history of ventricular tachycardia/ventricular fibrillation (hazard ratio [HR], 5.55; 95% confidence interval [CI], 1.33–23.19; p = 0.019) and triple vessel disease (HR, 3.90; 95% CI, 1.38–11.05; p = 0.010) were associated with the risk of SCD within 3 months. However, preoperative EF (in 5% increments) was not predictive (HR per 5% increase, 0.98; 95% CI, 0.62–1.55; p = 0.935). Conclusions: For patients with LV dysfunction, the risk of SCD was the highest during the first 3 months after revascularization. Further risk classification and treatment strategy are warranted. Clinical Trial Registration: The name of the registry: Coronary Revascularization in Patients with Ischemic Heart Failure and Prevention of Sudden Cardiac Death. Registration number: ChiCTR2100044378.

Abstract Objective Stoke after revascularization including both percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) is an uncommon but devastating complication. Patients with reduced ejection fraction (EF) had an increased risk of stroke after revascularization. However, little is known about the determinants and outcomes of stroke among patients with reduced EF following revascularization. Materials and Methods A cohort study of patients with preoperative reduced EF (≤40%) who received revascularization by either PCI or CABG between January 1, 2005 and December 31, 2014 was performed. Multivariate logistic regression was used to identify independent correlates of stroke. Logistic regression models were applied to evaluate the association of stroke with clinical outcomes. Results A total of 1937 patients were enrolled in this study. Of these, 111 (5.7%) patients suffered from stroke during the median 3.5‐year follow‐up. Older age (odds ratio [OR], 1.03; 95% CI, 1.01–1.05; p = .009), history of hypertension (OR, 1.79; 95% CI, 1.18–2.73; p = .007), and history of stroke (OR, 2.00; 95% CI, 1.19–3.36; p = .008) were found to be independent predictors for stroke. Patients with and without stroke had similar risk of all‐cause death (OR, 0.91; 95% CI, 0.59–1.41; p = .670). However, stroke was associated with higher odds ratio of heart failure (HF) hospitalization (OR, 2.77; 95% CI, 1.74–4.40; p < .001) and composite end point (OR, 1.61; 95% CI, 1.07–2.42; p = .021). Conclusions Further research appears warranted to minimize the complication of stroke and improve long‐term outcomes among patients with reduced EF who underwent such high risk revascularization procedural.

BACKGROUND:Appropriate time for ejection fraction (EF) reassessment after revascularization in patients with left ventricular dysfunction has not been investigated comprehensively, although 3 months after revascularization is recommended to stratify the risk of sudden cardiac death (SCD). HYPOTHESIS:EF reassessed within different timeframe after revascularization may have incosistent contribution for risk stratification of SCD. METHODS:Patients who had EF ≤ 40% before revascularization and had EF reassessment at least once during follow-up were included. The role of early (<3 months) versus late (3-12 months) EF measurements in prediction of all-cause mortality and SCD were compared. RESULTS:A total of 1589 patients were identified. EF reassessed <3 months was lower than EF reassessed within 3-12 months (42.1 ± 9.7% vs. 45.8 ± 10.8%; p < .01). Among 1069 patients who had EF reassessed <3 months, EF ≤ 35% was associated with a higher risk of all-cause mortality (hazard ratio [HR], 1.67; 95% confidence interval [CI], 1.22-2.29; p < .01), but had no association with the risk of SCD (HR, 1.44; 95% CI, 0.84-2.48; p = .18). By contrast, among 595 patients who had EF reassessed within 3-12 months, EF ≤ 35% was associated with higher risks of both all-cause death (HR, 1.81; 95% CI, 1.06-3.10; p = .03) and SCD (HR, 2.71; 95% CI, 1.31-5.61; p < .01). The relative contribution of SCD to all-cause death was higher in patients with EF ≤ 35% than patients with EF > 35% when EF was reassessed within 3-12 months (p = .04). However, when EF was reassessed <3 months, the mode of death was similar in patients with EF ≤ 35% versus >35% (p = .85). CONCLUSIONS:3 to 12 months after revascularization may be appropriate for cardiac function reassessment and SCD risk stratification.

Aims For patients with ischemic heart failure who underwent revascularization, ejection fraction (EF) improvement is a major predictor of survival benefit. However, the association between left ventricular (LV) remodeling and outcomes has not been well-established. The aim of the study is to investigate the extent of LV remodeling after revascularization and its predictive role for long-term survival. Methods Patients with reduced EF (≤40%), who underwent either coronary artery bypass grafting or percutaneous coronary intervention, and had echocardiography reassessment 3 months after revascularization were enrolled in a real-world cohort study (No. ChiCTR2100044378). Patients were categorized into 4 groups according to whether LV end-systolic dimension (LVESD) reduction was ≤7% or >7%, and absolute EF improvement ≤5% or >5% Results A total of 923 patients were identified. The percentage of LVESD reduction was 4.5±18.4%. The median follow-up time was 3.4 years, during which 123 patients died. Patients with greater percentage of LVESD reduction had lower risk of all-cause death (hazard ratio [HR] per 1% decrement in LVESD, 0.98; 95% CI, 0.97-0.99; P <.001). A reduction in LVESD of 7.2% was the optimal cutoff value to predict survival. Compared to patients with LVESD reduced and EF improved, 2.11-fold (95% CI, 1.04-4.29), 3.56-fold (95% CI, 1.60-7.91), and 7.54-fold (95% CI, 4.20-13.53) higher mortality were found in LVESD unreduced but EF improved, LVESD reduced but EF unimproved, and LVESD unreduced and EF unimproved group, respectively. Conclusions After revascularization among patients with ischemic HF, a reduction in LVESD of 7% signifies clinically relevant revers remodeling. Combination of EF improvement and LVESD reduction might be more clinically precise approach of risk stratification in this population. Clinical Trial Registration The name of the registry: Coronary Revascularization in Patients with Ischemic Heart Failure and Prevention of Sudden Cardiac Death. Registration number: ChiCTR2100044378 (). ### Competing Interest Statement The authors have declared no competing interest. ### Clinical Trial Registration number: ChiCTR2100044378 (). ### Funding Statement No external funding was received. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: This study was approved by the ethics committee of theBeijingAnzhenHospital(No. 2021004X).Becausethis was a retrospective cohort study, written informed consent from the patients was waived. The study conforms with World Medical Association Declaration of Helsinki. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

In recent decades, myocardial regeneration through stem cell transplantation and tissue engineering has been viewed as a promising technique for treating myocardial infarction. As a result, the researcher attempts to see whether co-culturing modified mesenchymal stem cells with Au@Ch-SF macro-hydrogel and H9C2 may help with tissue regeneration and cardiac function recovery. The gold nanoparticles (Au) incorporated into the chitosan-silk fibroin hydrogel (Au@Ch-SF) were validated using spectral and microscopic examinations. The most essential elements of hydrogel groups were investigated in detail, including weight loss, mechanical strength, and drug release rate. Initially, the cardioblast cells (H9C2 cells) was incubated with Au@Ch-SF macro-hydrogel, followed by mesenchymal stem cells (2 × 105) were transplanted into the Au@Ch-SF macro-hydrogel+H9C2 culture at the ratio of 2:1. Further, cardiac phenotype development, cytokines expression and tissue regenerative performance of modified mesenchymal stem cells treatment were studied through various in vitro and in vivo analyses. The Au@Ch-SF macro-hydrogel gelation time was much faster than that of Ch and Ch-SF hydrogels, showing that Ch and SF exhibited greater intermolecular interactions. The obtained Au@Ch-SF macro-hydrogel has no toxicity on mesenchymal stem cells (MS) or cardiac myoblast (H9C2) cells, according to the biocompatibility investigation. MS cells co-cultured with Au@Ch-SF macro-hydrogel and H9C2 cells also stimulated cardiomyocyte fiber restoration, which has been confirmed in myocardial infarction rats using -MHC and Cx43 myocardial indicators. We developed a novel method of co-cultured therapy using MS cells, Au@Ch-SF macro-hydrogel, and H9C2 cells which could promote the regenerative activities in myocardial ischemia cells. These study findings show that co-cultured MS therapy might be effective for the treatment of myocardial injury.

Purpose: Ejection fraction (EF) has been reported to be a major predictor of improved survival in patients with heart failure. However, it is largely unknown whether the extent of improvement in EF affects the subsequent risk of mortality. This study sought to investigate change in EF after revascularization and the implication of these changes on clinical outcomes among patients with ischemic left ventricular dysfunction.Patients and Methods: We conducted a cohort study (No. ChiCTR2100044378) of patients with reduced EF (<= 40%) who received revascularization and had EF reassessment by echocardiography 3 months after revascularization. Patients were categorized according to the absolute change in EF: 1) EF worsened group (absolute decrease in EF >5%); 2) EF unchanged group (absolute change in EF -5% to 5%); 3) EF improved group (absolute increase in EF >5%). Results: Of 974 patients, 84 (8.6%) had EF worsened, 317 (32.5%) had EF unchanged and 573 (58.8%) had EF improved. The median follow-up time was 3.5 years, during which 143 patients died. For each 5-unit increments in EF, the risk of death decreased by 20% (hazard ratio, HR, per 5% increases, 0.80; 95% CI, 0.73-0.86; P<0.001). Compared with EF improvement group, patients with EF worsened (HR, 3.35; 95% CI, 2.07-5.42; P<0.001) and patients with EF unchanged (HR, 2.05; 95% CI, 1.40-3.01; P<0.001) had significantly higher risk of all-cause death.Conclusion: Changes in EF were inversely associated with the risk of mortality. The extent of EF improvement after revasculariza-tion might be a potential factor which defines clinical outcomes.

Objectives To investigate the predictive roles of pre-operative left ventricular (LV) size and ejection fraction (EF) in EF improvement and outcome following revascularization in patients with coronary artery disease (CAD) and LV dysfunction. Background Revascularization may improve EF and long-term outcomes of patients with LV dysfunction. However, the determinants of EF improvement have not yet been investigated comprehensively. Materials and methods Patients with EF measurements before and 3 months after revascularization were enrolled in a cohort study (No. ChiCTR2100044378). All patients had baseline EF ≤ 40%. EF improvement was defined as absolute increase in EF > 5%. According to LV end-systolic diameter (LVESD) (severely enlarged or not) and EF (≤35% or of 36–40%) at baseline, patients were categorized into four groups. Results A total of 939 patients were identified. A total of 549 (58.5%) had EF improved. Both LVESD [odds ratio (OR) per 1 mm decrease, 1.05; 95% CI, 1.04–1.07; P < 0.001] and EF (OR per 1% decrease, 1.06; 95% CI, 1.03–1.10; P < 0.001) at baseline were predictive of EF improvement after revascularization. Patients with LVESD not severely enlarged and EF ≤ 35% had higher odds of being in the EF improved group in comparison with other three groups both in unadjusted and adjusted analysis (all P < 0.001). The median follow-up time was 3.5 years. Patients with LVESD not severely enlarged and EF ≤ 35% had significantly lower risk of all-cause death in comparison with patients with LVESD severely enlarged and EF ≤ 35% [hazard ratio (HR), 2.73; 95% CI, 1.28–5.82; P = 0.009], and tended to have lower risk in comparison with patients with LVESD severely enlarged and EF of 36–40% (HR, 2.00; 95% CI, 0.93–4.27; P = 0.074). Conclusion Among CAD patients with reduced EF (≤ 40%) who underwent revascularization, smaller pre-operative LVESD and lower EF had greatest potential to have EF improvement and better outcome. Our findings imply the indication for revascularization in patients with LV dysfunction who presented with lower EF but smaller LV size.