BACKGROUND:Despite PCI, many acute coronary syndrome (ACS) patients experience major adverse cardiovascular events (MACE). Angiography is limited, and fractional flow reserve (FFR) is restricted by cost and specialized resource requirements. Optical coherence tomography (OCT)-derived FFR (OFR) allows functional assessment without hyperemia, but its prognostic role after PCI is unclear. AIMS:To investigate the association between post-PCI OFR and 1-year target vessel-related MACE in ACS patients and to develop machine learning-based models to explore risk stratification. METHODS:This single-center retrospective study included 719 ACS patients undergoing OCT-guided PCI at the Affiliated Hospital of Zunyi Medical University (May 2022 to December 2023). The primary endpoint was target vessel-related MACE (cardiac death, revascularization, myocardial infarction, or angina rehospitalization). Imaging features were selected by LASSO and Boruta, and machine learning-based classification models were built with XGBoost, random forest, support vector machine, logistic regression, and light gradient boosting. Performance was assessed using ROC curves and feature importance via GINI index.

In-stent neoatherosclerosis (ISNA) is the leading cause of in-stent restenosis (ISR) and stent thrombosis, often signifying stent placement failure. Prior studies have demonstrated an association between uric acid (UA) levels and ISNA, while high-density lipoprotein (HDL) dysfunction may contribute to both target lesion revascularization and ISNA progression. However, no comprehensive study has evaluated the combined role of UA and HDL in ISNA. The UA to HDL ratio (UHR), an integrative metabolic-inflammatory biomarker, has been studied across various cardiovascular and metabolic disorders. This study examines the association between UHR and ISNA and assesses whether UHR predicts ISNA more accurately than UA or HDL alone. We conducted a retrospective cross-sectional study using clinical data from the Affiliated Hospital of Zunyi Medical University (2014–2025). Multivariable logistic regression models were employed to assess the association between the UHR and ISNA, with adjustments for clinically relevant confounders. Potential nonlinear relationships were examined using restricted cubic spline (RCS) regression with three knots. To validate the predictive utility of UHR, we performed subgroup analyses stratified by sex, age and comorbidities, along with ROC curve analysis to determine the optimal cutoff value and area under the curve (AUC). In multivariable regression analysis of 514 participants, each unit increase in UHR was associated with a 14.1

Heart failure (HF) is a progressive disease with complex pathogenesis involving inflammation, immune dysfunction, and metabolic abnormalities. Although C-reactive protein (CRP) is an established HF marker, the CRP-to-lymphocyte ratio (CLR) integrates inflammatory and immune responses. Sleep duration is also critical for cardiovascular health, but the joint impact of CLR and sleep on HF remains unclear. This study examined their association using 14,900 participants (659 with HF) from 2015 to 2023 NHANES data. CLR was calculated as high-sensitivity CRP divided by lymphocyte count, and sleep duration was self-reported. Multivariable logistic regression analyzed the relationships, adjusting for demographic and clinical confounders. Restricted cubic spline models assessed nonlinearity, and subgroup analyses were performed. Higher CLR was strongly associated with increased HF risk (highest quartile OR = 7.49, 95% CI: 5.89–9.52, p < 0.001). Short sleep (< 7 h) also correlated with a higher risk (OR = 1.60, 95% CI: 1.25–2.54, p = 0.017). Nonlinear trends revealed inflection points for CLR (7.83, 11.05) and sleep duration (6.97, 7.07 h), with extreme values linked to greater risk. In conclusion, both elevated CLR and inadequate sleep are independent risk factors for HF, emphasizing their combined role in HF pathogenesis. Further research should investigate underlying mechanisms and assess whether targeting inflammation and sleep can improve HF outcomes.

BACKGROUND:Neoatherosclerosis (NA) and treatment modality may influence outcomes in patients with in-stent restenosis (ISR). This study evaluated the prognostic impact of different NA patterns and percutaneous coronary intervention (PCI) strategies guided by optical coherence tomography (OCT). METHODS:We retrospectively analyzed 288 ISR lesions with OCT-defined NA treated between January 2015 and December 2023. Lesions were classified as lipidic, calcified, or mixed NA. The primary endpoint was 1-year target lesion failure (TLF), defined as a composite of cardiac death, nonfatal myocardial infarction, and clinically driven target lesion revascularization (CD-TLR). Cox regression, interaction analysis, and propensity score matching (PSM) were performed. RESULTS:No significant differences in TLF (p = 0.420) or CD-TLR (p = 0.650) were observed among NA patterns. After adjustment for clinical and procedural covariates, DES reimplantation was associated with a lower risk of TLF (hazard ratio [HR] 0.390, 95% confidence interval [CI] 0.157-0.974; p = 0.044) and CD-TLR (HR: 0.341, 95% CI: 0.114-0.925; p = 0.039) compared with DCB angioplasty. In patients with lipidic NA, a similar trend was observed (TLF: HR: 0.287; 95% CI: 0.097-0.849; p = 0.024; CD-TLR: HR: 0.171; 95% CI: 0.039-0.750; p = 0.019). However, no significant interaction was observed between the NA pattern and treatment modality (p for interaction = 0.543). CONCLUSION:No significant differences in clinical outcomes were observed across NA patterns. Although DES showed numerically favorable outcomes in lipidic NA, no significant interaction between NA pattern and treatment modality was detected. And these findings are hypothesis-generating and may relate to the additional mechanical scaffolding and plaque sealing provided by DES in lipidic NA.

In-stent restenosis (ISR) remains a major complication of percutaneous coronary intervention (PCI), with diabetes mellitus (DM) and prediabetes amplifying risk through endothelial dysfunction and chronic inflammation. Although intravascular imaging techniques, such as optical coherence tomography (OCT), improve ISR management, evidence of their prognostic benefits in patients with DM or prediabetes remains limited. This study aimed to compare clinical outcomes between OCT- and angiography-guided PCI in patients with DM or prediabetes experiencing ISR. This single-center, retrospective study included 314 patients with DM or prediabetes who underwent PCI for ISR. Patients were stratified into 2 groups: OCT-guided ( n = 215) and angiography-guided ( n = 99) groups. Baseline characteristics, procedural parameters, and clinical outcomes were analyzed. The primary endpoint was the occurrence of major adverse cardiovascular events (MACEs), defined as a composite of cardiovascular death, myocardial infarction, and revascularization. OCT-guided PCI significantly reduced the 3-year risk of MACEs (hazard ratio [HR]: 0.45, 95% confidence interval [CI]: 0.22–0.92; P = 0.047) and yielded superior angiographic results, including larger minimal lumen diameter (2.27 vs. 1.99 mm, P < 0.01), lower residual stenosis (15.98% vs. 27.12%, P < 0.01), and enhanced lumen gain (1.85 mm [interquartile range: 1.45–2.12] vs. 1.60 mm [interquartile range: 1.23–1.98]; P = 0.02). Cox regression analysis identified OCT guidance (HR: 0.47, 95% CI: 0.33–0.68), the use of drug-eluting stent (HR: 0.53, 95% CI: 0.31–0.92), and larger pre-PCI reference lumen diameter (HR: 0.66, 95% CI: 0.44–0.99) as independent protective factors against 3-year MACEs. Conversely, prior heart failure (HR: 3.6; 95% CI: 2.14–6.07) was an independent risk factor. Subgroup analyses showed significantly enhanced MACE reduction in nonsmokers, patients without prior heart failure, and drug-eluting stent users (interaction P < 0.05). OCT-guided PCI significantly improves 3-year outcomes in patients with DM or prediabetes experiencing ISR, particularly among nonsmokers, patients without prior heart failure, and recipients of drug-eluting stents.

The relationship between in-stent neoatherosclerosis (ISNA) and chronic kidney disease (CKD) was investigated among patients exhibiting in-stent restenosis (ISR) after drug-eluting stent (DES) implantation. A total of 220 patients with confirmed in-stent restenosis (ISR) via coronary arteriography between 2020 and 2023 were enrolled. Patients were stratified into three groups based on estimated glomerular filtration rate (eGFR) levels: (1) normal renal function (eGFR ≥ 90 mL/min/1.73 m², n = 80), (2) mild renal impairment (60 ≤ eGFR < 90 mL/min/1.73 m², n = 86), and (3) kidney failure (eGFR < 60 mL/min/1.73 m², n = 54). Baseline clinical characteristics, angiographic parameters, and optical coherence tomography (OCT) data were collected and analyzed across all groups. No significant differences in angiographic characteristics were found between the three groups (p > 0.05). Patients with kidney failure demonstrated significantly higher rates of both in-stent neoatherosclerosis (ISNA) (68.5% vs. 46.5% vs. 42.5%; p < 0.05) and thin-cap fibroatheroma (TCFA) within ISR lesions (40.7% vs. 22.1% vs. 22.5%; p < 0.05) compared to those with mild or normal renal function, respectively. Lower eGFR levels were associated with a higher incidence of ISNA and reduced neointima stability.

ABSTRACT Background Coronary artery plaque rupture (PR) is closely associated with immune‐inflammatory responses. The systemic inflammatory index (SII) and the systemic inflammatory response index (SIRI) have shown potential in predicting the occurrence of PR. Objective This study aims to establish a machine learning (ML) model that integrates baseline patient characteristics, SII, and SIRI to predict PR. The goal is to identify high‐risk PR patients before intravascular imaging examinations. Methods We included 337 patients with acute coronary syndrome who underwent emergency percutaneous coronary intervention and coronary optical coherence tomography (OCT) at the Affiliated Hospital of Zunyi Medical University, China, from May 2023 to October 2023. PR was determined by OCT images. Through manual feature selection, nine features, including SII and SIRI, were included, and an ML model was built using the XGBoost algorithm. Model performance was evaluated using receiver operating characteristic curves and calibration curves. SHAP values were used to assess the contribution of each feature to the model. Results The ML model demonstrated a higher area under the curve value (AUC = 0.81) compared to using SII or SIRI alone for prediction. The ML model also showed good calibration. SHAP values revealed that the top three features in the ML model were SII, LDL‐C, and SIRI. Conclusion The immuno‐inflammatory index, which integrates comprehensive clinical characteristics, can predict the occurrence of PR. However, large‐scale, multicenter studies are needed to confirm the generalizability of the predictive model.

BACKGROUND:In-stent neoatherosclerosis (ISNA) is the primary cause of in-stent restenosis (ISR). The neutrophil-to-high-density lipoprotein cholesterol ratio (NHR) has been independently associated with atherosclerosis and coronary artery stenosis. AIMS:To assess whether NHR predicts ISNA and vulnerable plaques in ISR patients using optical coherence tomography (OCT). METHODS:This cross-sectional study enrolled 216 individuals with 220 ISR lesions who percutaneous coronary intervention guided by OCT between July 2018 and November 2022. Participants were stratified into tertiles based on NHR: tertile 1 (NHR <3.464; n = 72), tertile 2 (3.464 ≤NHR ≤5.131; n = 72), and tertile 3 (NHR >5.131; n = 72). The clinical baseline, angiographic, and OCT characteristics were recorded and analyzed. Associations between NHR, ISNA, and thin fibrous caps (TCFA) were analyzed using both univariable and multivariable logistic regression analyses. Receiver operating characteristic curve analysis was conducted to assess the diagnostic capability of NHR for identifying ISNA and TCFA. RESULTS:The highest NHR tertile had higher incidences of ISNA and TCFA than the lowest tertile. NHR positively correlated with ISNA and plaque vulnerability. NHR was independently associated with ISNA and TCFA in multivariable models (ISNA: OR, 1.318; 95% CI, 1.145- 1.516; TCFA: OR, 1.369; 95% CI, 1.183-1.584). The areas under the curve were 0.656 for ISNA and 0.717 for TCFA. Receiver operating characteristic-derived cut-offs were NHR 4.058 for ISNA (sensitivity 69.72%; specificity 59.81%) and 4.109 for TCFA (sensitivity 83.93%; specificity 56.88%). CONCLUSIONS:In patients with DES-ISR, NHR was independently associated with OCT-defined ISNA and TCFA, with modest discrimination; moreover, larger prospective studies are needed to validate these findings.

BACKGROUND:The role of lipid markers in acute coronary syndrome remains incompletely understood, particularly for novel indices such as the Castelli risk indices (CRI-I, CRI-II) and cholesterol index (CHOINDEX). AIMS:This study aims to elucidate the relationship between novel lipid markers and plaque rupture. MATERIAL AND METHODS:In this single-center retrospective study, 649 patients with acute coronary syndrome undergoing optical coherence tomography were stratified into plaque rupture (n = 130) and non-rupture (n = 519) groups. Lipid indices included the following: CRI-I - total cholesterol/high-density lipoprotein cholesterol (HDL-C), CRI-II - low-density lipoprotein cholesterol (LDL-C)/HDL-C, and CHOINDEX - LDL-C/HDL-C. Multivariable logistic regression identified independent predictors of plaque rupture. Model performance was assessed using area under the curve and integrated discrimination improvement. RESULTS:The plaque rupture group had higher proportions of males (89.2% vs. 80%; P = 0.01) and smokers (57.7% vs. 44.9%; P = 0.009), with elevated LDL-C mean 3.14 vs. 2.83 mmol/l), apolipoprotein B (APOB; 1.03 vs. 0.85 g/l), CRI-I (4.75 vs. 3.91), CRI-II (3.11 vs. 2.45), and CHOINDEX (1.97 vs. 1.65; all P <0.01). Multivariable analysis identified CRI-I (odds ratio [OR], 1.57), CRI-II (OR, 2.09), CHOINDEX (OR, 0.40), and APOB (OR, 5.50) as independent predictors. The combined model (traditional factors + novel indices) showed superior discrimination (area under the curve = 0.775 vs. 0.622; integrated discrimination improvement = 0.059; P <0.001). CONCLUSION:The combined assessment of CRI-II, CRI-I, CHOINDEX, and APOB, in conjunction with traditional cardiovascular risk factors, exhibits robust diagnostic efficacy for plaque rupture.

The optical flow ratio (OFR), derived from optical coherence tomography (OCT) images, serves as a physiological index, while the Triglyceride-Glucose Index (TyG) is an alternative measure of insulin resistance. Both indices are positively correlated with poor prognosis in patients with acute coronary syndrome (ACS), but the relationship between the TyG index, OFR, and their prognostic value remains unclear. We included ACS patients who underwent OCT between January 1, 2021, and March 31, 2023. The TyG index was calculated as Ln[fasting triglycerides (mg/dL) × fasting blood glucose (mg/dL)/2]. Patients were grouped into three categories (T1, T2, and T3) based on TyG tertiles. The primary endpoint was major adverse cardiovascular events (MACE). In our analysis, the T3 group showed a significantly higher incidence of MACE (P < 0.05), with a progressive decrease in vessel-level OFR observed as the TyG index increased, demonstrating a linear correlation (r = - 0.0146, P < 0.001). The restricted cubic splines (RCS) model revealed a nonlinear relationship between the TyG index and the likelihood of MACE (P for nonlinear < 0.021). Additionally, the cumulative incidence of MACE was significantly higher in patients with a higher TyG index (all Log-rank P < 0.001).These findings suggest a nonlinear relationship between the TyG index and MACE, and a linear association between the TyG index and vessel-level OFR. The combination of the TyG index and OFR significantly improved discriminatory ability (c-index: 0.720 vs. 0.757; P < 0.001) and reclassification ability (net reclassification index [NRI]: 0.373; integrated discrimination improvement [IDI]: 0.031; P < 0.0001) for predicting MACE compared to vessel-level OFR alone. This combination effectively identifies high-risk ACS patients.

The aim of this study was to investigate the relationship between quantitative flow ratio (QFR) after drug-coated balloon (DCB) treatment for in-stent restenosis (ISR) and between neointimal characteristics assessed by optical coherence tomography (OCT) and clinical outcomes. This single-center, retrospective, observational cohort study included ISR patients who underwent DCB angioplasty under OCT guidance. The primary outcome of the study was a target vessel failure (TVF), defined as a composite endpoint of cardiovascular death, target vessel myocardial infarction and target vessel revascularization. During a median follow-up of 756 days (IQR: 443.25, 1134.50), 204 ISR patients underwent OCT-guided DCB angioplasty, resulting in TVF development in 27 patients. At the post-procedural DCB angioplasty, the vessel-level QFR was significantly lower in the TVF group (0.89 [IQR: 0.87, 0.93] vs. 0.93 [IQR: 0.91, 0.96]; P < 0.001) than in the non-TVF group. Analysis of the qualitative characteristics of ISR lesions showed a significantly higher incidence of heterogeneous neointima in the TVF group compared with the non-TVF group (13 [48.15%] vs. 32 [18.08%]; P < 0.001). In the multivariable Cox regression analysis, low vessel-level QFR (HR per 0.1 increase: 0.11; 95% CI: 0.03–0.41; P < 0.001) and heterogeneous neointima were independently associated with TVF. The TVF rate of vessels with the 2 features was 10.69 times higher than that of all other vessels (95%CI [2.05–55.79]; log-rank P < 0.0001). Vessel-level QFR and heterogeneous neointima were independent factors associated with TVF in ISR patients after DCB angioplasty. Adding the QFR measure-ment to OCT findings may enable better discrimination of patients with subsequent TVF post-DCB angioplasty for ISR.

BACKGROUND:Remnant cholesterol (RC) in triglyceride-rich lipoproteins (TRLs) is strongly associated with atherosclerotic cardiovascular disease (ASCVD). However, its relationship with the physiological features of the culprit vessel in patients following acute coronary syndrome (ACS) remains unclear. OBJECTIVE:To explore the relationships between RC and the culprit vessel physiological features in ACS patients. METHODS:This study retrospectively enrolled 657 patients with ACS who underwent optical coherence tomography (OCT) examination. The patients were divided into 3 groups based on RC tertiles. OCT images were analyzed using OCT automatic recognition software, which identified plaque composition, minimum lumen area (MLA), minimum fibrous cap thickness, maximum lipid angle, and a functional parameter, the optical flow ratio (OFR). RESULTS:Patients with higher RC levels exhibited larger lipid plaque volumes (22.43 vs 26.20 vs 29.53; P = .002) and lower OFR (0.74 vs 0.82 vs 0.84; P < .001) compared to those with lower RC levels. Elevated RC was identified as an independent predictor of OFR ≤0.8 (odds ratio per 1-unit increase: 2.364, 95% CI: 1.491-3.748, P < .001). Incorporating RC into a baseline model enhanced its predictive value for OFR ≤0.8, increasing the area under the curve (AUC) from 0.641 (95% CI: 0.598-0.683) to 0.720 (95% CI: 0.681-0.758; P < .001). CONCLUSIONS:There is a significantly positive relationship between the RC and potentially severe myocardial ischemia and the vulnerable plaques in patients with ACS.

The association between red cell distribution width-to-albumin ratio (RAR) and clinical outcomes in cardiovascular disease (CVD) patients with diabetes mellitus (DM) or pre-DM remains unclear, and its underlying mechanisms are not fully understood. This population-dependent prospective cohort study enrolled 3224 United States (U.S.) participants from the National Health and Nutrition Examination Survey (NHANES) (2001–2018) who had both CVD and either DM or pre-DM. Using the National Death Index data, the cohort’s mortality outcomes were tracked until December 31, 2019. Cox proportional hazard models and restricted cubic spline regressions were employed to investigate the associations between RAR and mortality outcomes. Notably, mediation analyses were performed to quantify the contribution of inflammatory markers, including neutrophils, monocytes, the neutrophil-to-lymphocyte ratio (NLR), and the systemic immune-inflammation index (SII), in the RAR-mortality relationship. During a median 78-month follow-up, 1,223 deaths occurred (483 cardiovascular-related). Elevated RAR was significantly associated with increased all-cause mortality (hazard ratio = 1.43, 95% CI: 1.31–1.56) and cardiovascular mortality (1.44, 1.28–1.62). NLR and SII exhibited significant mediating effects (8.8–10.79% for all-cause; 9.58–11.99% for cardiovascular mortality). Elevated RAR was significantly associated with increased risk of all-cause mortality and cardiovascular mortality among patients with CVD and DM or pre-DM. Systemic inflammation significantly mediated these associations. RAR may serve as a practical prognostic marker in this high-risk population.

Background : Acute coronary syndrome (ACS) remains a leading global cause of mortality. Although optical coherence tomography (OCT) provides detailed assessment of adverse-outcome-associated vulnerable plaque features, and the atherogenic index of plasma (AIP) is a novel lipid-related predictor of atherosclerotic cardiovascular disease, their interrelationship and combined prognostic value in ACS patients remain unclear. Objective: This study aims to examine the association between the atherogenic index of plasma (AIP) and OCT-defined vulnerable plaque features with clinical outcomes in patients with acute coronary syndrome (ACS). Methods: This retrospective single-center study enrolled 1,324 ACS patients undergoing OCT-guided PCI. AIP was calculated as log₁₀(TG/HDL-C). Vulnerable plaques were defined by four OCT features: thin-cap fibroatheroma (TCFA), lipid-to-cap ratio (LCR ≥0.33), macrophage infiltration, and cholesterol crystals. Primary outcome was MACEs (composite of all-cause death, cardiovascular death, unplanned revascularization, in-stent restenosis, angina rehospitalization, and heart failure rehospitalization). Multivariable Cox regression, Kaplan-Meier analysis, ROC curves, and mediation analysis were used. Results: During a median 441-day follow-up, 15.5% (206/1330) of patients experienced MACEs. Fully adjusted analyses revealed that both elevated AIP (≥0.21; HR=1.61, 95%CI:1.18–2.19) and all OCT-defined vulnerable plaque features (LCR≥0.33: HR=1.98; TCFA: HR=1.89; macrophage: HR=1.52; cholesterol crystals: HR=1.47; all P<0.05) independently predicted MACEs. Patients with high AIP plus ≥2 vulnerable plaque features had the highest MACEs risk (P<0.001). Adding AIP to a baseline model (C=0.59) improved prediction (ΔC=0.04; NRI=0.182, P=0.016), with further enhancement after incorporating plaque features (C=0.72; NRI=0.471, P<0.001). Vulnerable plaque features mediated 5.7–15.5% of AIP-associated cardiovascular risk (P<0.05). Conclusion: AIP and OCT-defined vulnerable plaque features serve as independent predictors of MACEs in ACS patients. Their combined assessment significantly enhances risk stratification. Furthermore, plaque features partially mediate AIP-associated cardiovascular risk.

In-stent neoatherosclerosis (ISNA) is a key mechanism underlying drug-eluting stent in-stent restenosis (DES-ISR), with inflammation playing a critical role. This study aimed to assess the association between the systemic immune-response index (SIRI) and ISNA in DES-ISR patients. A retrospective analysis included 212 patients with DES-ISR who underwent coronary angiography and optical coherence tomography (OCT) at least 12 months after stent implantation. SIRI was calculated as (neutrophil count × monocyte count)/lymphocyte count and divided into tertiles. Multivariate logistic regression, smooth curve fitting, threshold effect, and subgroup analyses were performed to evaluate the relationship between SIRI and ISNA risk. Higher SIRI tertiles were associated with ISNA and thin-cap fibroatheroma (all P < 0.05). Multivariate analysis identified SIRI as an independent risk factor for ISNA (OR per unit increase 1.23, 95

BACKGROUND:Hypoxia-induced pulmonary artery hypertension (HPH) is a complication of chronic hypoxic lung disease and the third most common type of pulmonary artery hypertension (PAH). Epigenetic mechanisms play essential roles in the pathogenesis of HPH. N6-methyladenosine (m6A) is an important modified RNA nucleotide involved in a variety of biological processes and an important regulator of epigenetic processes. To date, the precise role of m6A and regulatory molecules in HPH remains unclear. METHODS:HPH model and pulmonary artery smooth muscle cells (PASMCs) were constructed from which m6A changes were observed and screened for AlkB homolog 5 (Alkbh5). Alkbh5 knock-in (KI) and knock-out (KO) mice were constructed to observe the effects on m6A and evaluate right ventricular systolic pressure (RVSP), left ventricular and septal weight [RV/(LV + S)], and pulmonary vascular remodeling in the context of HPH. Additionally, the effects of Alkbh5 knockdown using adenovirus were examined in vitro on m6A, specifically in PASMCs with regard to proliferation, migration and cytochrome P450 1A1 (Cyp1a1) mRNA stability. RESULTS:In both HPH mice lung tissues and hypoxic PASMCs, a decrease in m6A was observed, accompanied by a significant up-regulation of Alkbh5 expression. Loss of Alkbh5 attenuated the proliferation and migration of hypoxic PASMCs in vitro, with an associated increase in m6A modification. Furthermore, Alkbh5 KO mice exhibited reduced RVSP, RV/(LV + S), and attenuated vascular remodeling in HPH mice. Mechanistically, loss of Alkbh5 inhibited Cyp1a1 mRNA decay and increased its expression through an m6A-dependent post-transcriptional mechanism, which hindered the proliferation and migration of hypoxic PASMCs. CONCLUSION:The current study highlights the loss of Alkbh5 impedes the proliferation and migration of PASMCs by inhibiting post-transcriptional Cyp1a1 mRNA decay in an m6A-dependent manner.

Background: Monocyte-to-high-density lipoprotein cholesterol ratio (MHR) is an independent predictor of atherosclerosis and in-stent restenosis (ISR). However, the association between MHR and the incidence of in-stent neoatherosclerosis (ISNA) remains to be validated. Methods: This study included 216 patients with acute coronary syndrome who had 220 ISR lesions and had undergone optical coherence tomography (OCT). All eligible patients were divided into three groups according to their MHR tertile level. OCT characteristics were comparatively analyzed between groups of different MHR levels, and univariate and multivariate logistic regression analyses were constructed to assess correlations be-tween MHR level and ISNA as well as in-stent thin-cap fibroatheroma (TCFA). A receiver operating characteristic curve was used to determine the optimal MHR thresholds for predicting ISNA and in-stent TCFA. Results: The incidence of ISNA (70.3% vs. 61.1% vs. 20.3%, P < 0.001) and in-stent TCFA (40.5% vs. 31.9% vs. 6.8%, P < 0.001) was the highest in the third tertile, followed by the second and first tertiles, respectively. Multivariate analysis revealed that MHR was independently associated with ISNA (odds ratio [OR], 7.212; 95% confidence interval [CI], 1.287-40.416; P = 0.025) and in-stent TCFA (OR, 5.610; 95% CI, 1.743-18.051; P = 0.004) after adjusting for other clinical factors. The area under the curve was 0.745 (95% CI, 0.678-0.811; P < 0.001) for the prediction of ISNA and 0.718 (95% CI, 0.637-0.778; P < 0.001) for the prediction of in-stent TCFA. Conclusion: MHR levels are an independent risk factor for ISNA.

The therapeutic efficacy of bone marrow mesenchymal stem cells (BMSCs) in myocardial infarction (MI) is hindered by poor cell survival. This study explored the role of N6-methyladenosine (m6A) regulation, specifically YTHDC1, in improving BMSC transplantation for MI. By screening m6A-related regulators in hypoxia and serum deprivation (HSD)-induced BMSC apoptosis, YTHDC1 was found to be downregulated. Overexpression of Ythdc1 in BMSCs reduced apoptosis markers, reactive oxygen species (ROS) release, and improved cell survival under HSD conditions. Conversely, Ythdc1 knockdown enhanced apoptosis. In rat MI models, transplantation of Ythdc1-overexpressing BMSCs improved cardiac function and reduced myocardial fibrosis. Mechanistically, YTHDC1 interacts with nuclear factor kappa B (NF-κB) inhibitor-alpha mRNA, suggesting its involvement in BMSC survival pathways. This study identifies YTHDC1 as a potential target to enhance BMSC efficacy in MI therapy.

Neoatherosclerosis is a major cause of stent failure after percutaneous coronary intervention. Metabolism such as hyperuricemia is associated with in-stent restenosis (ISR). However, the association between serum uric acid (sUA) levels and in-stent neoatherosclerosis (ISNA) has never been validated.A total of 216 patients with 220 ISR lesions who had undergone optical coherence tomography (OCT) of culprit stents were included in this study. According to their sUA levels, eligible patients were divided into two groups [normal-sUA group: sUA < 7 mg/dL, n = 126, and high-sUA group: sUA ≥ 7 mg/dL, n = 90]. OCT findings were analyzed and compared between the normal- and high-sUA groups.The incidence of ISNA (63.0% versus 43.0%, P = 0.004) was significantly higher in the high-sUA group than in the normal-sUA group. Lipid plaques (66.3% versus 43.0%, P < 0.001) and thin-cap fibroatheroma (38.0% versus 18.0%, P = 0.001) were observed more frequently in the restenotic tissue structure in patients in the high-sUA group than in those in the normal-sUA group. Meanwhile, univariate (OR: 1.208, 95% CI: 1.037-1.407; P = 0.015) and multivariate (OR: 1.254, 95% CI: 1.048-1.501; P = 0.013) logistic regression analyses indicated that sUA levels were an independent risk factor for ISNA after adjusting for relevant risk factors.The high-sUA levels were an independent risk factor for the occurrence of neoatherosclerosis in patients with ISR via OCT.

BACKGROUND:Percutaneous coronary intervention (PCI) has become the primary treatment for coronary artery disease. However, while PCI effectively addresses severe stenosis or occlusive lesions in target vessels, the progression of non-target vessel plaque remains a critical determinant of long-term patient prognosis. AIMS:The purpose of this study was to investigate the impact of non-target vascular plaque progression on prognosis after PCI for ISR. METHODS:This study included 195 patients diagnosed with ISR and multivessel disease who underwent successful PCI with drug-eluting stent (DES) placement, along with intraoperative optical coherence tomography (OCT) assessment of the culprit stent. Subsequent rechecked coronary angiography categorized eligible patients into non-target lesion progression (N-TLP) and no-N-TLP groups. We evaluated the baseline morphological characteristics of N-TLP by OCT and investigated the relationship between N-TLP, non-culprit vessel-related major adverse cardiovascular events (NCV-MACE), and pan-vascular disease-related clinical events (PVD-CE) incidence. RESULTS:Multivariate logistic regression analysis revealed that diabetes mellitus (OR 3.616, 95% CI: 1.735-7.537; P = 0.001), uric acid level (OR 1.005, 95% CI: 1.001-1.009; P = 0.006), in-stent neoatherosclerosis (ISNA) (OR 1.334, 95% CI: 1.114-1.985; P = 0.047) and heterogeneous neointima morphology (OR 2.48, 95% CI: 1.18-5.43; P = 0.019) were independent predictors for N-TLP. Furthermore, N-TLP was associated with a high incidence of NCV-MACE (19.4% vs 6.9%, P = 0.009) and PVD-CE (83.9% [95% CI: 79.7%-88.3%] vs 93.1% [95% CI: 88.4%-98.0%], P = 0.038) after PCI in ISR patients. CONCLUSION:Diabetes, uric acid levels, ISNA, and heterogeneous neointima are predictive factors for subsequent rapid plaque progression, with N-TLP exacerbating the incidence of NCV-MACE and PVD-CE after PCI.