Background:Chronic total occlusion (CTO) is a particularly challenging subtype of ischemic heart disease, significantly elevating the risk of heart failure and sudden cardiac death. Percutaneous coronary intervention (PCI) is the primary revascularization approach. However, the success rate of antegrade PCI (A-PCI) for CTO remains relatively low. Although the distal vessel diameter is recognized as a critical anatomic parameter in A-PCI, it has received limited attention in studies of related populations. Methods:This retrospective study included 502 CTO patients treated with antegrade PCI from July 2023 to September 2024. The relationship between the distal vessel diameter and the antegrade crossing success rate was investigated using logistic regression analysis and receiver operating characteristic curve analysis. Results:Antegrade crossing success was achieved in 72.5% (364 of 502 patients). The distal vessel diameter was significantly smaller in the failure group (1.60 ± 0.39 mm) compared to the success group (1.94 ± 0.41 mm; P < 0.001). In the multivariate logistic regression, distal vessel diameter was the most potent independent predictor of success. Each 0.5-mm increase in diameter was associated with more than triple the odds of successful crossing (odds ratio: 3.06; 95% confidence interval: 2.22-4.32; P < 0.001). This positive predictor had a greater predictive magnitude than the strongest negative predictor, proximal cap ambiguity (odds ratio: 0.35; 95% confidence interval: 0.21-0.58; P < 0.001). Conclusions:Distal vessel diameter is the most powerful independent angiographic predictor of antegrade crossing success in CTO-PCI, with a predictive significance surpassing that of established proximal lesion characteristics such as cap ambiguity.
Pediatric high myopia (HM) is increasingly recognized as a heterogeneous condition, arising either idiopathically or in association with underlying ocular or genetic disorders. Disease-associated HM may show distinct biometric characteristics, yet comparative data in children remain limited. This study characterized ocular biometry in isolated HM (IHM) and disease-associated HM related to familial exudative vitreoretinopathy (FEVR), myelinated retinal nerve fibers (MRNF), Stickler syndrome (SS), and epiretinal membrane (ERM). We retrospectively analyzed patients aged ≤ 18 years with HM, defined as spherical equivalent (SE) ≤ − 5.0 diopters (D) or axial length (AL) ≥ 26.0 mm, who underwent comprehensive examinations. Biometric parameters were obtained using the IOLMaster 700. Linear mixed-effects models accounted for inter-eye correlation, and estimated marginal means with Benjamini–Hochberg–adjusted pairwise comparisons were used for statistical inference. A total of 131 patients (186 eyes) were included. Of 186 affected eyes, 37.1
Objective To characterize clinical features, management, and outcomes of pediatric macular hole (MH) and to outline an etiology-guided aid. Design A retrospective, consecutive case series. Participants Pediatric MH patients diagnosed, surgically treated, and followed at a tertiary centre (March 2012 to January 2025). Methods Clinical data (age, sex, etiology, best-correct visual acuity [BCVA], intraocular pressure, axial length, MH size, and imaging) were reviewed. Etiology was classified as traumatic, secondary, or idiopathic. Vitreoretinal techniques and adjuncts were recorded. Results Eighty-eight eyes of 88 patients were included: traumatic 51/88 (58%), secondary 25/88 (28%), and idiopathic 12/88 (14%). At baseline, idiopathic MHs had better BCVA than traumatic (p = 0.05) and secondary (p = 0.003), while secondary MHs had longer axial length than traumatic MHs (p = 0.023). Imaging patterns differed by etiology (acute-injury changes in traumatic; proliferative/tractional features in secondary; relatively “pure” in idiopathic). Surgery reflected these patterns: internal limiting membrane flap/covering in 33% of traumatic MH; multiple adjuncts in secondary eyes (laser 56% with anti-vascular endothelial growth factor/steroid/buckle/oil); and primarily inert-gas tamponade in idiopathic MH (75%). Primary complete closure was 82%; final complete closure after reintervention was 84%. Mean final BCVA improved to 0.90 logMAR (≈20/160; p < 0.001), and the proportion with BCVA >20/200 rose from 47% to 68%. Visual gains were greatest in idiopathic and traumatic. Conclusions An etiology-informed, size/edge/traction-guided approach was associated with meaningful—though limited—visual improvement and high closure. These practice-informing data support early recognition, tailored surgery, and proactive complication management; a decision aid is provided. Prospective studies are needed to standardize thresholds and validate outcomes.
OBJECTIVE:This study aims to screen potential targets of Curcumin (Cur) in Myocardial ischaemia-reperfusion injury (MIRI) using network pharmacology and molecular docking, and to experimentally validate whether Cur mitigates MIRI by modulating the NLRP3 inflammasome and pyroptosis via the Nrf2/HO-1 pathway. METHODS:Potential Cur-MIRI targets were identified from public databases and analysed by topological algorithms; molecular docking assessed binding affinity. Cardioprotective effects were validated in vivo using a murine LAD ligation model (30 min ischaemia/24 h reperfusion) and in vitro using H9C2 cardiomyocytes subjected to hypoxia/reoxygenation (H/R). Cur was given as pretreatment. Mechanistic assays included tissue immunofluorescence, mtROS and JC-1 staining, ELISA for cytokines, and Western blotting; Nrf2 was silenced by siRNA to test dependency. RESULTS:Network analysis revealed 481 common targets enriched in apoptosis, TNF and NOD-like receptor pathways. Docking showed favourable binding to NLRP3 (-8.14 kcal/mol) and Nrf2 (-7.02 kcal/mol). In vivo Cur reduced myocardial injury markers, improved echocardiographic function, attenuated inflammation and mitochondrial ultrastructural damage, and decreased NLRP3/caspase-1 expression. In vitro Cur lowered IL-1β/IL-18 and mtROS, preserved mitochondrial membrane potential, reduced apoptosis, upregulated Nrf2/HO-1 and downregulated pyroptosis proteins (NLRP3, ASC, caspase-1, GSDMD). Nrf2 silencing abolished these effects. CONCLUSION:Combining in silico and experimental evidence, Cur attenuates MIRI by activating Nrf2/HO-1 to inhibit NLRP3 inflammasome-mediated pyroptosis.
Background Among patients with acute coronary syndromes at both high bleeding and ischemic risk (birisk), extended clopidogrel monotherapy after 9 to 12 months of dual‐antiplatelet therapy reduces bleeding without increasing ischemia. Whether this benefit extends to birisk patients with diabetes is unknown. Methods This prespecified subgroup analysis of the OPT‐BIRISK (Optimal Antiplatelet Therapy for High Bleeding and Ischemic Risk Patients) trial included birisk patients with acute coronary syndrome who had completed 9 to 12 months of dual‐antiplatelet therapy after percutaneous coronary intervention. Patients were then randomized 1:1 to 9 months of clopidogrel plus placebo versus clopidogrel plus aspirin. Outcomes were compared by diabetes status. The primary end point was Bleeding Academic Research Consortium type 2, 3, or 5 bleeding at 9 months after randomization. The key secondary end point was major adverse cardiac and cerebral events, defined as a composite outcome of all‐cause death, myocardial infarction, stroke, or clinically driven revascularization. Results Of 7758 patients, 4072 (52.5%) had diabetes. Clopidogrel monotherapy decreased Bleeding Academic Research Consortium type 2, 3, or 5 bleeding (2.1% versus 3.2%; hazard ratio [HR], 0.66 [95% CI, 0.45–0.97]) with no increase in major adverse cardiac and cerebral events (2.9% versus 3.6%; HR, 0.79 [95% CI, 0.56–1.12]) compared with clopidogrel plus aspirin in patients with diabetes. Outcomes were consistent in patients without diabetes, with no significant interactions by diabetes status. Conclusions In birisk patients with acute coronary syndrome who were stable on dual‐antiplatelet therapy with clopidogrel plus aspirin for 9 to 12 months after percutaneous coronary intervention, clopidogrel monotherapy for an additional 9 months reduced clinically relevant bleeding without increasing ischemic events compared with continued dual‐antiplatelet therapy, irrespective of diabetes status. Registration URL: https://clinicaltrials.gov ; Unique identifier: NCT03431142.
OBJECTIVES:To investigate the association between serum fibroblast growth factor 21 (FGF21) levels and the severity of coronary artery calcification (CAC) in patients with chronic total occlusion (CTO), as well as the complexity and outcomes of percutaneous coronary intervention (PCI). METHODS:We enrolled 128 CTO patients who underwent PCI and preprocedural coronary computed tomography angiography, dividing them into severe CAC (n = 48) and nonsevere CAC (n = 80) groups according to an Agatston score of greater than or equal to 400. RESULTS:Serum FGF21 levels were significantly lower in patients with severe CAC, negatively correlated with CAC scores, and independently associated with severe CAC after multivariable adjustment [odds ratio (OR) per 1-SD increase: 0.481, 95% confidence interval (CI): 0.244-0.947; P < 0.05]. Patients with low FGF21 levels had significantly higher complexity scores, increased use of guidewires, longer procedural times, and lower procedural success rates (all P < 0.05). Receiver operating characteristic analysis identified 226.13 pg/ml as the optimal cut-off value of serum FGF21 for predicting procedural success. The area under the curve was 0.664 (95% CI: 0.527-0.802; P = 0.029). CONCLUSION:Serum FGF21 levels were negatively correlated with CAC severity and independently predicted severe CAC in patients with CTO. Serum FGF21 was associated with procedural difficulty and had a diagnostic value for procedural success.
Neurofibromatosis type 1 (NF1) is a multisystem genetic disorder caused by mutations in the NF1 gene and is commonly associated with ocular manifestations such as Lisch nodules, optic pathway gliomas, and choroidal abnormalities. Retinal structural changes are rarely reported. The authors describe a 3-year-old girl with NF1 who presented with decreased vision in her left eye. Ophthalmic imaging revealed an epiretinal fibrovascular membrane with vitreoretinal traction, cystic macular changes, and localized tractional retinal detachment (TRD) with a retinal tear. RetCam (Clarity Medical Sysetms, Inc) imaging and fluorescein angiography demonstrated vitreous opacities, fibrovascular adhesions, and vascular leakage. Systemic examination identified multiple café-au-lait spots and a plexiform neurofibroma confirmed by histopathology. The patient underwent pars plana vitrectomy with membrane removal and silicone oil tamponade, resulting in stable retinal attachment during follow-up. This case expands the spectrum of retinal manifestations associated with NF1 and highlights the importance of regular ophthalmic surveillance in affected children.
Background: Coronary artery calcification (CAC) is a strong predictor of long-term adverse outcomes in patients with coronary artery disease (CAD). Meanwhile, insulin resistance (IR) is a key metabolic disorder that accelerates CAC progression through multiple pathways. Fibroblast growth factor 21 (FGF21) improves glucolipid metabolism and has been associated with vascular calcification. However, the relationship between serum FGF21 level and CAC severity in patients with varying degrees of IR remains unclear. Methods: A total of 128 patients with CAD who underwent preprocedural coronary computed tomography angiography and percutaneous coronary intervention were enrolled. Patients were stratified by triglyceride–glucose (TyG) index into high (TyG >8.62, n = 62) and low (TyG ≤8.62, n = 66) groups. Associations between FGF21 levels and severe CAC were analyzed under varying degrees of IR. Results: In patients with a TyG index >8.62, serum FGF21 levels were significantly lower in those with severe CAC, and were negatively correlated with CAC scores. Multivariable analysis revealed that serum FGF21 levels were independently associated with severe CAC (odds ratio (OR) per 1-standard deviation (SD) increase: 0.261; 95% confidence interval (CI): 0.073, 0.933; p < 0.05). In contrast, serum FGF21 levels among patients with a TyG index ≤8.62 did not differ significantly between the severe and non-severe CAC groups, and no independent association between serum FGF21 level and severe CAC was observed after adjustment. Importantly, a significant interaction was observed between the TyG index and FGF21 level (p for interaction = 0.035). Moreover, the protective association between FGF21 and CAC was primarily observed in patients with a high TyG index. Conclusions: Lower serum FGF21 levels in patients with CAD can identify individuals at increased risk of severe CAC, particularly among those with a higher degree of IR. Serum FGF21 levels may serve as a novel biomarker for CAC risk stratification in metabolically susceptible patients.
miRNA, circRNA, and lncRNA play crucial roles in the pathogenesis and progression of myocardial ischemia-reperfusion injury (MI/RI). This study aims to provide valuable insights into miRNA, circRNA, lncRNA, and MI/RI from a bibliometric standpoint, with the goal of fostering further advancements in this area. The relevant literature in the field of miRNA, circRNA, lncRNA, and MI/RI was retrieved from the Science Citation Index Expanded (SCI-E) database within Web of Science. The “Analyze Results” and “Citation Report” functions in WOS were utilized to compile the annual publication and citation counts in this field. Microsoft Office Excel 2019 was used to organize and visualize the data. Furthermore, bibliometric and visualization analyses of countries/regions, institutions, authors, keywords, and references were conducted using the bibliometric visualization software CiteSpace. A total of 858 publications were included for further analysis in this field. The literature was published across 297 journals, with Molecular Medicine Reports contributing the highest number of publications. Researchers from 45 countries participated in studies within this field, with those from China contributing the most publications. The research hotspots in this field primarily focus on three areas: the role of miRNA, circRNA, and lncRNA in the pathogenesis of MI/RI, their potential as therapeutic targets, and their role as biomarkers. Among these, circular RNA, therapy target, inflammatory response, and cardiomyocyte ferroptosis are likely to emerge as emerging trends in this field. The overall development of research in this field is on the rise. The compilation of research hotspots and emerging trends in this area may provide researchers with more references and assistance in selecting research directions, ultimately benefiting MI/RI patients.
Background: Chronic total occlusion (CTO) is a complex and difficult type of coronary lesion for which elective secondary intervention after subintimal plaque modification (SPM) can improve the success rate. This study sought to determine the most appropriate timing for secondary interval interventions to maximize the benefit to the patient. Methods: This study retrospectively included patients who failed their first CTO percutaneous coronary intervention (PCI) at Beijing Anzhen Hospital Department of Cardiology from January 2019 to December 2022. We reviewed the clinical characteristics, procedural features, and outcomes of patients who underwent SPM and returned to our institution for a second CTO-PCI. Results: Of the 2847 patients who visited our institution between January 2019 and December 2022, 528 underwent SPM and returned to our institution on an elective basis for a secondary procedure. Of these, 236 procedures were performed within 30 days (Group I), and 292 were performed between 30 and 90 days (Group II). After the intervention, the occluded segment was successfully opened in 170 (72.0%) Group I and 248 (84.9%) Group II participants. When analyzing the factors for operational failure, we found that different intervals, diabetes mellitus, hyperlipidemia, and a history of previous PCI or percutaneous coronary angioplasty (PTCA) were the reasons for the secondary intervention failure. When analyzing the safety of the procedure, we found that pericardial effusion was the most common complication after the procedure, with an incidence of 7.4%. There was no notable variation in the incidence of pericardial effusion between the two groups, 8.9% vs. 6.2% (p = 0.232). Conclusions: Higher success rates were observed when secondary procedures were performed between 30 and 90 days instead of within 30 days after the initial CTO-PCI SPM, with no significant difference in safety noted between the two groups.
Background: The incidence of unstable angina (UA), a type of cardiovascular disease (CVD), has increased in recent years. Meanwhile, timely percutaneous coronary intervention (PCI) or percutaneous transluminal coronary angioplasty (PTCA) procedures are crucial for patients with UA who also have diabetes mellitus (DM). Additionally, exploring other factors that may influence the prognosis of these patients could provide long-term benefits. The systemic immune-inflammation index (SII), a novel marker for assessing inflammation levels, has been shown to correlate with the long-term prognosis of various diseases. Thus, this study aimed to investigate the predictive value of the SII for the long-term prognosis of patients with UA and DM after revascularization. Methods: A total of 937 UA patients who underwent revascularization, of which 359 also had DM, were included in this study. Patients were divided into two groups: the low SII group (<622.675 × 109/L; n = 219, 61.0%) and the high SII group (≥622.675 × 109/L; n = 140, 39.0%). The primary outcome was the frequency of major adverse cardiovascular and cerebrovascular events (MACCEs). The secondary outcome was the incidence of all-cause death. Results: Of the 359 patients who visited our institution between January 2018 and January 2020, 23 patients (10.5%) in the low SII group experienced MACCEs, whereas 34 cases (24.3%) in the high SII group experienced MACCEs, showing a statistically significant difference (p < 0.001). After conducting univariate and multivariate regression analyses on the endpoint events, we identified several risk factors for MACCEs. These risk factors included high SII levels, a history of myocardial infarction (MI), prior PCI or coronary artery bypass grafting (CABG), elevated brain natriuretic peptide (BNP), and the lack of angiotensin-converting enzyme inhibitors (ACEI) or statin use. Upon adjusting for covariates including age, sex, body mass index (BMI), BNP, smoking, hypertension, PCI or CABG history, MI history, statin use, ACEI use, and the presence of three-vessel coronary disease, only high SII levels remained a risk factor for MACCEs (HR: 0.155, 95% CI: 0.063–0.382; p = 0.001). However, high SII levels were not identified as a risk factor for other individual endpoint events, including non-fatal stroke, cardiovascular death, non-fatal MI, or cardiac rehospitalization. Conclusion: Elevated SII levels following percutaneous intervention are associated with poor outcomes in patients with UA and DM. Therefore, regular monitoring and controlling inflammation levels may help improve long-term outcomes.
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.
Objectives: To create a nomogram using single photon emission computed tomography (SPECT) myocardial perfusion imaging and 18F-FDG positron emissions tomography (PET) gated myocardial metabolism imaging to forecast major adverse cardiovascular events (MACE) in chronic total occlusion (CTO) patients treated with optimal medical therapy (OMT). Methods: A total of 257 patients who received OMT between January 2016 and December 2021 were included in this retrospective study. Patients were randomly divided into development (n=179) and validation (n=78) cohorts. A thorough evaluation was conducted, encompassing clinical features and imaging analysis, which involved assessing myocardial perfusion and metabolism. Independent risk factors were identified using least absolute shrinkage and selection operator (LASSO) and multivariate Cox regression analyses. Calibration curves and decision curve analysis (DCA) were used to evaluate the clinical usefulness. Results: In the development cohort, 53 patients (29.6%) experienced MACE out of 179 patients, while in the validation cohort, MACE occurred in 23 (29.5%) patients out of 78. The PET-left ventricular end-systolic volume (P-ESV) (HR 1.01; 95% CI 1.003-1.017; p=0.003), hibernating myocardium / total perfusion defect (HM/TPD) (HR 1.053; 95% CI 1.038-1.069; p<0.001), PET-left ventricular ejection fraction (P-LVEF) (HR 0.862; 95% CI 0.788-0.943; p=0.001), and left anterior descending branch (LAD) (HR 2.303; 95% CI 1.086-4.884; p=0.03) were significantly associated with MACE and were used to develop the nomogram. The nomogram demonstrated excellent discrimination with C-indexes of 0.931 and 0.911 in the development and validation cohorts. DCA determined that the model exhibited a considerably superior net advantage in predicting MACE. Conclusion: A new nomogram integrating clinical factors and imaging features was created to predict the risk of MACE in patients with CTO.
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.
OBJECTIVE:To investigate the underlying protein molecular mechanisms of"Qi stagnation and blood stasis syndrome"(QS)and"Qi deficiency and blood stasis syndrome"(QD),as two subtypes of coronary artery disease(CAD)in Traditional Chinese Medicine(TCM),following percutaneous coronary intervention(PCI). METHODS:In this study,a total of 227 CAD patients with QS and 211 CAD patients with QD were enrolled;all participants underwent PCI.Label-free quantification proteomics were employed to analyze the changes in serum in two subtypes of CAD patients before and 6 months after PCI,aiming to elucidate the intervention mechanism of PCI in treating CAD characterized by two different TCM syndromes. RESULTS:Biochemical analysis revealed significant changes in tumor necrosis factor-α,high density lipoprotein cholesterol,blood stasis clinical symptoms observation,and Gensini levels in both patient groups post-PCI;Proteomic analysis identified 79 and 95 differentially expressed proteins in the QS and QD patient groups,respectively,compared to their control groups.complement C8 alpha chain,complement factor H,apolipoprotein H,apolipoprotein B,plasminogen,carbonic anhydrase 2,and complement factor I were altered in both comparison groups.Furthermore,enrichment analysis demonstrated that cell adhesion and connectivity-related processes underwent changes in QS patients post-PCI,whereas lipid metabolism-related pathways,including the peroxisome proliferator-activated receptor signaling pathway and extracellular matrix receptor interaction,underwent changes in the QD group.The protein-protein interaction network analysis further enriched 52 node proteins,including apolipoprotein B,lipoprotein(a),complement C5,apolipoprotein A4,complement C8 alpha chain,complement C8 beta chain,complement C8 gamma chain,apolipoprotein H,apolipoprotein A-Ⅱ,albumin,complement C4-B,apolipoprotein C3,among others.The functional network of these proteins is posited to contribute to the pathophysiology of CAD characterized by TCM syndromes. CONCLUSION:The current quantitative proteomic study has preliminarily identified biomarkers of CAD in different TCM subtypes treated with PCI,potentially laying the groundwork for understanding the protein profiles associated with the treatment of various TCM subtypes of CAD.
Background and Objectives: Chronic total occlusion (CTO) is a complex lesion of coronary artery disease (CAD) with a detection rate of approximately 25% on coronary angiography. CTO patients generally experience poor quality of life and prognosis. This study aims to evaluate the association between the estimated glucose disposal rate (eGDR), a surrogate marker for insulin resistance (IR), and the prognosis of CTO PCI patients, as well as to investigate the potential role of the systemic immune-inflammation index (SII) in this process. Methods: We retrospectively included 1482 non-diabetic patients who underwent successful CTO PCI at Anzhen Hospital between January 2018 and December 2021. The primary endpoint was major adverse cardiovascular events (MACEs). Clinical characteristics, biochemical markers, and interventional records were collected, and the eGDR and SII were calculated. Cox regression, restricted cubic splines (RCSs), receiver operating characteristic (ROC) analysis, and Kaplan–Meier curves were used to assess associations. Results: MACEs occurred in 158 patients (10.67%). Patients with MACEs had lower eGDR and higher SII levels. A high eGDR significantly reduced MACE risk (Q4 vs. Q1: HR 0.06, 95% CI 0.03–0.12), while a high SII increased it (Q4 vs. Q1: HR 3.32, 95% CI 1.78–6.33). The combination of low eGDRs and high SIIs predicted the highest MACE risk (HR 4.36, 95% CI 2.71–6.01). The SII partially mediated the relationship between eGDR and MACEs. Conclusions: A low eGDR and high SII are significant predictors of poor prognosis in non-diabetic CTO PCI patients. Combining the eGDR and the SII provides a comprehensive assessment for better predicting cardiovascular outcomes.
The mechanisms through which aging increases heart injury remain partially understood. Protein phosphorylation plays a critical regulatory role in cell survival and death. Using an unbiased phosphoproteomics approach, we aimed to identify the proteins whose phosphorylation could be causatively related to aging-related cardiomyocyte apoptosis and elucidate the underlying mechanisms. Comparative phosphoproteomics was conducted on cardiac tissues obtained from young (8 weeks) and aged (24 months) mice. Our findings revealed that the Mammalian Target of Rapamycin phosphorylation at T1262 (mTORT1262) was reduced in the aging heart. Immunohistochemical and Western blot analyses confirmed these findings in aging myocardia and D-galactose-induced senescent AC16 cardiomyocytes. In hypoxia/reoxygenation cardiomyocytes, mTORT1262 phosphorylation deficiency (mTORT1262A, lentivirus-mediated transfection) inhibited AKT1, suppressed NF-κB, activated FOXO1/3a signaling, and ultimately exacerbated apoptosis. Conversely, mTORT1262 pseudophosphorylation (mTORT1262E) exhibited opposite effects. Through bioinformatics and CO-IP, purinergic receptor P2X4 (P2X4R) was found to be the possible receptor responsible for mTORT1262 phosphorylation. Knockdown of P2X4R increased apoptosis, whereas its overexpression decreased it. In senescent cardiomyocytes, P2X4R expression and mTORT1262 and AKT1S473 phosphorylation were reduced, NF-κB signaling was suppressed, and FOXO1/3a signaling was activated. We demonstrated that P2X4R downregulation and the subsequent reduction of mTORT1262 phosphorylation is a novel mechanism contributing to cardiomyocyte apoptosis in aging hearts. The P2X4R-mTOR-AKT1 signaling pathway represents a potential therapeutic target against accelerated cardiac injury in aging.
Background Calcified lesions are one of the most challenging cases for PCI, where optimal angiographic results and satisfying outcomes are hard to achieve.Methods We evaluated the baseline clinical, procedures characteristics and outcomes of patients with severe coronary artery calcification (CAC) who underwent coronary intravascular lithotripsy (IVL) and rotational atherectomy (RA).Results Respectively 152 and 238 patients who underwent IVL and RA are enrolled from January 2023 to November 2023. Regarding demographic characteristics, the gender proportion, medical history of PCI and smoke history among groups reach statistical significance. Left anterior descending and right coronary artery were the main vessels treated in both groups. The 2.5 and 3.0 mm IVL balloons and 1.5 mm burr were the most commonly used. 99.3% cases were successfully implanted drug-eluting stents after IVL balloon pre-treatment, which was higher than in the group treated with RA. During hospitalization, there were no serious adverse events in the IVL group, but there were two adverse events in the RA group. Procedural complications were higher in the RA group than the IVL group (5.5% vs. 0.7%, P = 0.027).Conclusions IVL appears to be safe and effective for the treatment of severe CAC lesions compared to RA.
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