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.

Cardiovascular disease is currently a major global challenge, and its causes are complex, encompassing genetic, lifestyle, environmental, and other factors. Ubiquitination, an important post-translational protein modification, is closely associated with cardiovascular disease and is involved in the regulation of protein degradation, signaling, and gene expression. An increasing number of studies have shown that ubiquitination plays a key regulatory role in the development and progression of cardiovascular disease. Recent research has elucidated the crucial role of ubiquitination modifications in governing various cellular processes, signaling pathways, and protein homeostasis within cardiovascular contexts. Specifically, these modifications have been implicated in cardiomyocyte injury and hypertrophy, macrophage inflammation, phenotypic changes in smooth muscle cells, and activation of fibroblasts. This review summarizes the role of ubiquitination modifications in recent years, focusing on the recognition of different substrate proteins by E3 ubiquitin ligases. These ligases are involved in the regulation of various cardiovascular disorders, such as atherosclerosis, myocardial ischemia/reperfusion injury, cardiac remodeling, cardiac arrhythmia, and hypertension. The findings provide new insights into the prevention and treatment of cardiovascular disease.

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.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a risk factor for cardiovascular events. However, MASLD’s relationship with optical coherence tomography (OCT)-defined coronary plaque vulnerability in patients with acute coronary syndrome (ACS) remains unclear. Moreover, the mediating role of plaque vulnerability in the association between MASLD and major adverse cardiovascular and cerebrovascular events (MACCE) has rarely been investigated. Therefore, this study used OCT to examine the association between MASLD and coronary plaque vulnerability in ACS patients, to assess the impact of MASLD on MACCE, and to explore whether plaque vulnerability mediates this relationship. A total of 820 patients with ACS were enrolled in this study. All patients underwent OCT-guided percutaneous coronary intervention (PCI) and completed abdominal ultrasound (US) or non-contrast computed tomography (CT) examinations. Patients meeting the diagnostic criteria for MASLD were categorized into the MASLD group, while those who did not were assigned to the non-MASLD group. The MASLD group had a significantly higher prevalence of multivessel disease, more complex coronary artery disease on OCT, and higher detection rates of lipid-rich plaques, cholesterol crystals, and thin-cap fibroatheroma (TCFA). Multivariate analysis confirmed that MASLD was independently associated with these vulnerable plaque features and served as an independent risk factor for major adverse cardiovascular and cerebrovascular events (MACCE) (adjusted hazard ratio [aHR] = 2.05, 95

Oxidised 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (oxPAPC), dendritic cells (DCs), and long non-coding RNAs (lncRNAs) play crucial roles in atherosclerosis (AS). This study aimed to determine whether oxPAPC-induced DC-derived lncRNAs contribute to AS and to elucidate the underlying regulatory mechanisms. DCs were treated with increasing oxPAPC concentrations to assess transcriptomic changes. RNA sequencing was used to identify differential expression of lncRNAs. ChIP-Seq and RNA pull-down assays were used to assess direct binding between lncRNA CYP1B1-AS1 and NFATC2. The association between CYP1B1-AS1 and CYP1B1 was assessed using Pearson's correlation analysis. Elevated serum oxPAPC levels were confirmed in patients with coronary heart disease. In vitro, sustained oxPAPC stimulation activated the TLR4-MD2 pathway in DCs. CYP1B1-AS1 was identified as the key oxPAPC-induced DC-derived lncRNA, with Gm33055 as its murine homologue. RNA sequencing revealed oxPAPC-driven alterations in DC chemotaxis, differentiation, and lymphocyte activation. Analysis of human atherosclerotic plaque-derived DCs showed significant CYP1B1-AS1 upregulation. Gm33055 enhanced Cyp1b1 expression in murine DCs. Mechanistically, oxPAPC promoted NFATC2 nuclear translocation. NFATC2 binds to the CYP1B1-AS1 promoter, whereas CYP1B1-AS1 directly interacts with NFATC2, forming a positive regulatory loop. Adoptive transfer of m-CYP1B1-AS1-expressing DCs into Apoe-/- mice accelerated AS progression. These findings identify a DC-derived lncRNA-mediated regulatory axis that promotes AS and suggest potential therapeutic targets.

Serum Angiopoietin-2 (Ang2) is a novel indicator of vascular inflammation that has demonstrated predictive potential in multiple studies. However, the association between Ang2 and the presence of layered plaques (LP) in patients with acute coronary syndrome (ACS) has not been well-established. The aim of the present study was to investigate the observational association of serum levels of Ang2 with LP by optical coherence tomography (OCT). This study was a retrospective observational study. A total of 101 consecutive ACS patients who transferred from the emergency department to the cardiology department were included, mainly patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI). Preoperative OCT images were collected from all patients. According to the presence or absence of LP in the target lesion, the patients were divided into the LP group (n = 38) and the non-layered plaque (NLP) group (n = 63). The concentration of Ang2 was measured by enzyme-linked immunosorbent assay (ELISA). The binary logistic regression model was used to assess the relationship between Ang2 and LP, and the receiver operating characteristic (ROC) curve was used to evaluate the ability of Ang2 to discriminate LP in ACS lesions. Information about Ang2 was obtained through online databases and literature review. There was a significant difference in Ang2 concentration between the LP group and the NLP group (18.97 ng/mL, 95

BACKGROUND:The constant resistance ratio (cRR) is a novel nonhyperemic pressure ratio based on piezoresistive pressure microcatheter (PMC) measurements. With repeated measurements in randomized order of PMC and pressure wire techniques, this study aimed primarily to validate the diagnostic performance of cRR compared with fractional flow reserve (FFR) in coronary lesions of 30% to 90% diameter stenosis. METHODS:SUPREME II (Sensor-Equipped Ultrathin Pressure Microcatheter Versus Pressure Wire for Physiological Measurements) was a multicenter, prospective study that included 466 patients (483 vessels) from 11 centers. All target vessels were assessed using both pressure wire and PMC separately in randomized order under resting and hyperemic conditions. The primary end point was the diagnostic accuracy of the cRR using a PMC-based FFR of ≤0.80 as the reference standard. Secondary end points included the cRR "gray zone" of the cRR-FFR hybrid strategy and the proportion of patients in whom diagnosed was achieved without vasodilator use. RESULTS:The optimal cRR cutoff was 0.89, which correctly classified 82.8% of the patients, with a sensitivity and specificity of 87.0% and 80.1%, respectively, and achieved an area under the curve of 0.92 with FFRPMC as reference (area under the curve 0.90 with FFRpressure wire as reference). If FFR was added for decision-making in cases of cRR values between 0.85 and 0.91, a cRR--FFR hybrid strategy achieved a 95.3% agreement with the FFR-only strategy and allowed 68.5% of the patients to not require using vasodilator. CONCLUSIONS:In coronary stenosis of 30% to 90% diameter stenosis, cRR measurements were highly feasible. The diagnostic accuracy of cRR with FFRPMC as reference was excellent. Further, a cRR-FFR hybrid strategy may reduce vasodilator use without compromising diagnostic accuracy. REGISTRATION:URL: https://clinicaltrials.gov/study/NCT05417763; Unique Identifier: NCT05417763.

Following the global increase in atherosclerotic cardiovascular diseases, the demand for the effective identification of high-risk factors that lead to atherosclerotic plaque rupture and the search for new therapeutic targets has also increased. Neovascularization within plaques is widely recognized as an important indicator of plaque vulnerability. Thus, the timely detection of neovascularization within plaques and early intervention treatment can help reduce the potential adverse cardiovascular events caused by plaque rupture. This article introduces the formation mechanism, clinical significance, detection techniques, and prevention strategies for neovascularizing atherosclerotic plaques.

ABSTRACT Intravascular lithotripsy (IVL) is a promising therapy for calcified coronary lesions. This study evaluated the safety and effectiveness of a novel IVL system. The COronary CAlcified Lesion Lithotripsy Procedure (COCALP) study (No. ChiCTR2300073280) was a prospective, multicenter, single‐arm trial involving 266 patients with severely calcified coronary lesions. The primary endpoint was procedural success, defined as successful stent implantation with ≤30% residual stenosis and no in‐hospital major adverse cardiovascular events (MACE). In a subgroup, calcium morphology was evaluated by optical coherence tomography (OCT) assessment. A total of 266 patients were included. The procedural success rate was 97.4% (95% confidence interval [CI]: 0.947–0.989), with the lower limit of the CI exceeding the prespecified performance goal (p < 0.001). No MACE occurred intraoperatively. During hospitalization, MACE occurred in five patients (1.9%), all of which were myocardial infarctions. MACE rates at 1 and 6 months were 2.3 and 3.4%, respectively. In the OCT subgroup (n = 76), IVL induced a 76.8% rate of calcification fracture. The minimal lumen area increased from 1.77 ± 0.72 to 2.59 ± 1.11 mm2 following IVL (p < 0.001), and further expanded to 5.22 ± 1.69 mm2 poststenting (p < 0.001). The novel IVL system demonstrated high effectiveness and safety, supporting its use for treating severely calcified coronary lesions and enhancing stent implantation success.

A rare but deadly side effect of coronary procedures is coronary artery rupture. The 63-year-old male patient with coronary atherosclerotic heart disease who presented with typical symptoms is the subject of this case report. Acute myocardial infarction was not detected by echocardiography, myocardial damage indicators, or electrocardiograms. Two vessels had lesions found by CAG inspection, necessitating surgery. During the surgery, a coronary artery rupture occurred, and the IVUS test showed that the affected arteries had negative vessel remodeling. In clinical practice, coronary artery rupture is quite uncommon and mostly only occurs in case reports. Early detection and prompt treatment are crucial because there is a dearth of information on how to manage this disorder.

Ferroptosis is a regulated form of cell death that is dependent on reactive oxygen species (ROS) and iron metabolism. Ferroptosis can participate in the formation and rupture of atherosclerotic plaque by regulating apoptosis. However, the mechanism of vascular endothelial cells (VECs) ferroptosis in the occurrence and development of atherosclerosis (AS) requires further exploration. Previous studies have shown that peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) can improve mitochondrial dysfunction and apoptosis induced by oxidized low-density lipoprotein (oxLDL), but its specific role in VECs ferroptosis remains unclear. In this study, we found that oxLDL can induce VECs ferroptosis, and mitochondria are key to oxLDL-induced VECs ferroptosis. As a key regulator of mitochondrial function, the protein expression of PGC-1α was lower in oxLDL-treated VECs. Moreover, overexpression of PGC-1α inhibited oxLDL-induced VECs ferroptosis, whereas the role of PGC-1α was affected by its upstream regulatory molecule AMPK in this process. This study explores the new idea of oxLDL-induced VECs ferroptosis mediated by AMPK/PGC-1α to better understand the pathogenesis of vascular lesions caused by high lipid levels and provides a theoretical basis for the early prevention of AS.

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.

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.

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: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.

Introduction：Few studies have evaluated different patterns of in-stent restenosis by optical coherence tomography (OCT). This study aims to identify in vivo predictors for focal restenosis in patients with in-stent restenosis (ISR). Methods: The study recruited patients with ISR who underwent OCT examination in the Cardiology Department of the Affiliated Hospital of Zunyi Medical University from October 2018 to December 2022. Based on the angiographic classification of ISR lesions, the patients were divided into two groups: the focal group (n=58) and the non-focal group (n=158). Results： The white blood cell count was higher in the non-focal group than those in focal type (7.8±3.0 vs. 6.6±2.1, P = 0.007). The prevalence of lipid rich plaque was higher in patients with focal ISR (65.5% vs. 42.4%, P = 0.003). The occurrence of red thrombus (27.8% vs. 12.1%, P = 0.016) and white thrombus (41.1% vs. 24.1%, P = 0.021) was higher in the non-focal group. Multivariate analysis showed that low density lipoprotein cholesterol C (odds ratio [OR]:3.341, 95% confidence interval [CI]: 1.714-9.784, P = 0.046) was independently associated with focal restenosis. While white blood cell count (OR: 0.814, 95% CI: 0.657-0.913, P = 0.047) and stent malapposition (OR: 0.228, 95% CI: 0.057-0.896, P = 0.037) were independently associated with non-focal restenosis. Conclusion：There were significant differences in clinical baselines and OCT identified morphological characteristics in patients between focal and non-focal group. Low density lipoprotein cholesterol C was independent associated with focal restenosis. White blood cell count and stent malapposition were correlated with non-focal restenosis.

Myocardial infarction with nonobstructive coronary artery (MINOCA) is a heterogeneous disease with different pathophysiological mechanisms and prognosis. In recent years, it has been found that the incidence of major cardiovascular adverse events in MINOCA is similar to that of myocardial infarction with coronary artery disease (MI-CAD), and it is difficult to clarify the pathogenesis of both through coronary angiography (CAG). Therefore, the aim of this study is to investigate the clinical features, plaque characteristics and prognosis of patients with MINOCA and MI-CAD through optical coherence tomography (OCT). A total of 553 culprit lesions from AMI patients who underwent CAG and OCT were retrospectively analysed. Patients were subsequently divided into two groups: the MINOCA group and the MI-CAD group. The clinical characteristics, plaque characteristics and prognosis of the two groups were compared. The primary endpoint was defined as a composite of major adverse cardiac events (MACE), including cardiac death, non-fatal myocardial infarction, target lesion revascularization, stroke, and rehospitalisation for angina or heart failure. (1) Patients with MINOCA exhibited a lower incidence of ST-segment elevated myocardial infarction (STEMI) and a less frequent history of combined drug-eluting stent (DES) compared to those with MI-CAD. Additionally, they demonstrated lower levels of low density lipoprotein cholesterol (LDL-C), total cholesterol (TC), triglycerides (TG), peak troponin T (peak TnT) and peak creatine kinase (peak CK). The MINOCA group had more lesions in the left anterior descending (LAD) and fewer in the left circumflex (LCX). Additionally, they demonstrated a lower prevalence of multibranch vasculopathy and a diminished post-discharge use of aspirin, P2Y12 receptor inhibitors, beta-blockers, angiotensin converting enzyme inhibitor/angiotensin receptor blockers (ACEI/ARBs), and a higher proportion of conservative treatment compared to DES. The frequency of plaque rupture, calcified plaque, cholesterol crystals, macrophages infiltration, microvessels, thin-cap fibroatheroma (TCFA), and thrombus were found to be lower in the MINOCA group than in the MI-CAD group, with these differences being statistically significant (P < 0.05); (2) No significant difference was observed in the incidence of MACE at 30-days and 1 year between patients in the MINOCA and MI-CAD groups (P > 0.05). Compared with MI-CAD patients, MINOCA patients had fewer high-risk plaques on OCT and were more likely to be treated conservatively, with lower rates of stenting and less post-discharge pharmacological treatment. Both groups had similar rates of MACE at 30-day and 1 year, highlighting the importance of individualising treatment for MINOCA patients. Patients with MINOCA who develop MACE are more likely to exhibit high-risk OCT plaque features, with macrophage infiltration identified as an independent risk factor. OCT plaque features such as plaque rupture, plaque erosion, cholesterol crystals, macrophages, microvessels, TCFA may have played different roles in the progression of the two groups of patients.