Background:Myocardial ischemia/reperfusion (I/R) injury (MIRI) is a major contributor to cardiovascular morbidity, characterized by inflammatory responses and cardiomyocyte death. Ginsenoside Rb2 (Rb2), a bioactive compound from Panax ginseng, has shown potential cardioprotective effects, but its mechanisms in I/R injury remain unclear. Macrophage polarization refers to the process by which macrophages dynamically shift between pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes in response to microenvironmental signals. This study aimed to investigate whether Rb2 could participate in the progression of MIRI by regulating macrophage polarization. Methods:In vitro, THP-1-derived macrophages were co-cultured with AC16 cardiomyocytes under hypoxia/reoxygenation (H/R) conditions and treated with Rb2 (0, 25, 50, or 100 µM) for 24 h. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay. Macrophage polarization (CD86/CD206) was evaluated by immunofluorescence (IF), and apoptosis by terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) staining. Gene expression of inflammatory markers [interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, arginase-1 (Arg-1), IL-10, transforming growth factor-β (TGF-β)] was analyzed by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Inhibitor of kappa B kinase (IKKα) lactylation was assessed by immunoprecipitation (IP) and Western blot. In vivo, a murine MIRI model was established in male C57BL/6 mice by transient occlusion of the left anterior descending (LAD) coronary artery for 30 min, followed by 24 h of reperfusion. Rb2 was administered intraperitoneally at 10 mg/kg daily for 14 consecutive days prior to I/R induction. Cardiac function was assessed by echocardiography, infarct size by triphenyltetrazolium chloride (TTC) staining, and macrophage markers (CD86, CD206) by immunohistochemistry (IHC). Serum cardiac troponin T (cTnT) levels were measured by enzyme-linked immunosorbent assay (ELISA), and inflammatory gene expression in cardiac tissues was analyzed by RT-qPCR. IKKα lactylation in cardiac tissues was evaluated by IP and Western blot. Molecular docking, surface plasmon resonance (SPR), and bioinformatics were used to validate Rb2-IKKα interactions. Results:Rb2 treatment enhanced cell viability (104.2±3.1 vs. 88.7±2.8, P<0.001), promoted M2 polarization (P<0.001), reduced apoptosis (29.6±2.1 vs. 10.1±1.8, P<0.001), and improved cardiac function post-I/R [cTNT, 532±53 vs. 125±22, P<0.001; left ventricular ejection fraction (LVEF), 41±6 vs. 61±4, P<0.001; left ventricular fractional shortening (LVFS), 20±3 vs. 31±2, P<0.01; Infarct size, 63±4 vs. 20±4, P<0.001]. Mechanistically, Rb2 directly bound to IKKα, inhibited its lactylation at K617 site, and destabilized the protein. Overexpression of IKKα reversed Rb2's protective effects. Conclusions:Rb2 attenuated MIRI by modulating macrophage polarization via IKKα lactylation inhibition, offering a potential therapeutic strategy for MIRI treatment.
Background: The coronary slow flow (CSF) phenomenon following primary percutaneous coronary intervention (PPCI) for acute ST-segment elevation myocardial infarction (STEMI) represents a severe complication associated with adverse clinical outcomes. The endothelial glycocalyx (EG) serves as a pivotal barrier maintaining microvascular integrity; however, the kinetics of its degradation and its specific association with CSF remain incompletely understood. Therefore, this study aims to investigate the correlation between serum markers of EG shedding and the incidence of CSF in patients with STEMI. Methods: In this prospective observational study, we consecutively enrolled 82 patients with STEMI who underwent emergent percutaneous coronary intervention (PCI) between August and November 2025. CSF was defined as a post-procedural corrected thrombolysis in myocardial infarction (TIMI) frame count (CTFC) >27 frames. Post-procedural TIMI flow grade was recorded concurrently, and no-reflow was defined as TIMI flow grade <3. Serum syndecan-1 (SDC-1) and hyaluronic acid (HA) were measured pre-procedure, immediately after PCI, and 24 hours after PCI. Multivariable logistic regression was used to evaluate the association between pre-procedural biomarkers and CSF, with continuous variables standardized as z-scores. As sensitivity analyses, we performed linear regression using CTFC as a continuous outcome and Firth's penalized logistic regression for no-reflow. Discriminative performance was assessed using receiver operating characteristic (ROC) curves. Results: Compared with the normal flow group, the CSF group had higher pre-procedural levels of SDC-1 and HA. Longitudinal analyses showed a more pronounced immediate post-PCI increase in HA in the CSF group, which remained elevated at 24 hours. Both SDC-1 and HA also remained higher at 24 hours in the CSF group. After adjustment for age, symptom-to-treatment time, total stent length, and admission diastolic blood pressure, higher pre-procedural SDC-1 [odds ratio (OR) =5.03; 95% confidence interval (CI): 2.39-10.60; P<0.001] and HA (OR =3.56; 95% CI: 1.92-6.60; P<0.001) were independently associated with CSF. These associations were directionally consistent in sensitivity analyses using CTFC as a continuous outcome and no-reflow as an endpoint. ROC analysis showed that pre-procedural SDC-1 had higher discriminative ability [area under the curve (AUC) =0.88] than HA (AUC =0.84). Conclusions: Severe degradation of the EG, characterized by elevated serum levels of SDC-1 and HA, is independently associated with the post-procedural CSF phenomenon in patients with STEMI. Pre-procedural SDC-1 appeared to have a stronger association with CSF and numerically higher discriminative performance than HA. These findings suggest that therapeutic strategies aimed at preserving the glycocalyx may offer novel avenues for ameliorating coronary microvascular dysfunction. The study was registered in the Chinese Clinical Trial Registry (Identifier: ChiCTR2500107421).
Comparing angiographic findings of patients presenting with acute coronary syndrome (ACS) in the Middle East/Gulf (MEG) and North America (NA) may shed light onto how coronary artery disease (CAD) complexity at time of ACS presentation impacts immediate management and clinical outcomes. Therefore, we compared outcomes in concurrent ACS patients between MEG and NA. Consecutive patients with ACS were identified at 2 locations in an international health system. Extent of epicardial coronary disease was determined using Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) score by trained investigators at both locations and compared using appropriate testing. In addition, in-hospital outcomes, including death, stroke and major bleeding were compared between the two groups. Between January and December 2017, 158 patients in MEG and 381 in NA were admitted with ACS. Patients in MEG were younger (57.3±11.5 vs. 65.0±12.1 years; P<0.001) than those in NA, more likely to have diabetes (51.9% vs. 28.9%; P<0.001). MEG patients had more complex CAD (SYNTAX score: 23.5±12.3 vs. 13.2±8.6; P<0.001) and were more likely to receive surgical or hybrid revascularization [odds ratio (OR) 2.1, 95% confidence interval (CI): 1.4-3.1] but less likely to receive percutaneous coronary interventions (OR 0.3, 95% CI: 0.2-0.5). These findings suggest that patients in the MEG present at the time of their first clinical event with more severe CAD, potentially driven by a higher prevalence and poorer control of diabetes. Further studies are needed to explore genetic, environmental, and metabolic factors contributing to rapid CAD progression in MEG populations.
Background:ST-segment elevation myocardial infarction (STEMI) is usually associated with impaired systolic function, but heart failure with preserved ejection fraction (HFpEF) may also occur and remains under-recognized in this setting. We aimed to investigate the prevalence, clinical predictors, and outcomes of HFpEF in STEMI patients with preserved left ventricular ejection fraction (LVEF). Methods:We retrospectively analyzed 421 STEMI patients who underwent successful percutaneous coronary intervention (PCI). Among them, 280 patients with LVEF ≥50% on 1-month follow-up echocardiography were included. Patients were classified as HFpEF or non-HFpEF according to the Heart Failure Association Pre-test assessment, Echocardiography and natriuretic peptide, Functional testing, Final etiology (HFA-PEFF) score, with scores ≥5 defining HFpEF. The primary endpoint was a composite of cardiovascular (CV) death or hospitalization for heart failure (HF). Results:Eighty-eight patients (31.4%) were classified as HFpEF. Compared with the non-HFpEF group, these patients were older (mean age 70 years), more frequently female (46.6% vs. 16.1%), and less likely to be current smokers (31.8% vs. 51.0%). During a median follow-up of 3 years, 2 patients (0.7%) died from CV causes and 29 (10.4%) were hospitalized for HF. The incidence of HF hospitalization was significantly higher in the HFpEF group (17.0% vs. 7.3%). In multivariable Cox regression, HFpEF was independently associated with the composite outcome [hazard ratio (HR) 2.45; 95% confidence interval (CI): 1.10-5.44]. Conclusions:In STEMI patients with preserved LVEF, a substantial proportion developed HFpEF, which was associated with increased risks of HF hospitalization and mortality. The HFA-PEFF score provides incremental prognostic value in this population and may help identify high-risk patients for closer monitoring and tailored management.
Background:A patent foramen ovale (PFO) is a common congenital cardiac condition characterized by a persistent communication between the right and left atria, which can facilitate a right-to-left shunt (RLS). This study aimed to determine the diagnostic accuracy, reproducibility, and prognostic value of PFO shunt volume quantified by three-dimensional transesophageal echocardiography (3D-TEE) combined with right-heart contrast echocardiography. Methods:In this prospective study, 100 patients with suspected PFO were prospectively enrolled and allocated in a 7:3 ratio to a training cohort (n=70) and a validation cohort (n=30). Each participant underwent two-dimensional transthoracic echocardiography (2D-TTE), two-dimensional transesophageal echocardiography (2D-TEE), and 3D-TEE. The total shunt volume (V_total) was calculated using voxel-based grey-scale integration. The optimal cut-off value was determined in the training set with the Youden index and then applied to the validation set. A multi-modality "hard reference" standard served as the diagnostic gold standard for method comparison. Reproducibility was evaluated with intraclass correlation coefficients (ICCs). All patients were followed for 36 months; stroke or transient ischemic attack (TIA) risk was analyzed with Kaplan-Meier curves and Firth-penalized Cox models, and changes in migraine frequency and residual shunt volume were recorded. Results:Eight baseline 3D structural indices, including tunnel length, slit width, leaflet excursion and shunt volume, showed no significant difference between cohorts (P>0.05). V_total, V_peak and t_dur demonstrated excellent repeatability (ICC =0.91-0.94; coefficient of variation 6.96-8.27%). The optimal threshold of 22.93 µL yielded an area under the curve (AUC) of 0.92 in the training set and 0.89 in the validation set (DeLong, P=0.27), with a sensitivity of 92%, specificity of 89%, and a diagnostic odds ratio (DOR) of 89.78, outperforming 2D-TTE and 2D-TEE. Kaplan-Meier analysis showed a 3-year stroke/TIA-free survival of 79% for shunt volume ≥22.93 µL versus 96% below the threshold (12 events, log-rank P=0.01); V_total ≥23 µL remained an independent predictor [hazard ratio (HR) =5.27, P=0.04]. Migraine frequency fell significantly over follow-up (P=0.001), and residual shunt volume at six months was lower after closure than with medical therapy (P<0.001). Conclusions:3D-TEE with right-heart contrast precisely quantifies PFO shunt volume; a threshold of 22.93 µL is reproducible and predicts both diagnostic status and long-term outcomes, supporting its use in stroke risk stratification, closure decision-making and therapeutic monitoring.
Background:Although a number of studies involving small-vessel de novo coronary disease have indicated that drug-coated balloons (DCBs) angioplasty, provides clinical benefits, the clinical value of DCB in large-vessel lesions remains unclear. We therefore conducted a real-world study to evaluate the midterm clinical outcomes of DCB treatment in patients with de novo coronary lesions >3.0 mm. Methods:We performed a retrospective study of 1,514 consecutive patients who received paclitaxel DCB angioplasty to treat de novo coronary lesions at Beijing Anzhen Hospital between June 2019 and November 2021. Lesions with a reference vessel diameter (RVD) ≥3.0 mm were defined as large-vessel disease (LVD), and lesions with an RVD ≤2.75 mm were defined as small-vessel disease (SVD). The LVD and SVD groups included 462 and 1,052 patients, respectively. The end points of the study were all-cause death, myocardial infarction (MI), stroke, and target vessel revascularization (TVR). Outcomes were compared between the LVD and SVD groups. The median follow-up was 34.2 months [interquartile range (IQR), 31.3 to 39.7 months] in the overall cohort. Results:Of the 1,514 patients, 43 (2.8%) died, 21 (1.4%) experienced MI, and 21 (1.4%) experienced stroke; 167 (11.0%) underwent TVR. No significant differences were observed in mortality rate (LVD: 2.4%; SVD: 3.0%; P=0.32), MI (LVD: 1.1%; SVD: 1.5%; P=0.37), stroke (LVD: 0.9%; SVD: 1.6%, P=0.19) and TVR (LVD: 11.9%; SVD: 10.6%, P=0.92). After multivariate adjustment, the adjusted hazard ratios (HRs) [95% confidence interval (CI)] for LVD versus SVD were 1.092 (0.447-2.670; P=0.85) for death, 1.424 (0.464-4.369; P=0.54) for MI, 1.604 (0.529-4.864; P=0.40) for stroke, and 0.995 (0.719-1.378; P=0.98) for TVR, with no significant differences observed in any endpoints between the two groups. Conclusions:The findings from this study indicate that the prognosis of DCB for patients with de novo lesions in vessels exceeding 3.0 mm are not significantly different compared to those of DCB for patients with SVD.
Background: Pulmonary hypertension (PH) is a comorbidity closely associated with high-grade mitral valve regurgitation (MR), for which transcatheter edge-to-edge mitral valve repair (M-TEER) is a valuable treatment method. To date, conflicting evidence exists regarding the impact of PH on treatment outcomes due to divergent PH definitions between studies and the updated guideline definitions. This study aimed to investigate the prevalence of PH and its respective subtypes and their impact on long-term survival after M-TEER. Methods: In this monocentric cohort study, all patients who underwent M-TEER and provided right heart catheterization (RHC) data were analyzed. PH and its respective subtypes were defined according to the current guidelines. Differences in long-term survival were analyzed using the Kaplan-Meier method, and independent predictors of mortality were analyzed using uni-and multivariable Cox regression analyses. Results: A total of 183 patients underwent M-TEER, but 58 patients had to be excluded from further analysis due to insufficient hemodynamic recordings. Among the included patients, 77.6% (97/125) revealed concomitant PH. Combined post-and precapillary PH (Cpc-PH) was the most common subtype in 56.7% (55/97) of patients. This subtype was associated with significantly greater morbidity compared with isolated postcapillary PH (Ipc-PH), which was the second most common subtype, observed in 39.2% (38/97) of the patients. Longterm survival significantly deteriorated in PH patients, while Ipc-PH patients presented a nonsignificant trend towards better survival compared to those with Cpc-PH. Although there was a significant correlation between noninvasive and invasive measurements of pulmonary artery systolic pressure (PASP) among Cpc-PH patients, PASP was significantly underestimated by noninvasive measurements in both PH cohorts. Conclusions: The early differentiation of patients undergoing M-TEER with respect to PH and its complicating comorbidities could represent a potential approach to improve long-term outcomes. Invasive RHC measurements remain crucial for classifying PH subgroups and their underlying PASP.
Background:Pulmonary hypertension (PH) is a heterogeneous condition with diverse aetiologies and clinical presentations, driven by remodelling of the pulmonary vasculature and right ventricular (RV) myocardium, progressing to right heart failure (RHF) with poor prognosis. Cardiovascular remodelling is characterized by re-expression of extra-domain A containing fibronectin (ED-A+ Fn), which our prior studies identified as a key pathogenetic mediator in monocrotaline-induced PH. This study investigated the role of ED-A+ Fn in the progression of hypoxia-associated PH and subsequent RHF, corresponding to clinical group 3 PH, associated with lung diseases and/or hypoxia. We employed the mouse model of Sugen5416/hypoxia (SuHx) induced PH, that reproduces essential features of both group 1 (pulmonary arterial hypertension) and 3 PH, comparing ED-A+ Fn knockout (KO) mice with wild-type (WT) controls (strain: Black 6, C57BL/6). Methods:PH was induced in male mice (n=26) employing the Sugen5416/hypoxia model. Animals were allocated to four experimental groups: normoxic WT controls (WTNx, n=8), WT mice with SuHx-induced PH (WTSuHx, n=8), normoxic ED-A+ Fn KO controls (KONx, n=5) and ED-A+ Fn KO mice with SuHx-induced PH (KOSuHx, n=5). Echocardiographic assessment of RV morphological structure and function was conducted, including measurements of basal RV diameter (RVbasal), right atrial (RA) area (RAarea), tricuspid annular plane systolic excursion (TAPSE) and fractional area change (FAC). Right heart catheterization (RHC) was performed to measure RV systolic pressure (RVPsys), followed by histological and immunohistochemical analyses of tissue samples. Results:RHC demonstrated a significant increase in RVPsys in WTSuHx mice (85.2±11.4 mmHg) as opposed to WTNx (45.2±4.6 mmHg, P=0.006), KONx (38.9±4 mmHg, P=0.02) and KOSuHx (49.8±9.5 mmHg, P=0.02). Echocardiographic assessment revealed significant impairment in WTSuHx mice, including a markedly increased RVbasal (2.57±0.15 mm, P=0.01) relative to KOSuHx mice (2.14±0.19 mm). Histological analysis showed pronounced pulmonary tissue damage induced by PH in WTSuHx (5.63±0.7, P=0.006) and KOSuHx (2.7±0.98, P=0.03) compared to their respective normoxic controls, with significantly greater impairment observed in WTSuHx versus KOSuHx (P=0.01). The degree of RV myocardial injury was markedly greater in WTSuHx (0.88±0.41) versus WTNx (0.06±0.17, P=0.006), while KO groups displayed no significant differences. Pulmonary vasculopathy and immune cell infiltration, assessed by immunohistochemical analysis, were significantly exacerbated in WTSuHx relative to all other experimental groups. Conclusions:Beyond its established pathogenetic role in monocrotaline-induced PH, our study additionally identifies ED-A+ Fn as a critical mediator in the preclinical SuHx model of PH. These findings underscore the involvement of ED-A+ Fn in both clinical group 1 and group 3 of PH, as well as in subsequent development of RHF. Given the limited availability of effective therapies, ED-A+ Fn represents a promising biomarker and therapeutic target, with potential of mitigating deleterious PH-mediated tissue remodelling, for instance, through administration of specific neutralizing antibodies.
Background and Objective:Immune checkpoint inhibitors (ICIs) are widely used in cancer treatment and have shown substantial clinical benefit. Although the incidence of ICI-associated cardiac injury is uncommon, such events may lead to severe complications and high mortality. Current tools for evaluating cardiac injury include serum biomarkers, electrocardiogram (ECG), echocardiography, cardiac magnetic resonance imaging, coronary angiography, and endomyocardial biopsy. Among these, ECG is widely used because of its convenience and practicality and serves as an important screening tool. This review summarizes ECG manifestations associated with ICI-associated cardiac injury to further clarify the clinical role of ECG in this setting. Methods:A literature search was conducted in PubMed for English-language literature published from February 23, 2010 to February 13, 2026 using predefined keywords related to immune checkpoint inhibitors, ECG, and cardiac injury. Key Content and Findings:ECG, as a diagnostic and monitoring tool for cardiotoxicity, has both advantages and limitations. Common ECG manifestations include arrhythmias such as premature atrial contractions, premature ventricular contractions, atrial fibrillation or atrial flutter, ventricular tachycardia (or ventricular fibrillation), and atrioventricular block, as well as QRS complex prolongation, low QRS voltage, and ST-segment and T-wave (ST-T) abnormalities. Among these findings, conduction disturbances, tachyarrhythmias (particularly ventricular tachycardia), and ST-T segment abnormalities are associated with higher mortality. However, ECG alone has limited diagnostic specificity, and its value is improved when combined with other diagnostic modalities. Conclusions:ECG is an important noninvasive tool for monitoring ICI-associated cardiac injury and plays a crucial role in screening and diagnosis. However, important knowledge gaps remain, including the lack of specific ECG markers for early diagnosis, limited evidence on ECG features that distinguish ICI-associated myocarditis from other causes of cardiac injury, insufficient understanding of the temporal evolution of ECG abnormalities, and the absence of validated ECG-based risk stratification or early warning models. Future research should focus on the development of early prediction models and further elucidation of injury mechanisms to improve cardiac safety during ICI therapy.
Background:Obesity is a common comorbidity among patients undergoing transcatheter aortic valve replacement (TAVR) and may influence valve hemodynamics. The impact of body mass index (BMI) and valve size on post-TAVR echo-derived gradients is not fully understood; however, it is clinically important for optimizing outcomes, particularly in high-BMI populations, where procedural success may be affected. This study aims to determine the relationship between BMI and post-procedural gradients. Methods:This retrospective cohort study was conducted at a single large academic medical center to study patients who underwent balloon-expandable TAVR between 2021 and 2023. Patients had pre-procedural computed tomography (CT) and echocardiographic data and completed a 30-day follow-up echocardiogram. Patients were stratified based on BMI (<30 vs. ≥30 kg/m2) and valve size (20/23 vs. 26/29 mm). Mean 30-day echocardiogram gradients, measured with Doppler echocardiography, were compared across groups. A total of 180 patients were identified and stratified into 4 groups: high-BMI small valve (n=26); high-BMI large valve (n=33); low-BMI small valve (n=47); and low-BMI large valve (n=74). Both univariate analysis and multivariate analysis compared different groups and the impacts of individual variables on mean 30-day echocardiogram gradients. Results:The groups were similar in demographics and clinical characteristics, except for age, which was significantly lower in the high BMI group (P<0.001). Low-BMI patients with large valves had significantly lower gradients than high-BMI patients with small valves (P=0.002). Among high-BMI patients, small valves were associated with significantly higher gradients than large valves (P=0.009). In low-BMI patients, gradients were similar regardless of valve size (P=0.16). In small valve patients, there was a trend for higher gradients in high versus low BMI (P=0.056). Conclusions:Both BMI and valve size impact 30-day echo-derived gradients after balloon-expandable TAVR. High BMI and small valves are associated with higher gradients. With larger valves, the impact of BMI on valve gradient is attenuated. Additionally, for low-BMI patients, valve size has less impact on gradients. This study suggests that BMI is a crucial factor impacting gradients, and suggests that future research into the role of weight loss in TAVR treatment should be conducted.
Background:Cardiovascular complications are the primary cause of mortality in patients with Duchenne muscular dystrophy (DMD). However, the dynamic progression underlying myocardial damage in DMD has not yet been fully elucidated. This study aimed to quantitatively assess myocardial dysfunction in patients with DMD across different age groups via cardiac magnetic resonance (CMR) tissue tracking technology. Methods:Between August 2018 and January 2020, 110 patients with DMD diagnosed at the Pediatric Neurology Outpatient Department of West China Second University Hospital were consecutively and prospectively included in the study. The patients were categorized into three age groups: 3-6, 7-10, and 11-14 years. Based on left ventricular ejection fraction (LVEF), the patients were further divided into a normal LVEF group (LVEF ≥55%) and a decreased LVEF group (LVEF <55%). Furthermore, based on the presence of delayed enhancement, patients were classified into late gadolinium enhancement (LGE)-positive and LGE-negative groups. Additionally, 69 healthy controls were recruited for comparison. Left ventricular functional parameters and CMR tissue tracking-related parameters, such as global and regional myocardial strain of the left ventricle, were assessed. These included radial, circumferential, and longitudinal peak strains at the base, middle, and apex of the left ventricle. Statistical analyses were conducted via the t-test. Results:A total of 99 patients and 61 healthy controls were included in the study. In comparison to the control group (n=21), patients aged 3-6 years in the DMD group (n=15) did not exhibit any decline. Patients aged 7-10 years in the DMD group (n=63), as compared with the control group (n=18), had lower LVEF (59.58%±7.09% vs. 63.39%±5.27%, P=0.044) and left ventricular global radial (37.34%±9.78% vs. 42.95%±9.22%, P=0.03), circumferential (-20.75%±3.77% vs. -22.09%±2.46%, P=0.03), and longitudinal (-13.91%±2.81% vs. -15.69%±2.52%, P=0.04) strain. Patients aged 11-14 years in the DMD group (n=21), as compared with the control group (n=22), demonstrated an even greater reduction in strain in the left ventricle for all parameters, except for LVEF. For patients in the normal LVEF group (n=77) or LGE-negative group (n=51), despite there being no significant difference in cardiac function compared with the control group, the global and regional myocardial strain of left ventricle was decreased. Conclusions:Myocardial dysfunction predominantly manifests in DMD among children older than 7 years, exhibiting a subtle progression that exacerbates with advancing age. The myocardial injury tends to develop from the basal epicardium toward the apical and endocardial regions.
Background:Artificial intelligence (AI) shows promise for improving electrocardiogram (ECG)-based acute myocardial infarction (AMI) detection, but clinical readiness remains uncertain. We aimed to conduct a systematic synthesis informed by a structured search of AI-enhanced ECG systems to evaluate their performance, validation quality, and implementation readiness. Methods:We conducted a structured search of PubMed and Embase (publication date limits: January 1, 2017, to August 31, 2025; last searched: February 18, 2026) for English-language human studies that developed or validated AI models for ECG-based AMI diagnosis, extracting data on architectures, clinical applications, validation approaches, and performance metrics; we excluded non-original publications and studies that were non-English or non-human studies or did not use ECG input or did not address AMI diagnosis. Results:We included 88 studies; the total number of participants was not estimable because sample sizes were inconsistently reported across studies. Among 88 identified studies, convolutional neural networks predominated (51/88, 58%). Most studies were retrospective (80/88, 91%) and used 12-lead ECG (64/88, 73%). Reported performance varied widely [area under the receiver operating characteristic curve (AUROC), 0.700-0.999; sensitivity, 67.7-100.0%; specificity, 73.3-100.0%], with promising results for detecting subtle ischemic patterns in non-ST-elevation and occlusion myocardial infarction (OMI). However, only 33/88 (37.5%) performed external validation. Public datasets were used in 50/88 (57%) and institutional patient cohorts in 43/88 (49%); several studies used both sources. More complex architectures did not consistently demonstrate superior accuracy, though heterogeneity in study designs limits definitive conclusions. Conclusions:AI demonstrates substantial technical potential for AMI detection, particularly for subtle ischemic patterns. However, critical gaps impede clinical deployment: insufficient external validation, reliance on curated datasets with limited generalizability, absence of standardized evaluation frameworks, and insufficient evidence on patient-centered outcomes. Future research must prioritize prospective multicenter validation, standardized benchmarks with rigorous reference standards, and real-world implementation studies examining clinical outcomes and workflow integration. Technical feasibility is established; clinical impact now depends on validation rigor and pragmatic deployment.
Background and Objective:Artificial intelligence (AI), extended reality (XR), and computational modelling are increasingly integrated with cross-sectional cardiovascular imaging, particularly computed tomography (CT) and cardiovascular magnetic resonance (CMR), to address the diagnostic and therapeutic complexity of congenital heart disease (CHD). Given the lifelong and heterogeneous nature of CHD, these technologies have the potential to enhance anatomical assessment, haemodynamic understanding, procedural planning, and personalised care. This narrative review aims to provide a structured overview of current developments, clinical applications, and translational challenges related to AI, XR, and computational modelling in CT- and CMR-based CHD imaging. Methods:A targeted literature search was performed in PubMed to identify representative and clinically relevant publications from January 2014 to October 2025, including early online articles. Search terms included combinations of "artificial intelligence", "deep learning", "extended reality", "virtual reality", "computational modelling", "computational fluid dynamics", "3D printing", "congenital heart disease", "cardiovascular magnetic resonance", and "computed tomography". English-language original articles, reviews, and consensus statements were considered. Given the narrative design, studies were selected based on relevance and methodological contribution rather than formal systematic screening. Key Content and Findings:AI applications now span the full imaging-to-decision continuum, including image reconstruction, automated segmentation, quantitative assessment, phenotype recognition, and decision support. XR technologies enhance spatial understanding and pre-procedural planning, while computational modelling and three-dimensional (3D) printing enable patient-specific haemodynamic simulation and procedural rehearsal. Public datasets and integrated AI-XR-modelling pipelines are emerging. However, most evidence derives from feasibility and single-centre studies, and lesion-specific external validation remains limited. Conclusions:AI, XR, and computational modelling hold significant promise for advancing cross-sectional imaging in CHD. Future progress will depend on multicentre collaboration, lesion-stratified validation, workflow integration, and governance frameworks tailored to lifelong congenital care. Demonstration of clinical outcome benefit will be essential for widespread adoption.
Background:A reproducible and reliable automated tool to measure right ventricle-to-left ventricle diameter ratio (RV/LV) in acute pulmonary embolism (PE) examinations on computed tomography pulmonary angiography (CTPA) can suggest right ventricle (RV) enlargement, however the relationship to outcomes has not been investigated. The purpose of this study was to assess the relationship between an automated RV/LV ratio determined by an artificial intelligence (AI) algorithm, on a set of examinations deemed positive for acute PE by an AI algorithm on CTPA studies in the emergency department (ED) and various clinical parameters in predicting mortality and outcomes. Methods:This retrospective study included ED patients who underwent CTPA from April 2022 to October 2023. A commercial AI algorithm was applied to CTPA images with acute PE. Associations of automated RV/LV >1 in acute PE examinations with variables including interventional treatment, 30- and 90-day mortality, intensive care unit (ICU) admission and stay length were studied. Results were analyzed with a logistic regression model and reported as odds ratios (ORs). Results:In a cohort of 408 examinations from 408 patients, 142 examinations (35%) had an RV/LV ≤1 and 266 (65%) had an RV/LV >1. Patients with RV/LV >1 were more likely to be admitted into ICU ±12 hours of CTPA (25% vs. 15%, P=0.02) and more likely to undergo interventional radiology (IR) procedures (6.8% vs. 0.7%, P=0.006) compared to those RV/LV ≤1. The same group had higher odds of ICU admission both before and after adjusting for simplified pulmonary embolism severity index (sPESI) [unadjusted OR: 1.90 (1.12, 3.33), P=0.02; adjusted OR: 2.00 (1.14, 3.64), P=0.02]. Conclusions:Automated detected RV/LV >1 in acute PE examinations on CTPA in the ED has an association with ICU admission.
Background: Atherosclerosis (AS) progression is closely associated with phenotypic transformation of vascular smooth muscle cells (VSMCs) and activation of the Janus kinase 1/signal transducer and activator of transcription 3 (JAK1/STAT3) signaling pathway. This study aimed to elucidate the active components and underlying mechanisms of the Tiaozhi Tongmai Formula (TZTMF) in ameliorating AS through both in vivo and in vitro experiments. Methods: The chemical constituents and serum pharmacochemistry of TZTMF were characterized using ultra-performance liquid chromatography-electrospray ionization-tandem mass spectrometry. An AS model was established in apolipoprotein E-deficient mice fed with a high-fat diet. The therapeutic effects of TZTMF were evaluated using hematoxylin and eosin, Movat pentachrome, and immunohistochemical staining, as well as western blot analysis. In hypoxia-stimulated mouse VSMCs, enzyme-linked immunosorbent assay, Transwell migration, wound-healing, immunofluorescence, western blot, and reverse transcription-quantitative polymerase chain reaction assays were conducted to assess cell viability and cellular responses to TZTMF. Results: A total of seventy-eight compounds were identified in TZTMF, of which thirty-nine were detected in serum. In vivo, TZTMF reduced AS progression, promoted plaque stabilization, and attenuated inflammation, abnormal proliferation, and phenotypic transformation of smooth muscle cells (SMCs) through downregulation of the JAK1/STAT3 signaling pathway. In vitro, TZTMF-containing serum suppressed hypoxia-induced SMC proliferation and migration, prevented the transition from the contractile to the synthetic phenotype, and decreased JAK1 and STAT3 expression at both the messenger RNA (mRNA) and protein levels. Furthermore, the regulatory effects of TZTMF on mouse aortic vascular smooth muscle (MOVAS) cells were largely mediated through the JAK1 pathway. Conclusions: TZTMF exerts anti-atherosclerotic effects in both in vivo and in vitro models. It contributes to plaque stabilization by enhancing collagen deposition, reducing inflammation, and suppressing SMC proliferation and phenotypic transformation, primarily through inhibition of the JAK1/STAT3 signaling pathway.
Background and Objective:Conventional interpretation of vascular imaging is often limited by qualitative assessments and inter-observer variability. Artificial intelligence (AI)-driven radiomics addresses these limitations by extracting high-dimensional quantitative features, providing superior characterization of complex vascular lesions, such as atherosclerotic plaques and calcifications. This review aims to summarize current AI applications in vascular imaging, focusing specifically on diagnosis, risk prediction, and the emerging field of radiogenomics. Methods:A comprehensive literature search of the PubMed database was conducted to retrieve relevant English-language articles published between 2015 and 2025. The search strategy strictly prioritized large-scale multicenter studies and pivotal clinical trials concerning AI in vascular imaging. Key Content and Findings:Integrating machine learning (ML) with multimodal imaging [ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI)] significantly enhances automated vascular identification, diagnostic consistency, and precise outcome prediction. Additionally, radiogenomics links imaging phenotypes with genetic profiles, providing deeper insights into the molecular mechanisms of vascular diseases. The review also critically addresses key challenges hindering the clinical translation of these AI technologies, particularly data heterogeneity, the lack of standardized protocols, and limited model interpretability. Conclusions:AI radiomics holds significant transformative potential for advancing personalized vascular medicine. Future efforts must prioritize methodological standardization and robust multicenter validation to facilitate the reliable clinical adoption of AI tools and inform healthcare policy making.
Background and Objective:Patients with pulmonary hypertension (PH) exhibit left heart alterations, in morphology, function, and tissue characteristics, which may critically correlate with the pathophysiological mechanisms and prognosis of PH. However, a comprehensive review that summarizes the role of left heart parameters derived from cardiac magnetic resonance (CMR) in PH remains lacking. This review summarizes CMR-derived left heart morphological, functional, and tissue characterization parameters for PH diagnosis, classification, severity assessment, and prognosis, aiming to enhance evidence-based PH management. Methods:A literature search was performed on the PubMed and China National Knowledge Infrastructure (CNKI) databases for articles published between January 2000 and December 2024. Key search terms incorporated "pulmonary hypertension", "cardiac magnetic resonance", "left ventricle", "left atrium", "diagnosis", and "prognosis". Studies were deemed eligible if they investigated the association between CMR-derived left heart parameters and the diagnosis or prognosis of patients with PH. Key Content and Findings:This review synthesizes the evidence on key CMR-derived left heart parameters in PH. Left atrial volume index and left ventricular eccentricity index aid in the diagnosis and mortality prediction of PH. Left atrial active strain and left ventricular global strain serve as sensitive markers for identifying left ventricular dysfunction and predicting prognosis in PH patients, respectively. Ventricular interdependence parameters, such as ventricular mass index and septal angle, have been confirmed to correlate with hemodynamic parameters in PH. Furthermore, a key tissue characterization parameter-the right ventricular/left ventricular blood pool T2 ratio (RVT2/LVT2)-demonstrates significant value in assessing disease severity in chronic thromboembolic PH (CTEPH) and may serve as a novel non-invasive imaging marker for predicting prognosis in these patients. Conclusions:CMR-derived left heart parameters provide valuable insights for the diagnosis, classification, severity assessment, and prognosis of PH.
Background and Objective: Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide despite substantial advancements in prevention, diagnostics, and therapeutics. The integration of artificial intelligence (AI) and machine learning (ML) is transforming cardiovascular medicine, with applications spanning electrocardiogram (ECG) interpretation, advanced imaging analysis, and risk prediction modelling. Authoritative guidelines, observational studies, systematic reviews, and meta-analyses have highlighted the diagnostic and prognostic potential in various domains, including AI-derived physiological age from ECG, automated plaque quantification in coronary computed tomography angiography (CTCA), and time to event survival prediction models. This review aims to synthesise contemporary evidence on AI in cardiovascular diagnostics, prevention, and rehabilitation, and to outline the methodological, ethical, and translational considerations for safe clinical adoption. Methods: A narrative review was conducted. The literature search was performed on PubMed/MEDLINE, Scopus, Embase, and Web of Science using relevant keywords, and articles published between January 2015, and August 2025 were included. Peer-reviewed studies, systematic reviews and meta-analyses, and position statements pertinent to AI in cardiovascular medicine were selected. Key Content and Findings: AI has achieved high accuracy in imaging interpretation, ECG-based arrhythmia detection, multimodal risk stratification, wearable-based screening, and adaptive cardiac rehabilitation. Survival models, such as Random Survival Forests and DeepSurv, have outperformed traditional Cox models in select datasets. Additionally, AI-derived physiological age from ECG shows associations with incident cardiovascular events and mortality. However, external validation is inconsistent, calibration is often inadequate, and reporting standards are variable. Equity, data privacy, interpretability, and workflow integration remain substantial barriers. Conclusions: AI can augment but not replace clinician judgment in cardiovascular care. Translation into routine practice requires rigorous multi-centre prospective trials, transparent reporting checklists, fairness assessments, and governance frameworks to ensure safety, generalizability, and equity. AI will likely play a significantly increasing role in enhancing patients' cardiovascular care.
