Myocardial infarction (MI) initiates sterile inflammation through the release of cytosolic DNA from necrotic cardiomyocytes, which aberrantly activates the cGAS-STING pathway in infiltrating macrophages and drives their polarization toward a pro-inflammatory M1 phenotype. Although the immunosuppressive oligodeoxynucleotide A151 can antagonize cGAS activation, its therapeutic utility is limited by enzymatic instability and inefficient cellular delivery. Here, we report a dual-biomimetic nanodecoy (A151@APPL) that integrates platelet membrane vesicles for infarct-specific targeting with arginine-modified phosphatidylserine lipids to promote macrophage uptake and enable nitric oxide-driven propulsion in redox-enriched tissue. This construct achieves efficient cytosolic delivery of A151 to lesional macrophages, suppressing the cGAS-STING axis, reducing pro-inflammatory cytokine expression, and reprogramming macrophages toward a reparative M2-like state. In a murine MI model, A151@APPL treatment attenuated ventricular inflammation, limited fibrotic remodeling, and restored cardiac performance. These findings establish a context-responsive delivery strategy that selectively modulates innate immune signaling and promotes cardiac repair following ischemic injury.

Heatwave (HW) exposure is increasing rapidly under climate change, yet its potential role in accelerating biological aging and the underlying mechanisms remain poorly understood. Leveraging data derived from the China Health and Retirement Longitudinal Study (CHARLS), a large population-based cohort in China, we examined whether exposure to HWs is linked to more rapid biological aging in adults of middle and advanced age. The Klemera–Doubal method (KDM) was applied to derive estimates of biological age (BA), and biological age acceleration (BAA) was calculated as biological age minus chronological age. HW exposure during the 12 months preceding BA assessments in 2011 and 2015 was quantified using 12 definitions based on different temperature threshold and duration. Longitudinal associations between HW exposure and BAA were evaluated using a difference-in-differences design. Among 2,318 participants (mean age, 58.7 years; 46.9% men), greater HW exposure was significantly associated with higher BAA. Under the most stringent (HW12; ≥4 consecutive days above the 97.5th percentile), each additional HW event and day increased BAA by 0.531 years [95% confidence interval (CI), 0.341 to 0.722] and 0.057 years (95% CI, 0.037 to 0.076). Stronger associations were observed among participants with body mass index ≥ 23 kg/m2, urban residents, and those living in southern or subtropical regions. HW exposure was also additionally associated with higher levels of total cholesterol and glycated hemoglobin A1c (HbA1c) levels. To explore potential biological mechanisms, transcriptomic profiling was performed in aged mice exposed to HW conditions. HW exposure induced 29 differentially expressed genes enriched in lipid metabolism and insulin resistance pathways, providing biological plausibility for the observed epidemiological associations. These results suggest that recurrent HW exposure may contribute to accelerated biological aging, potentially through metabolic disruption, and highlighting the vulnerability of aging populations to climate-related thermal stress and the need for targeted climate-adaptation strategies.

Background: Accelerated biological aging is characterized by an expedited deterioration of physiological systems. Phenotypic age (PA) derived from chronological age and 9 clinical biomarkers serves as a robust measure of this process, and phenotypic aging acceleration (PAA) was the discrepancy between phenotypic and chronological age. However, its association with major adverse cardiovascular events (MACEs) in stable coronary artery disease (SCAD) remains unclear. Methods: This cohort study enrolled 8672 patients with SCAD who underwent initial percutaneous coronary intervention (PCI). Accelerated biological aging was assessed using phenotypic aging calculations, and MACEs were defined as death (all-cause and cardiac mortality), non-fatal myocardial infarction (MI), non-fatal stroke, and unplanned revascularization. A cox proportional hazard model was employed for analysis. Results: Overall, the subjects were 64.7 ± 6.5 years old while the PA were 62.7 ± 12.3 years and the PAA was −2.8 (−6.4, 1.5) years. During overall 2.2 (1.4, 3.1) follow up years, 1147 MACEs were documented (165 all-cause mortality, 47 cardiac mortality, 918 unplanned revascularization, 43 non-fatal MI and 80 non-fatal strokes). Compared with phenotypically younger group (PAA < 0), phenotypically older group (PAA ≥ 0) showed higher risk for MACEs and components (all P values < 0.05). A positive dose-response association was identified between PAA and MACEs. For each 1-year PAA, there were 2.80%, 8.80%, 10.80%, 1.20%, 5.80%, 4.50% higher risk of MACEs, all-cause mortality, cardiac mortality, unplanned revascularization, non-fatal MI and non-fatal stroke, respectively (all P values < 0.05). Robust results were demonstrated in subgroup analysis. Conclusion: In SCAD patients undergoing PCI, accelerated biological aging is associated with an increased risk of MACEs, particularly death (all-cause and cardiac mortality) and unplanned revascularization.

Hypertensive left ventricular (LV) remodeling may influence coronary artery pathology due to anatomical proximity, yet its association with coronary chronic total occlusion (CTO) remains unclear. This cross-sectional, hypothesis-generating study included patients with coexisting coronary artery disease (CAD) and hypertension. LV geometry was classified by echocardiography as normal, concentric remodeling (CR), concentric hypertrophy (CH), or eccentric hypertrophy (EH). CTO was identified by coronary angiography. Logistic regression models were used to evaluate the association between LV geometry and CTO incidence. A total of 3430 patients were included, with a mean age of 65.3 years and 68.9% male. LV remodeling was present in 2427 (70.8%) patients. CTO lesions were identified in 300 (8.7%) patients, with incidence rates of 6.1% in normal geometry, 6.9% in CR, 9.9% in CH, and 12.7% in EH. Compared to normal geometry, LV remodeling was associated with a higher risk of CTO (OR, 1.696; 95% CI 1.258-2.285, p = 0.001), particularly in patients with CH (OR, 1.798; 95% CI 1.276-2.535, p = 0.001) and EH (OR, 2.355; 95% CI 1.656-3.349, p < 0.001). These observational findings suggest an association between LV remodeling and CTO in hypertensive CAD patients, although causal inference remains limited and further prospective investigations are warranted.

Mitochondrial quality control (MQC) mechanisms – including biogenesis, dynamics, mitophagy, proteostasis, the unfolded protein response, and mitochondrial-derived vesicles – play critical roles in the development of atherosclerosis. Dysregulation of these processes can lead to mitochondrial dysfunction, and subsequently the initiation of a pathological cascade characterized by oxidative stress, chronic inflammation, and the accumulation of lipids within arterial walls. Specifically, ROS overproduction and redox state imbalance are key molecular aspects that exacerbate mitochondrial damage, and create a self-perpetuating cycle of cellular injury and disease progression. Emerging therapeutic strategies targeting the modulation of MQC have promise in attenuating atherosclerotic progression by restoring mitochondrial biogenesis, restoring the balance of fusion and fission dynamics, enhancing the clearance of damaged mitochondria, and improving protein homeostasis. Advancing understanding of the molecular regulators and protein interaction networks within MQC pathways might facilitate the development of precision-targeted therapies. However, substantial challenges persist in translating these insights into clinical applications. This review explores the relationship between MQC mechanisms and atherosclerosis, focusing on the associated pathways and potential avenues for therapeutic intervention.

Angiopoietin-like protein 8 (ANGPTL8), a member of the angiopoietin-like protein (ANGPTL) family, is a physiological inhibitor of lipoprotein lipase (LPL), and plays a critical role in lipoprotein and triglyceride metabolism in response to nutritional cues. ANGPTL8 is implicated in a wide range of systemic and cellular processes and is closely associated with metabolic and cardiovascular diseases (CVD). Circulating ANGPTL8 is primarily secreted by the liver, with adipose tissue as a secondary source. Its expression is regulated by multiple transcription factors and microRNAs, and is responsive to fasting/refeeding states, hormonal signals, and stress conditions. In lipid metabolism, ANGPTL8 forms complexes with ANGPTL3 and ANGPTL4 to modulate LPL activity under fasting and feeding conditions. In glucose metabolism, ANGPTL8 plays a complex role. While some studies suggest it may improve glucose tolerance and insulin resistance, others indicate it could exacerbate glucose metabolism disorders and diabetes, or have no effect. Cardiovascular diseases are intricately linked to metabolic disorders and diseases. Increasing evidence also links ANGPTL8 to various cardiovascular pathologies, including atherosclerosis, hypertension, cardiomyopathy, cardiac hypertrophy, aortic aneurysm, and dissection. Given the strong interplay between metabolic dysregulation and CVDs, elucidating the role of ANGPTL8 in these processes is of significant interest. This review provides a balanced assessment of ANGPTL8’s roles in key pathophysiological processes, highlighting its established functions in metabolism alongside its emerging involvement in CVDs. Understanding the diverse functions of ANGPTL8 in various tissues and metabolic states will lead to new opportunities for therapeutic intervention in cardiometabolic disorders.

Chest pain is very common in emergency department. The management of chest pain is a priority for resident physicians. This study aimed to verify the teaching effects of the combination of bridge-in, objective, preassessment, participatory learning, post-assessment, and summary and case-based learning (BOPPPS-CBL) model in emergency chest pain management teaching for resident physicians. This randomized controlled trial study enrolled 118 resident physicians undergoing standardized training during their Cardiology Department rotation. They were randomized in two groups: traditional lecture-based learning (LBL) group and BOPPPS-CBL group. Pre-class test (30 points), post-class test (30 points), Mini clinical evaluation exercise (Mini-CEX), and direct observation of procedural skills (DOPS) were analyzed. The satisfaction of two teaching models and self-adjustment by two groups were further analyzed. A total of 118 resident physicians were enrolled and the mean age was 26.96 years and 57.6

AimsResearch on the triglyceride-glucose (TyG) index in patients with stable coronary artery disease (SCAD) remains relatively limited. Therefore, this study aims to investigate the association of the TyG index and its derived indicators, including the baseline TyG index, the baseline triglyceride glucose-body mass index (TyG-BMI), the mean TyG index, and the triglyceride glucose index-standard deviation (TyG-SD), with the prognosis of SCAD patients undergoing percutaneous coronary intervention (PCI).MethodsThis retrospective study enrolled 2,306 patients. The Cox proportional hazards model was utilized to evaluate the association between the four TyG indicators and major adverse cardiovascular and cerebrovascular events (MACCE). The predictive ability of the four TyG indicators for MACCE was assessed using the time-dependent receiver operating characteristic (ROC) curve. Kaplan-Meier survival analysis was employed to assess the prognostic differences among groups.ResultsAfter a median follow-up of 26.1 months, a total of 352 patients (15.3%) experienced MACCE. The Cox regression analysis revealed that under a fully adjusted model, when the four TyG indicators were stratified by tertiles, patients in the highest tertile of each TyG indicator had a significantly increased risk of MACCE compared to those in the lowest tertile. Specifically, the hazard ratio for baseline TyG index was 1.653 (95% confidence intervals (CI): 1.234-2.214), for baseline TyG-BMI was 2.467 (95%CI: 1.849-3.293), for mean TyG index was 2.451 (95%CI: 1.794-3.349), and for TyG-SD was 1.896 (95%CI: 1.430-2.513). Time-dependent ROC curve demonstrated that the mean TyG index had the strongest predictive ability for MACCE at each follow-up time point. The Kaplan-Meier analysis results showed that when the four TyG indicators were grouped by tertiles, there were significant differences in the cumulative incidence of MACCE among the three groups for each indicator (P < 0.05).ConclusionHigher levels of the TyG index and its derived indicators were each independently and positively associated with the risk of MACCE in SCAD patients undergoing PCI. Among these indicators, the mean TyG index demonstrated the greatest predictive value for the risk of MACCE at each follow-up time point. Consequently, tracking the long-term trends of the TyG index may be prioritized in clinical practice.

Introduction:Circulating very-long-chain saturated fatty acids (VLSFAs) may attenuate age-related cognitive decline, but their direct association with neurodegeneration biomarkers and the underlying mechanisms remain unclear. Methods:This cross-sectional study examined associations between circulating fatty acid profiles, neurodegeneration (assessed by serum neurofilament light chain, NfL), cognitive function, and hypertension in 1,677 U.S. adults from the National Health and Nutrition Examination Survey (NHANES) 2013-2014. Advanced statistical methods including weighted quantile sum (WQS) regression, Bayesian kernel machine regression (BKMR), quantile g-computation (Qgcomp), and formal mediation analyses were employed. Results:The VLSFA mixture demonstrated significant inverse associations with serum NfL (β = -0.044, 95% CI: -0.076, -0.011) and the prevalence of hypertension (OR = 0.788, 95% CI: 0.672, 0.923). This association with NfL was non-linear, exhibiting a more pronounced protective effect at lower VLSFA concentrations. Higher VLSFA levels were significantly correlated with better cognitive performance, particularly in processing speed (Digit-Symbol Substitution Test) and memory (delayed recall). Hypertension was positively associated with NfL (β=4.133, 95% CI: 1.705, 6.562), an effect driven primarily by systolic blood pressure. Mediation analysis revealed that hypertension accounted for approximately 15-20% of the total association between VLSFAs and NfL. Discussion:Circulating VLSFAs are inversely associated with the neurodegeneration biomarker NfL and positively correlated with cognitive performance. This neuroprotective association appears to be partially mediated by blood pressure regulation pathways. These findings identify VLSFAs as a potential therapeutic target, warranting further longitudinal and interventional studies to confirm their role in mitigating neurodegeneration.

As a main cause of serious cardiovascular diseases, atherosclerosis is characterized by deposited lipid and cholesterol crystals (CCs), which is considered as a great challenge to the current treatments. In this study, a dual-track reverse cholesterol transport strategy is used to overcome the cumulative CCs in the atherosclerotic lesions via a targeting nanoplatform named as LPLCH. Endowed with the active targeting ability to the plaques, the nanoparticles can be efficiently internalized and achieve a pH-triggered charge conversion for the escape from lysosomes. During this procedure, the liver X receptor (LXR) agonists loaded in nanoparticles are replaced by the deposited lysosomal CCs, leading to a LXR mediated up-regulation of ATP-binding cassette transporte ABCA1/G1 with the local CCs carrying at the same time. Thus, the cumulative CCs are removed in a dual-track way of ABCA1/G1 mediated efflux and nanoparticle-based carrying. The in vivo investigations indicate that LPLCH exhibits a favorable inhibition on the plaque progression and a further reversal of formed lesions when under a healthy diet. And the RNA-sequencing suggests that the cholesterol transport also synergistically activates the anti-inflammation effect. The dual-track reverse cholesterol transport strategy performed by LPLCH delivers an exciting candidate for the effective inhibition and degradation of atherosclerosis.

Metabolic reprogramming is critical in the onset of pressure overload-induced cardiac remodeling. Our study reveals that proline dehydrogenase (PRODH), the key enzyme in proline metabolism, reprograms cardiomyocyte metabolism to protect against cardiac remodeling. We induced cardiac remodeling using transverse aortic constriction (TAC) in both cardiac-specific PRODH knockout and overexpression mice. Our results indicate that PRODH expression is suppressed after TAC. Cardiac-specific PRODH knockout mice exhibited worsened cardiac dysfunction, while mice with PRODH overexpression demonstrated a protective effect. In addition, we simulated cardiomyocyte hypertrophy in vitro using neonatal rat ventricular myocytes treated with phenylephrine. Through RNA sequencing, metabolomics, and metabolic flux analysis, we elucidated that PRODH overexpression in cardiomyocytes redirects proline catabolism to replenish tricarboxylic acid cycle intermediates, enhance energy production, and restore glutathione redox balance. Our findings suggest PRODH as a modulator of cardiac bioenergetics and redox homeostasis during cardiac remodeling induced by pressure overload. This highlights the potential of PRODH as a therapeutic target for cardiac remodeling.

Aims:Myocardial ischemia can affect traditional right ventricular (RV) pacing parameters, but it is unclear whether coronary artery disease (CAD) impact the pacing parameters and electrophysiological characteristics of left bundle branch area pacing (LBBaP) as a physiological pacing representative. Methods:Patients who underwent coronary angiography (CAG) after/before the LBBaP procedure and underwent percutaneous coronary intervention after LBBaP procedure were divided into CAD group and Non-CAD group according to visual CAG. Pacing parameters and electrophysiological characteristics were recorded at LBBaP implantation. Multivariate logistic regression analysis was implemented to evaluate the association between CAD and higher capture threshold. Sensitivity analyses were conducted to verify result stability. Results:A total of 176 patients met inclusion criteria (115 Non-CAD patients and 61 CAD patients) with a mean age of 71.1 ± 9.0 years. Compared with the Non-CAD patients, CAD patients had the higher capture threshold (0.67 ± 0.22 V vs. 0.82 ± 0.28 V, P < 0.001) and lower R-wave amplitude (12.5 ± 4.8 mV vs. 10.1 ± 2.7 mV, P = 0.001). Moreover, CAD was independently associated with higher capture threshold (adjusted Odds ratio (OR) 3.418, 95% confidence interval (CI): 1.621-7.206, P = 0.001), which was further validated through sensitivity analyses. Conclusion:Patients without CAD might have safer pacing parameters in the LBBaP procedure. Besides, CAD might be the risk factor of capture threshold increase during permanent LBBaP implantation.

Purpose: Peripheral sensitivity of thyroid hormones (PSTH) plays a vital role in many renal diseases, but the relationship between PSTH and contrast-induced acute kidney injury (CI-AKI) is still not clear. Our study aimed to identify the association between PSTH and CI-AKI in euthyroid patients with stable coronary heart disease (SCAD) underwent coronary angiography (CAG). Methods: This is a retrospective cross-sectional study which enrolled 2482 euthyroid patients with SCAD underwent CAG. CI-AKI was defined by serum creatinine (Scr) elevation. The indicator of PSTH was serum free triiodothyronine / free thyroxine (FT3/FT4) ratio. Multivariable logistic regression analysis was performed with confounders being adjusted, while receiver operator characteristic (ROC) analysis was performed with area under ROC curve (AUC) being calculated. Besides, subgroup analysis was also conducted. Results: Overall, 297 (12.0%) patients were diagnosed with CI-AKI. Patients with CI-AKI had lower FT3/FT4 (2.34±0.46 vs. 2.54±0.48, P<0.001). Higher FT3/FT4 was proven to be negatively associated with the incidence of CI-AKI (adjusted OR [95%CI] = 0.573 [0.421 to 0.779], P < 0.001). A similar negative association was also observed for FT3 (adjusted OR [95%CI] = 0.524 [0.367 to 0.748], P < 0.001), but not for FT4. Furthermore, we found FT3/FT4 performed well in predicting the incidence of CI-AKI (AUC: 0.613). These findings between FT3/FT4 and CI-AKI were consistent across subgroups. Conclusion: PSTH was negatively associated with the incidence of CI-AKI in euthyroid patients with SCAD who underwent CAG.

BACKGROUND:Statins are lipid-lowering drugs with favorable anti-inflammatory effects. This study aimed to explore different statin-based lipid-lowering strategies to reduce high-sensitivity C-reactive protein (hs-CRP).HYPOTHESIS:The hypothesis is that different statin-based lipid-lowering strategies might reduce hs-CRP.METHODS:This retrospective study included 3653 patients who underwent percutaneous coronary intervention (PCI). Three statin-based lipid-lowering strategies were investigated, including different types of statins (atorvastatin vs. rosuvastatin), statin combined with ezetimibe therapy (vs. without), and intensive statin therapy (vs. regular). The hs-CRP levels and blood lipid indicators were measured at baseline and after 1-month lipid-lowering therapy. Multivariable linear regression analysis and structural equation mode analysis were conducted to verify the association between different lipid-lowering strategies, Δhs-CRP (%) and ΔLDL-C (%).RESULTS:Totally, 3653 patients were enrolled with an average age of 63.81 years. Multivariable linear regression demonstrated that statin combined with ezetimibe therapy was significantly associated with decreased Δhs-CRP (%) (β = -0.253, 95% CI: [-0.501 to -0.005], p = 0.045). The increased ΔLDL-C (%) was an independent predictor of elevated levels of Δhs-CRP (%) (β = 0.487, 95% CI: [0.15-0.824], p = 0.005). Furthermore, structural equation model analysis proved that statin combined with ezetimibe therapy (β = -0.300, p < 0.001) and intensive statin therapy (β = -0.032, p = 0.043) had an indirect negative effect on Δhs-CRP via ΔLDL-C.CONCLUSIONS:Compared with routine statin use, statin combined with ezetimibe therapy and intensive statin therapy could further reduce hs-CRP levels.

Terpenes have been shown to have an effect on metabolic status. However, it is unclear how they are associated with the metabolic syndrome (MetS) and whether insulin resistance (IR) mechanisms are involved. This cross-sectional study included data from the National Health and Nutrition Examination Survey (2013–2014). Serum terpenes (α- pinene, β- pinene, and limonene) were quantified by gas chromatography-tandem mass spectrometry. MetS was diagnosed by lipid, glucose, blood pressure, and waist circumference criteria. IR status was assessed using the homeostasis model assessment of insulin resistance (HOMA-IR) model and triglyceride-glucose index. Regression analysis models, mixed-effects models (weighted quantile sum regression models, quantile g-computation and Bayesian Kernel machine regression models), and mediation analysis were used for analysis. Among 1563 U.S. general population (mean age 39.0 years), 447 (28.6

Bilirubin is widely recognized to possess antioxidant and anti-inflammatory characteristics. However, the relationship between bilirubin and coronary artery disease (CAD) remains controversial, particularly in individuals receiving Percutaneous Coronary Intervention (PCI). Given that statins may enhance the production of heme oxygenase-1 (HO-1) and bilirubin, we investigated the long-term cardiovascular prognostic role of bilirubin levels elevated by statin use in patients undergoing PCI. Data of 6945 subjects undergoing PCI were enrolled in this study. We divided the patients into two groups based on serum total bilirubin (TB) levels detected prior to PCI. The high TB group consisted of patients with serum TB values > 8.4 μmmol/L, while the low TB group consisted of patients with serum TB values ≤ 8.4 μmmol/L. The median follow-up time was 836 days. Cox proportional hazards models were performed to evaluate the hazard ratios (HRs) and 95% confidence interval (CI) for the incidence of major adverse cardiovascular event (MACE) associated with bilirubin levels. The association between TB levels and risk of MACE was significant [adjusted HR = 0.557, 95% CI (0.59–0.96), p = 0.020). Linear analysis was performed to determine the association between preadmission usage of statin and bilirubin level. The preadmission usage of statin independently linearly increases TB [adjusted-β = 0.371, 95% CI (0.134–0.608), p = 0.002] and direct bilirubin (DB) [adjusted-β = 0.411, 95% CI (0.300–0.522), p < 0.001). Mediation analysis demonstrated a direct protective role of preadmission statins treatment (β = − 0.024, p < 0.01), TB (β = − 0.003, p < 0.05) and DB (β = − 0.009, p < 0.05). Furthermore, it was found that TB (4.0%) and DB (12.0%) mediated the relationship between preadmission statins therapy and MACE. Bilirubin has a protective effect against MACE. In patients with normal bilirubin level undergoing elective PCI, preadmission statin use elevated bilirubin levels, which were independently associated with a lower incidence of MACE over the long-term follow-up period.

Background: Biological age is a reliable indicator reflecting the real physiological state and aging status of individuals. This study was aimed at exploring the association between biological age and contrast-associated acute kidney injury (CA-AKI). Methods: This retrospective study was conducted on 4078 patients with coronary artery disease (CAD) undergoing coronary angiography (CAG). Biological age was calculated according to chronological age and blood biomarkers, and the “age gap,” reflecting retardation or acceleration of biological aging, was further determined. Logistic regression analysis was used to examine the association of the biological age and age gap with CA-AKI. Receiver operating characteristic (ROC) analysis and subgroup analysis were also conducted. Results: Among the 4078 patients (68.00 [61.00, 74.00] years, 2680 (65.7%) men), 725 CA-AKI cases were identified. Older biological age (≥79.3 vs. <79.3 years, OR [95% CI] = 3.319 [2.714 to 4.059]) and greater age gap (≥1.12 vs. <1.12, OR [95% CI] = 2.700 [2.240 to 3.256]) were independent risk factors for CA-AKI (both P <0.001). ROC analysis indicated that biological age (AUC = 0.672) and age gap (AUC = 0.672) had better predictive ability for CA-AKI than chronological age (AUC = 0.583). Subgroup analysis also indicated similar findings (all P <0.001). Conclusion: Biological age was found to be an independent risk factor for CA-AKI after CAG, with better predictive value than chronological age.

BACKGROUND:Percutaneous coronary intervention (PCI)-related myocardial infarction (MI), especially the distal type associated with microvascular dysfunction, is not an uncommon complication of the procedure. Specific lesion features, the echo-attenuated plaques (EA) in particular, are well-established contributors to the pathogenesis of distal-type MI. These plaques are prone to disruption during PCI, leading to microvascular thrombosis and distal embolism. Tenecteplase (TNK), a 3rd-generation thrombolytic drug, has demonstrated effective thrombolytic capacity without significantly increasing the bleeding risk. Our study aims to evaluate whether a low-dose intracoronary TNK administration prior to PCI in patients with intravascular ultrasound (IVUS)-detected EA can reduce the occurrence of PCI-related MI and improve clinical outcomes. METHODS:This trial is designed as a multicenter, prospective randomized controlled trial with a 1-month follow-up. The primary outcome of the study is the incidence of PCI-related myocardial infarction (MI) occurring within 48 h after PCI, which serves as a valid surrogate endpoint for assessing the efficacy of tenecteplase-based PCI in preventing future major adverse cardiovascular events (MACE) in patients with EA (Bulluck, et. al, Eur Heart J 42:2630-42, 2021) {1b.1}. Secondary outcomes include the proportion of patients with elevated postoperative high-sensitivity cTnI exceeding 5, 10, 35, and 70 times of the normal baseline, incidence of coronary slow flow after stent implantation and post-dilation, frame count of angiographic flow after stent implantation and post-dilation, as well as the incidence of MACE during hospitalization and at the 1-month follow-up. DISCUSSION:This trial may demonstrate that an immediate intracoronary administration of low-dose TNK following PCI can effectively lower the incidence of PMI in patients with EA, while confirming the safety of this therapeutic approach. TRIAL REGISTRATION:Chinese Clinical Trial Registry ( ChiCTR2400084840 ). Registered on May 27, 2024.

AimsStress hyperglycemia ratio (SHR), an emerging indicator of critical illness, exhibits a significant association with adverse cardiovascular outcomes. The primary aim of this research endeavor is to evaluate the association between fasting SHR and contrast-induced acute kidney injury (CI-AKI).MethodsThis cross-sectional study comprised 3,137 patients who underwent coronary angiography (CAG) or percutaneous coronary intervention (PCI). The calculation of fasting SHR involved dividing the admission fasting blood glucose by the estimated mean glucose obtained from glycosylated hemoglobin. CI-AKI was assessed based on elevated serum creatinine (Scr) levels. To investigate the relationship between fasting SHR and the proportion of SCr elevation, piecewise linear regression analysis was conducted. Modified Poisson’s regression analysis was implemented to evaluate the correlation between fasting SHR and CI-AKI. Subgroup analysis and sensitivity analysis were conducted to explore result stability.ResultsAmong the total population, 482 (15.4%) patients experienced CI-AKI. Piecewise linear regression analysis revealed significant associations between the proportion of SCr elevation and fasting SHR on both sides (≤ 0.8 and > 0.8) [β = -12.651, 95% CI (−23.281 to −2.022), P = 0.020; β = 8.274, 95% CI (4.176 to 12.372), P < 0.001]. The Modified Poisson’s regression analysis demonstrated a statistically significant correlation between both the lowest and highest levels of fasting SHR and an increased incidence of CI-AKI [(SHR < 0.7 vs. 0.7 ≤ SHR < 0.9) β = 1.828, 95% CI (1.345 to 2.486), P < 0.001; (SHR ≥ 1.3 vs. 0.7 ≤ SHR < 0.9) β = 2.896, 95% CI (2.087 to 4.019), P < 0.001], which was further validated through subgroup and sensitivity analyses.ConclusionIn populations undergoing CAG or PCI, both lowest and highest levels of fasting SHR were significantly associated with an increased occurrence of CI-AKI.