Doxorubicin (DOX)-induced cardiomyopathy remains therapeutically challenging due to the absence of pathway-specific interventions. Ferroptosis of cardiac microvascular endothelial cells (CMECs) is a major driver of disease progression, yet precise therapeutic strategies remain limited. Here, mechanistic analyses identified lncRNA TUG1 as an upstream promoter of CMEC ferroptosis through the miR-153-5p/MMP2-TIMP2/TFR-1 axis. Guided by this mechanism, a translational construct was developed by cloaking mesoporous silica nanoparticles carrying TUG1-targeting siRNA with neutrophil membranes (NM@si-TUG1/MSN). The neutrophil membrane coating enabled robust cardiac tropism and preferential CMEC uptake. In a murine model of DOX-induced cardiomyopathy, NM@si-TUG1/MSN accumulated in the heart, achieved effective TUG1 knockdown, and markedly reduced ferroptosis. Relative to free siRNA and uncoated nanoparticles, the nanocomplex produced superior outcomes, including restoration of microvascular integrity, reduced fibrosis, and significant improvement in cardiac function. This study characterizes a regulatory axis in DOX-induced cardiomyopathy and demonstrates a targeted biomimetic nanotherapy that interrupts microvascular ferroptosis and limits disease progression. The data support the feasibility of this approach for clinical translation.

BackgroundCardiovascular disease is the leading cause of death worldwide, and its risk is closely linked to metabolic abnormalities. Through summary-data-based mendelian randomization and colocalization analysis, we investigate the causal relationships between plasma proteins, six cardiovascular diseases (atrial fibrillation, coronary artery disease, heart failure, venous thromboembolism, peripheral artery disease and stroke), and 19 metabolic traits (including anthropometric phenotypes, blood pressure, glycemic phenotypes, inflammatory phenotypes, kidney-related phenotypes, lipidemic phenotypes, and liver-related phenotypes).ResultsWe identify 49 proteins genetically associated with cardiovascular diseases, validated across two proteomic platforms. Among them, 35 are also associated with one or more metabolic phenotypes, with six showing evidence of colocalization. These six candidate proteins are classified into three categories based on drug development status, with PCSK9 already successful in therapies for cardiovascular diseases and hypercholesterolemia. DUSP13B, LRIG1, APOH, INHBC, and GUSB also demonstrate high therapeutic potential. Further phenome-wide MR analysis indicates that INHBC, APOH and DUSP13B represent promising therapeutic targets for cardiovascular diseases characterized by metabolic disorders.ConclusionsOverall, this study revealed causal plasma proteins underlying the onset of cardiovascular diseases and metabolic abnormalities, advancing the understanding of disease mechanisms and facilitating drug discovery.

Background: Evidence on mortality benefits of general health checks comes mainly from higher-resource settings. We examined variation by resource setting, baseline risk, modifiable risk-factor change, and allocation strategy. Methods: We analysed six longitudinal cohorts from 17 countries and a real-world and population-based cohort in northwestern China. Health-check receipt was time varying and the outcome was all-cause mortality. Cohort-specific Cox models were fitted; the northwestern China analysis also included instrumental-variable models, mediation analysis, absolute-benefit estimation, and six-year allocation simulations. Findings: The multinational cohorts included 149,620 participants and 2,803,872 person-years; the the Northwest China Real-world and Population-based Cohort (NCRP) included 14,505,733 participants and 89,829,304 person-years. Health checks were not associated with mortality in the US or European cohorts, but were associated with lower mortality in cohorts from Mexico, Indonesia, and China (hazard ratios 0.726–0.898). In northwestern China, annual health checks were associated with lower subsequent-year mortality (hazard ratio 0.828 [95% CI 0.822–0.835]), with directionally consistent instrumental-variable estimates. Absolute benefit increased with risk burden, and modifiable risk-factor improvement mediated 16.3% (95% CI 15.59–16.96) of the association. With 10 million annual examinations, risk-targeted allocation was estimated to avert 10,284 deaths per year versus 7,717 with population-wide allocation. Interpretation: Associations varied by resource context and baseline risk. Risk-targeted implementation might improve efficiency in lower-resource settings, although the observational and modelled findings should not be interpreted as causal effects.

Transcatheter aortic valve replacement (TAVR), also known as transcatheter aortic valve implantation (TAVI), is an interventional technology in which an artificial aortic valve is compressed and assembled outside the body, then delivered through a catheter and implanted at the site of the diseased aortic valve, thereby functionally replacing the native valve. Two versions of the Chinese expert consensus on TAVR were issued in China in 2015 and 2020, respectively. To promptly update the field's understanding of TAVR and to promote its broader, more standardized, and higher-quality application in China, an expert panel has developed this new version of the consensus. This consensus includes substantial updates compared with the previous version, covering topics such as the epidemiology of aortic valve disease, recent advances in TAVR research, indications, procedural standards, post-procedural antithrombotic therapy, prevention and management of complications, management of special cases, and future development trends. This consensus integrates international research evidence and references international guidelines to ensure rigor and evidence-based recommendations, while also incorporating domestic research findings and clinical practice in China, thereby enhancing both its forward-looking perspective and practical applicability.

BACKGROUND:Residual left ventricular (LV) hypertrophy and incomplete reverse remodelling after transcatheter aortic valve replacement (TAVR) are associated with adverse outcomes. Whether renin-angiotensin system inhibitors (RASi) promote reverse remodelling in patients with heart failure and LV ejection fraction (LVEF) ≥40% following TAVR remains uncertain. METHODS:In this multicentre, prospective, randomised, open-label, blinded-endpoint trial, patients aged ≥60 years with symptomatic severe aortic stenosis, LVEF ≥40% and successful TAVR were randomly assigned (1:1) to standard care alone or standard care plus RASi (ACE inhibitor, angiotensin II receptor blocker or angiotensin receptor-neprilysin inhibitor). The primary endpoint was change in LV mass index (LVMI) at 12 months. Secondary endpoints included changes in LV volumes, LVEF, N-terminal pro-B-type natriuretic peptide (NT-proBNP) and functional status. RESULTS:A total of 200 patients were randomised; 194 were included in the modified intention-to-treat analysis (RASi n=95; control n=99). At 12 months, RASi therapy was associated with a greater reduction in LVMI compared with control (adjusted mean difference -12.77 g/m², 95% CI -24.73 to -0.81; p=0.036). Consistent improvements were observed in LV end-diastolic and end-systolic volumes. Functional status (New York Heart Association class) improved modestly in the RASi group. No significant differences were observed in LVEF or NT-proBNP. CONCLUSION:In patients with heart failure and LVEF ≥40% following TAVR, RAS inhibition led to enhanced reverse LV remodelling over 12 months, reflected by greater regression of LV mass and volumes. These findings support the potential role for RASi in modifying post-TAVR myocardial remodelling, although larger trials are required to determine whether these structural benefits translate into improved clinical outcomes. TRIAL REGISTRATION NUMBER:ChiCTR2100042266.

Acute aortic dissection (AAD) is a life-threatening emergency without established effective monitoring biomarkers. This study aimed to explore biomarkers to optimize the diagnosis of AAD. AAD related genes were screened by spatial transcriptomics experiments, and their encoded proteins were validated in aortic tissues. We measured plasma levels of candidate proteins in 302 participants (173 AAD cases, 129 controls), finding higher PTMA, ADAMTS8, and CD36 in AAD. Case-control analysis revealed that elevated levels of those proteins along with D-dimer, increased systolic blood pressure (SBP), height and smoking history were risk factors for AAD. A multi-marker score comprising D-dimer, ADAMTS8, height, SBP, and age was developed for AAD diagnosis, achieving an AUC of 0.921 (95%CI 0.889-0.952), with 77.5% sensitivity and 96.5% specificity. We further validated the diagnostic performance of the multi-marker score in an independent validation set including healthy controls and patients with chest pain. Our findings indicate that PTMA, ADAMTS8, and CD36 are potential biomarkers associated with AAD. The multi-marker score effectively discriminates AAD from both healthy controls and non-AAD acute chest pain conditions, and may serve as a rapid, cost-effective auxiliary diagnostic tool.

There is ongoing discussion in the medical community on the effect of metformin in cardiac arrhythmias. Investigating the causal relationship between metformin and arrhythmias was the target of the research. We utilized the Mendelian randomization (MR)-based platform to collect genome-wide association data linking arrhythmias and metformin. We utilized SNPs connected to metformin as instrumental variables (IVs) to evaluate the causative link between metformin and arrhythmia through two-sample MR analysis. Four statistical techniques were employed: MR-Egger regression, weighted median estimator, weighted mode method, and inverse-variance weighted (IVW) method. The impact of individual SNPs on the outcomes of IVW analyses was investigated using the leave-one-out method, and the study's possible bias was examined using a funnel plot to guarantee the results' robustness. We identified 40 independent single nucleotide polymorphisms (SNPs) of genome-wide significance from GWAS data for metformin as IVs. The IVW method supported a causal relationship between metformin and reduced incidence of arrhythmia (OR = 0.0093; 95% CI = 0.002-0.055; P = 2.72E-07). MR-Egger regression indicated that there is no need to consider the effect of gene pleiotropy on the results of the study (intercept = 0.0014; P = .874). Although the MR-Egger method didn't pinpoint a causal link, it did reveal a similar directionality in the β values (OR = 0.0056; 95% CI = 9.384E-06 to 3.369; P = .1207). Fortunately, the weighted median and weighted mode techniques demonstrated a causal link between metformin and a decreased arrhythmia risk (OR = 0.004; 95% CI = 0.0003-0.052, P = .000023; OR = 0.0025; 95% CI = 7.418E-05 to 0.085, P = .001915). Neither Cochran Q test nor the funnel plot showed signs of directional pleiotropy, heterogeneity, or asymmetry. The sensitivity of the method was analyzed by leave-one-out method, and the results suggested that the method was stable. With the MR method, we've substantiated a potential cause-and-effect link between metformin usage and cardiac arrhythmia.

Background Heart failure (HF) frequently complicates chronic nonrheumatic aortic regurgitation (CNRAR), yet the prognostic impact of fasting plasma glucose (FPG) and its inflammatory mechanisms remain unclear. We assessed whether FPG predicts HF in CNRAR and quantified inflammation-mediated effects. Methods We analyzed 13,200 CNRAR patients from Northwest China. The endpoint was new-onset HF. Post-discharge FPG was measured before an endpoint. Multivariable Cox models, competing-risk analysis, restricted cubic splines (RCSs), sensitivity analyses, inverse probability of treatment weighting (IPTW) and mediation analysis were performed. In addition, 13,200 CNRAR patients were 1:1 propensity matched to 2,774,530 general population participants to estimate relative hazard ratios (RHRs). External validation included 418 CNRAR or mixed aortic stenosis-regurgitation cases from the UK Biobank. Results During 535-day median follow-up, higher FPG demonstrated a dose-risk association. Compared with normoglycemia, FPG 6.1–7.0 and 7.0–16.7 mmol/L were associated with 17.1% (HR 1.171, 95% CI 1.026–1.337) and 26.2% (HR 1.262, 95% CI 1.102–1.446) higher HF risk; each 1.0 mmol/L increase conferred a 4.0% higher risk. White blood cells (WBC) accounted for 13.26% of the mediated effect on heart failure. Compared with the general population, CNRAR showed greater vulnerability at 6.1–7.0 mmol/L (RHR 1.270, 95% CI 1.037–1.555), while RHR at ≥ 7.0 mmol/L was non-significant (RHR 1.076, 95% CI 0.901–1.284). In UK Biobank, FPG ≥ 6.1 mmol/L was associated with higher HF risk (HR 1.713, 95% CI 1.044–2.808). Conclusions Elevated FPG independently predicts HF in CNRAR, partially through inflammation, supporting intensified glycemic and inflammatory risk management.

While air pollution is a recognized cardiovascular risk, its specific impact on aortic stenosis (AS) remains poorly characterized. This study investigates the association between air pollution and incident AS, integrating gene-environment interactions and network toxicology. Based on the UK Biobank as the primary cohort, long-term air pollution exposure (per standard deviation increase) is associated with an increased risk of AS, with HRs and 95% CIs of 1.60 (1.55,1.66) for PM2.5, 1.37 (1.32, 1.41) for PM10, 1.37 (1.32, 1.42) for NO2, and 1.36 (1.31, 1.41) for NOx. The observed associations demonstrate high consistency across a suite of advanced internal methodological validations and are further replicated in the Tianshan Community Cohort. There are joint and interactive effects of genetic susceptibility and air pollutants on AS risk. Network toxicology and bioinformatics analyses reveal key PM-AS target genes enriched in the lipid and atherosclerosis, fluid shear stress and atherosclerosis, and IL-17 signaling pathway. In conclusion, long-term exposure to PM2.5, PM10, NO2, and NOx is significantly associated with an increased AS risk, with a potential interaction between environmental exposure and genetic susceptibility.

OBJECTIVE:This study was aimed at analyzing the correlation of serum γKlotho with the long-term prognosis of multivessel coronary artery disease (MVD) and develop a predictive model to predict an accurate long-term prognosis. METHODS:We enrolled 969 MVD patients and classified them into three groups: training (n = 552), internal validation (n = 224), and external validation (n = 193) groups, respectively. The training group data helped in establishing a prognostic model. Univariable Cox regression analyses were conducted using serum and clinical γKlotho levels. Thereafter, the least absolute shrinkage and selection operator (LASSO) regression model was utilized for optimizing feature selection. Additionally, we constructed a prognosis prediction nomogram with multivariate Cox regression results by incorporating features screened with the LASSO model. Moreover, the as-constructed prognosis model's discriminability, consistency, and clinical usefulness were assessed by receiver operating characteristic (ROC) curve, C-index, decision curve analysis (DCA), and calibration plot analysis, respectively. RESULT:Included in our prognosis prediction nomogram, the predictors of the long-term prognosis of MVD patients were age, BMI, diabetes mellitus (DM), antiplatelets, LDL-C, LVDD, and serum γKlotho level. Consequently, this nomogram displayed high discriminability, according to ROC and C-index analyses. Moreover, according to the calibration plot, the nomogram's probabilities exhibited high consistency with the actual levels. Based on DCA, this nomogram displayed good clinical usefulness. CONCLUSION:Higher serum γKlotho levels correlated with the poor prognosis of MVD patients, our predictive model exhibited better predictive ability and clinical usefulness.

The global burden, secular trends, and future projections of ischemic cardio-cerebrovascular disease (ICCVD), a composite indicator of ischemic heart disease (IHD) and ischemic stroke (IS), have not been specifically described in women. This study was aimed at estimating the global ICCVD burden from 1990 to 2021, and the projected burden from 2022 to 2050, in women. Age-standardized incidence, prevalence, mortality, and disability-adjusted life years (DALYs) with 95% uncertainty intervals (UI), and corresponding average annual percentage change (AAPC) with 95% confidence intervals (CI) and associated P-values, were calculated for women at global, regional, and national levels according to data from Global Burden of Disease 2021. Age-specific patterns, DALYs attributable to risk factors, and DALY projections to 2050 were also examined. In women, the global age-standardized prevalence of ICCVD increased from 3063 (95% UI: 2786 to 3339) per 100,000 population in 1990 to 3127 (2778 to 3476) per 100,000 population in 2021, and the AAPC was 0.03% (95% CI: 0.02% to 0.05%), whereas the incidence, mortality, and DALYs decreased (all P < 0.001). Notably, the age-standardized ICCVD incidence among women resurged in the past decade (0.29%), following a decline from 1990 to 2011 (−0.66%), whereas men experienced a consistent decline between 1990 and 2021. Low-middle Sociodemographic Index (SDI) countries consistently exhibited the highest age-standardized ICCVD incidence among women from 1990 to 2021, whereas only middle SDI countries demonstrated an increasing trend in age-standardized incidence over this period. Age-specific incidence rates increased among people younger than 60 years (0.14%) but decreased among people older than 60 years (−0.55%). High systolic blood pressure remained the leading risk factor for ICCVD in women, whereas high temperatures exhibited the most rapid relative increase in associated DALYs. DALYs for ICCVD in women are projected to continue declining through 2050, but the fatal burden will remain substantial, accounting for 87.4% of the total burden in 2050. ICCVD has posed a severe burden on women, largely driven by a notable resurgence in its incidence and prevalence over the past decade, alongside a pronounced increase in early-onset cases. Despite the projected decreasing trend in DALYs by 2050, the fatal burden is expected to remain the leading health threat. Our findings highlight the urgent need for public health strategies focusing on risk factor management and effective treatment to mitigate the ICCVD burden among women.

To systematically review and analyze the impact of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors on circulating inflammation, focusing on their underlying mechanisms and clinical application prospects, this review comprehensively summarizes recent studies addressing the molecular basis, nonclassical pathologic mechanisms, clinical evidence in multisystem diseases, therapeutic advances, and combined intervention strategies associated with PCSK9 and its inhibitors, highlighting their anti-inflammatory potential and personalized management strategies. PCSK9 participates in circulating inflammation primarily through multiple signaling pathways, including the NOD-like receptor family pyrin domain containing 3 inflammasome and the Toll-like receptor 4/nuclear factor kappa B axis. Clinical evidence indicates that PCSK9 inhibitors have limited direct effects on traditional inflammatory biomarkers. However, they show benefits in improving atherosclerotic plaque stability and modulating immune-inflammatory gene expression. The anti-inflammatory effects of PCSK9 inhibitors in circulating inflammation might not be directly reflected through changes in conventional inflammatory biomarkers. Future research should further explore their nonclassical mechanisms and optimize personalized risk stratification strategies, integrating multiomics and multiple biomarkers for precise inflammation management.

ABSTRACT Although single‐cell studies have profiled diseased aorta, mechanisms driving aortic dissection (AD) remain largely elusive owing to limited cohorts. Here, we integrate single‐cell and spatial transcriptomic data from 110 thoracic aortic samples (80 individuals; control, aneurysm, dissection; 767 018 high‐quality cells) to generate a comprehensive thoracic‐aorta cellular—molecular atlas. We identify an elastin‐rich fibroblast subset (Fibro_C1_FBN1+; FBN1, MFAP5, LOX) that declines with age and is markedly depleted in AD, linking fibroblast loss to increased aortic wall vulnerability and dissection risk. Vascular smooth muscle cells (vSMCs) undergo ENO1‐driven glycolytic reprogramming under hypoxia, lose contractility and adopt a synthetic, MIF‐secreting phenotype that engages macrophage receptors to promote macrophage recruitment and pro‐inflammatory polarization, leading aggregated macrophages to upregulate proteolytic and fibrinolytic pathways and thereby accelerate extracellular‐matrix degradation. In vitro and in vivo, ENO1 knockdown inhibits vSMC switching, reduces macrophage inflammation, and slows AD progression. This stromal‐immune axis suggests potential therapeutic targets in AD.

Stanford type A aortic dissection (AAD) is a life-threatening cardiovascular disease characterized by tearing in the aortic wall. Using spatial transcriptomics and multiplex immunofluorescence, we comprehensively analyzed ascending aortas from eight AAD patients across different severities and segments. We demonstrate that SPP1-driven inflammatory signaling intensifies with AAD severity, identifying a nine-gene, layer-anchored severity scale: MYL6/CALD1/MYH9 (mild); CCL2/CP/COL4A1 (moderate); and TMSB4X/ATP5F1E/PKM (severe). Importantly, the collagen-remodeling triad COL1A1/COL3A1/MMP2 is concurrently up-regulated in the brachiocephalic, left subclavian, and left common carotid arteries, often before the ascending aorta meets surgical diameter thresholds. These molecular signatures provide a critical foundation for non-invasive biomarker discovery, risk stratification, and precision pharmacotherapy targeting the SPP1-inflammatory axis, ultimately offering new insights into AAD mechanisms and therapeutic targets.

BackgroundAortic dissection (AD) is a life-threatening cardiovascular disease. ARHGAP27 can regulate cytoskeleton and cellular functions, which may be related to the phenotypic switching of vascular smooth muscle cells (VSMCs) in AD. However, the role of ARHGAP27 in AD has not been reported yet.MethodsThe AD-related data sets were downloaded from GEO database to screen differential genes. HE and IHC staining was used to detect the pathological changes and the expression level of ARHGAP27 in AD tissue. AD cell models were constructed in vitro by inducing HAVSMCs with PDGF-BB to evaluate the effects of ARHGAP27 overexpression or knockdown on cell survival, migration, invasion and phenotypic switching. Rescue experiments were performed using the ROCK activator LPA to test pathway specificity.ResultsARHGAP27 was significantly upregulated in the dataset and the tissue. In vitro experiments have shown that overexpression of ARHGAP27 can further promote the survival, migration and invasion of VSMCs, and the expression of synthetic phenotypic proteins MMP2 and MMP9, and inhibit the expression of contraction phenotypes α-SMA and SM22α. Knockdown of ARHGAP27-2 can obtain the opposite result. In terms of mechanism, PDGF-BB down-regulates the expression levels of RhoA, ROCK1/2, and up-regulates the phosphorylation levels of YAP in VSMCs. Overexpression of ARHGAP27 further enhances the effect of PDGF-BB, while knockdown of ARHGAP27-1 and ARHGAP27-2 inhibits the effect of PDGF-BB. Treatment with LPA would reverse the effects produced by ARHGAP27 overexpression.ConclusionARHGAP27 is upregulated in AD and accelerates its pathological progression by regulating the RhoA/ROCK/YAP pathway.

Background: Aortic dissection and myocardial infarction are two common and life-threatening cardiovascular emergencies characterized by sudden onset, high mortality, and overlapping clinical symptoms such as chest pain and respiratory distress, which make accurate and timely clinical differentiation particularly challenging. Current mainstream diagnostic techniques, including computed tomography and transesophageal echocardiography, provide valuable anatomical and functional information but are often costly, time-consuming, and insensitive to early-stage biochemical alterations, which may result in missed or incorrect diagnoses in emergency settings. Aortic dissection often requires immediate repair of the damaged vessel to prevent further expansion or rupture, whereas myocardial infarction requires rapid restoration of blood flow to the myocardium. The treatment approaches for the two conditions are distinct, and misdiagnosis can result in severe consequences. Therefore, more convenient, rapid, and efficient diagnostic methods are urgently needed. Methods: Vibrational spectroscopy is a noninvasive analytical technique with high sensitivity to molecular and biochemical changes in biological samples, and Raman spectroscopy and infrared spectroscopy target distinct molecular vibrational modes, providing complementary pathological information. In this study, a multimodal attention fusion network was developed to integrate Raman spectroscopy and infrared spectroscopy data for rapid disease classification. Results: Experimental results demonstrated that the proposed method achieved a diagnostic accuracy of 94.06 % and a specificity of 97.03 % percent in distinguishing aortic dissection, myocardial infarction, and non-critical cases. Conclusion: This method provides an innovative and efficient decision-support tool for the clinical differentiation of aortic dissection and myocardial infarction, offering significant clinical value.

Background:Published studies have reported inconsistent findings regarding the association between preprocedural red cell distribution width (RDW) and adverse outcomes after percutaneous coronary intervention (PCI), and earlier reviews no longer reflect the currently available evidence. This updated systematic review and meta-analysis was conducted to reassess the association between preprocedural RDW and adverse outcomes in patients with coronary artery disease (CAD) undergoing PCI. Methods:PubMed, Embase, Web of Science, and the Cochrane Library were searched from inception to November 22, 2025. Standard major adverse cardiovascular events (MACE), all-cause mortality (ACM), and cardiovascular mortality (CVM) were prespecified as the primary outcomes, whereas PCI-specific stent-related outcomes were analyzed separately as exploratory outcomes. Hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (CIs) were extracted for quantitative synthesis when appropriate. Results:Twenty-four studies comprising 31 comparison groups and approximately 83,000 patients were included in the meta-analysis. Elevated preprocedural RDW was associated with higher risks of ACM (HR 1.46, 95% CI 1.31-1.63) and CVM (HR 1.66, 95% CI 1.33-2.07), with the most consistent association observed for ACM. The HR-based analysis of standard MACE showed a statistically significant association (HR 1.24, 95% CI 1.06-1.45; p = 0.007), but the finding was unstable in sensitivity analysis and should therefore be interpreted cautiously. After endpoint reclassification, only one study remained eligible for the OR-based analysis of standard MACE, precluding quantitative synthesis. In-stent restenosis (ISR) was analyzed separately as an exploratory stent-related outcome when eligible studies were available. Conclusions:Elevated preprocedural RDW was associated with adverse outcomes after PCI. The most consistent association was observed for ACM, whereas the evidence for CVM and standard MACE was less certain. PCI-specific stent-related outcomes should be interpreted as exploratory. Further prospective multicenter studies with standardized endpoint definitions and harmonized RDW cutoff values are warranted. Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO/view/CRD420251249457, PROSPERO, CRD420251249457.

BACKGROUND:Aortic dissection and myocardial infarction are two life-threatening acute cardiovascular conditions with similar clinical presentations but fundamentally different treatment strategies. Misdiagnosis between these diseases can severely endanger patient survival, highlighting the urgent need for efficient and non-invasive differential diagnostic methods. Vibrational spectroscopy, characterized by its non-invasiveness, high throughput, and molecular sensitivity, offers a promising approach for early biochemical disease identification. However, single spectral modalities are limited in diagnostic performance due to insufficient complementary information. RESULTS:To address these limitations, we propose MSFusion, a multimodal deep learning model that integrates infrared and Raman spectroscopy data for precise diagnosis and survival prognosis prediction of aortic dissection. MSFusion employs a three-branch multiscale convolutional architecture to extract hierarchical spectral representations, incorporates a cross-modal attention module to promote semantic synergy and complementary interaction between modalities, and utilizes a bidirectional multiscale fusion mechanism to align local and global features across multiple granularities.Experimental results demonstrate that MSFusion achieves 95.63% accuracy and 98.79% AUC in distinguishing aortic dissection from myocardial infarction, significantly outperforming unimodal and conventional fusion approaches. For survival prognosis, the model is further extended by incorporating clinical indicators to predict postoperative survival outcomes, achieving 81.82% accuracy and 70.00% AUC, showing its capability for effective clinical risk stratification. SIGNIFICANCE:This study presents a multimodal deep learning framework that combines vibrational spectroscopy with clinical data for rapid and non-invasive diagnosis of aortic dissection. MSFusion effectively enhances diagnostic precision and prognostic reliability, providing a promising tool for intelligent cardiovascular disease assessment and clinical decision support.

BACKGROUND AND AIMS:The efficacy of prophylactic mechanical circulatory support with micro-axial flow pump or veno-arterial extracorporeal membrane oxygenation (VA-ECMO) in patients with severely reduced left ventricular ejection fraction (LVEF) undergoing high-risk percutaneous coronary intervention (PCI) remains unclear. METHODS:Patients with complex three-vessel disease, unprotected left main coronary disease or last patent conduit and LVEF ≤ 35% were assigned to receive either a micro-axial flow pump (SynFlow 3.0) or VA-ECMO support during a non-emergent high-risk PCI procedure in this prospective, multicentre, randomized, open-label, non-inferiority trial. The primary endpoint was the incidence of 30-day major adverse events, defined as any of: all-cause death, myocardial infarction, stroke/transient ischaemic attack, repeat revascularization, major bleeding, acute kidney injury, cardiopulmonary resuscitation/cardioversion, cardiac surgery/limb ischaemia, or serious device-related complications. Safety endpoints included adverse events and serious adverse events. RESULTS:The primary endpoint, 30-day major adverse events, occurred in 8 of 109 patients (7.34%) in the SynFlow 3.0 group and 13 of 113 patients (11.5%) in the VA-ECMO group (absolute difference adjusted for centre effect, -4.6%; 95% confidence interval, -12.6% to 3.5%; P for non-inferiority < .001). Patients with SynFlow 3.0 had shorter post-procedural hospital stay (4.1 days vs 5.2 days on average, P = .047) and fewer device-related adverse events (3.7% vs 11.5%; P = .041). Anaemia occurred more often with VA-ECMO than with SynFlow 3.0 (20.4% vs 9.2%; P = .023). CONCLUSIONS:The prophylactic use of a micro-axial flow pump during high-risk PCI procedures was non-inferior to VA-ECMO in the incidence of 30-day major adverse events. The use of a micro-axial flow pump was associated with shorter post-procedural hospital stay and fewer device-related adverse events.