HSP70 contributes to pathogenesis of fulminant hepatitis induced by coronavirus.

Fulminant viral hepatitis (FH) represents a significant clinical challenge, with its pathogenesis not yet fully elucidated. Heat shock protein (HSP)70, a molecular chaperone protein with a broad range of cytoprotective functions, is upregulated in response to stress. However, the role of HSP70 in FH remains to be investigated. Notably, HSP70 expression is upregulated in the livers of coronavirus-infected mice and patients. Therefore, we investigated the mechanistic role of HSP70 in coronavirus-associated FH pathogenesis. FH was induced in HSP70-deficient (HSP70 KO) mice or in WT mice treated with the HSP70 inhibitor VER155008 when infected with the mouse hepatitis virus strain A59 (MHV-A59). MHV-A59-infected HSP70 KO mice exhibited significantly reduced liver damage and mortality. This effect was attributed to decreased infiltration of monocyte-macrophages and neutrophils in the liver of HSP70 KO mice, resulting in lower levels of inflammatory cytokines such as IL-1ß, TNFα, and IL-6, and a reduced viral load. Moreover, treatment with the HSP70 inhibitor VER155008 protected mice from MHV-A59-induced liver damage and FH mortality. In summary, HSP70 promotes coronavirus-induced FH pathogenesis by enhancing the infiltration of monocyte-macrophages and neutrophils and promoting the secretion of inflammatory cytokines. Therefore, HSP70 is a potential therapeutic target in viral FH intervention.

Galectin-3 induces pathogenic immunosuppressive macrophages through interaction with TREM2 in lung cancer.

BACKGROUND: High infiltration of tumor-associated macrophages (TAMs) is associated with tumor promotion and immunosuppression. The triggering receptor expressed on myeloid cells 2 (TREM2) is emerged as a key immunosuppressive regulator for TAMs, however, how TREM2-expressing TAMs are recruited and what ligands TREM2 interacts with to mediate immunosuppression is unknown. METHODS: Flow cytometry and single-cell RNA sequencing were used to analyze TREM2 expression. Mechanistically, mass spectrometry and immunoprecipitation were employed to identify proteins binding to TREM2. Phagocytosis and co-culture experiments were used to explore the in vitro functions of galectin3-TREM2 pair. Establishment of TREM2f/f-Lyz2-cre mice to validate the role of TREM2 signaling pathway in lung carcinogenesis. GB1107 were further supplemented to validate the therapeutic effect of Galectin3 based on TREM2 signaling regulation. RESULTS: This study identified that abundant TREM2+ macrophages were recruited at the intra-tumor site through the CCL2-CCR2 chemotactic axis. Galectin-3 impaired TREM2-mediated phagocytosis and promoted the conversion of TREM2+ macrophages to immunosuppressive TAMs with attenuated antigen presentation and co-stimulatory functions both in vitro both in vivo, and galectin-3 is a potential ligand for TREM2. Genetic and pharmacological blockade of TREM2 and galectin-3 significantly inhibited lung cancer progression in subcutaneous and orthotopic cancer models by remodeling the tumor immune microenvironment. CONCLUSION: Our findings revealed a previously unknown association between galectin-3 and TREM2 in TAMs of lung cancer, and suggested simultaneous inhibition of galectin3 and TREM2 as potent therapeutic approach for lung cancer therapy.

Multifunctional Bispecific Nanovesicles Targeting SLAMF7 Trigger Potent Antitumor Immunity.

The effectiveness of immune checkpoint inhibitor (ICI) therapy is hindered by the ineffective infiltration and functioning of cytotoxic T cells and the immunosuppressive tumor microenvironment (TME). Signaling lymphocytic activation molecule family member 7 (SLAMF7) is a pivotal co-stimulatory receptor thought to simultaneously trigger NK-cell, T-cell, and macrophage antitumor cytotoxicity. However, the potential of this collaborative immune stimulation in antitumor immunity for solid tumors is underexplored due to the exclusive expression of SLAMF7 by hematopoietic cells. Here, we report the development and characterization of multifunctional bispecific nanovesicles (NVs) targeting SLAMF7 and glypican-3-a hepatocellular carcinoma (HCC)-specific tumor antigen. We found that by effectively "decorating" the surfaces of solid tumors with SLAMF7, these NVs directly induced potent and specific antitumor immunity and remodeled the immunosuppressive TME, sensitizing the tumors to programmed cell death protein 1 (PD1) blockade. Our findings highlight the potential of SLAMF7-targeted multifunctional bispecific NVs as an anticancer strategy with implications for designing next-generation targeted cancer therapies.

Pyroptotic Macrophage-Derived Microvesicles Accelerate Formation of Neutrophil Extracellular Traps via GSDMD-N-expressing Mitochondrial Transfer during Sepsis.

Macrophage pyroptosis and neutrophil extracellular traps (NETs) play a critical role in sepsis pathophysiology; however, the role of macrophage pyroptosis in the regulation of NETs formation during sepsis is unknown. Here, we showed that macrophages transfer mitochondria to neutrophils through microvesicles following pyroptosis; this process induces mitochondrial dysfunction and triggers the induction of NETs formation through mitochondrial reactive oxygen species (mtROS)/Gasdermin D (GSDMD) axis. These pyroptotic macrophage-derived microvesicles can induce tissues damage, coagulation, and NETs formation in vivo. Disulfiram partly inhibits these effects in a mouse model of sepsis. Pyroptotic macrophage-derived microvesicles induce NETs formation through mitochondrial transfer, both in vitro and in vivo. Microvesicles-mediated NETs formation depends on the presence of GSDMD-N-expressing mitochondria in the microvesicles. This study elucidates a microvesicles-based pathway for NETs formation during sepsis and proposes a microvesicles-based intervention measure for sepsis management.

Diagnostic performance of ultrasonic flow ratio versus quantitative flow ratio for assessment of coronary stenosis.

BACKGROUND: Ultrasonic flow ratio (UFR) is a novel intravascular ultrasound (IVUS)-derived modality for fast computation of fractional flow reserve (FFR) without pressure wires and adenosine. AIMS: This study was sought to compare the diagnostic performance of UFR and quantitative flow ratio (QFR), using FFR as the reference standard. METHODS: This is a retrospective study enrolling consecutive patients with intermediate coronary artery lesions (diameter stenosis of 30%-90% by visual estimation) for IVUS and FFR measurement. UFR and QFR were performed offline in a core-lab by independent analysts blinded to FFR. RESULTS: From December 2022 to May 2023, a total of 78 eligible patients were enrolled. IVUS and FFR measurements were successfully conducted in 104 vessels, finally 98 vessels with both FFR, UFR and QFR evaluation were analyzed. Mean FFR was 0.79 ± 0.12. UFR showed a strong correlation with FFR similar to QFR (r = 0.83 vs. 0.82, p = 0.795). Diagnostic accuracy of UFR was non-inferior to QFR (94% [89%-97%] versus 90% [84%-94%], p = 0.113). Sensitivity and specificity in identifying hemodynamically significant stenosis were comparable between UFR and QFR (sensitivity: 89% [79%-96%] versus 85% [74%-92%], p = 0.453; specificity: 97% [91%-99%] versus 95% [88%-99%], p = 0.625). The area under curve for UFR was 0.95 [0.90-0.98], non-inferior to QFR (difference = 0.021, p = 0.293), and significantly higher than minimum lumen area (MLA; difference = 0.13, p < 0.001). Diagnostic accuracy of UFR and QFR was not statically different in bifurcation nor non-bifurcation lesions. CONCLUSIONS: UFR showed excellent concordance with FFR, non-inferior to QFR, superior to MLA. UFR provides a potentiality for the integration of physiological assessment and intravascular imaging in clinical practice.

A Novel System for Transcatheter Aortic Valve Implantation: First-in-Man Study.

Transcatheter aortic valve implantation (TAVI) has become a therapeutic treatment for severe symptomatic patients with aortic stenosis. This study aimed to test a novel transcatheter aortic self-expandable bioprosthesis-the ScienCrown system (Lepu Medtech Inc., Beijing, China)-and evaluate the safety of the new device during TAVI. ScienCrown aortic valve implantation was performed on 10 patients. Clinical assessment was performed at baseline, post procedure, and after 1 year. Clinical outcomes and adverse events were assessed according to Valvular Academic Research Consortium-3 criteria. The mean age was 75.30 ± 4.78 years with a mean Society of Thoracic Surgeons score of 4.64 ± 3.23%. Device success was achieved in all patients (80% transfemoral, 20% transapical). After 1 year, there were no deaths, disabling strokes, myocardial infarctions, conversions to surgery, or major procedure-related complications. New pacemaker implantation was required in one patient (10%). ScienCrown implantation resulted in a reduction in mean valve gradient (63.00 ± 18.84 to 9.67 ± 4.97 mm Hg, p <0.001) and an increase in effective orifice area (0.57 ± 0.20 to 2.57 ± 0.59 cm2, p <0.001) at 1 year. Paravalvular leak was absent in 9 patients (90%), and there was a trace in one patient (10%). All patients were in New York Heart Association class I to II at a mean follow-up of 1 year. The experience showed that ScienCrown transcatheter aortic valve system was safely and successfully implanted for treatment of severe symptomatic aortic stenosis. The newer-generation device affords a stable implantation while providing optimal hemodynamic performance.

Effect of chemotherapy in tumor on coronary arteries: Mechanisms and management.

Coronary artery disease (CAD) is an important contributor to the cardiovascular burden in cancer survivors. The development of coronary ischemia events, myocardial infarction, and heart failure has been associated with many conventional chemotherapeutic agents, new targeted therapies, and immunotherapy. The most frequent pathological manifestations of chemotherapy-mediated coronary damage include acute vasospasm, acute thrombosis, accelerated atherosclerosis development, and microvascular dysfunction. Potential screening techniques for CAD patients include baseline risk factor evaluation, polygenic risk factors, and coronary artery calcium scores. Determining the risk requires consideration of both the type of chemotherapy and the type of cancer being treated. Cardiology-oncology guidelines offer some suggestions for the care of coronary artery disease, which might involve medication, lifestyle changes, and coronary revascularization.

Unsupervised Domain Adaptation on Person Reidentification via Dual-Level Asymmetric Mutual Learning.

Unsupervised domain adaptation (UDA) person reidentification (Re-ID) aims to identify pedestrian images within an unlabeled target domain with an auxiliary labeled source-domain dataset. Many existing works attempt to recover reliable identity information by considering multiple homogeneous networks. And take these generated labels to train the model in the target domain. However, these homogeneous networks identify people in approximate subspaces and equally exchange their knowledge with others or their mean net to improve their ability, inevitably limiting the scope of available knowledge and putting them into the same mistake. This article proposes a dual-level asymmetric mutual learning (DAML) method to learn discriminative representations from a broader knowledge scope with diverse embedding spaces. Specifically, two heterogeneous networks mutually learn knowledge from asymmetric subspaces through the pseudo label generation in a hard distillation manner. The knowledge transfer between two networks is based on an asymmetric mutual learning (AML) manner. The teacher network learns to identify both the target and source domain while adapting to the target domain distribution based on the knowledge of the student. Meanwhile, the student network is trained on the target dataset and employs the ground-truth label through the knowledge of the teacher. Extensive experiments in Market-1501, CUHK-SYSU, and MSMT17 public datasets verified the superiority of DAML over state-of-the-arts (SOTA).

HSPA13 modulates type I interferon antiviral pathway and NLRP3 inflammasome to restrict dengue virus infection in macrophages.

Dengue virus (DENV) is a type of arthropod-borne Flavivirus, which leads to a series of serious diseases like dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). DENV has a devastating health and economic impact worldwide. However, there are no suitable drugs to combat the virus. Here we reported that HSPA13, also known as stress chaperone (STCH), is a member of the HSP70 family and is a key regulator of type I interferon (IFN-I) and pro-inflammatory responses during DENV infection. HSPA13 expression was increased in macrophages infected with DENV or other Flaviviruses like Zika virus (ZIKV), Yellow fever virus (YFV) and Japanese encephalitis virus (JEV). Further, HSPA13 suppressed the replication of DENV and other Flaviviruses (ZIKV, JEV, YFV), which exhibited broad-spectrum antiviral effects. On the one hand, HSPA13 promoted production of IFN-ß and interferon-stimulated genes (ISGs, such as ISG15, OAS and IFIT3) by interacting with RIG-I and up-regulating RIG-I expression during DENV infection. On the other hand, HSPA13 enhanced NLRP3 inflammasome activation and IL-1ß secretion by interacting with ASC in DENV infection. We identified HSPA13 as a potential anti-DENV target. Our results provide clues for the development of antiviral drugs against DENV based on HSPA13 and reveal novel drug target against Flaviviruses.

Synergistic therapeutic antitumor effect of PD-1 blockade cellular vesicles in combination with Iguratimod and Rhodium nanoparticles.

Immune checkpoint blockade has emerged as a significant therapeutic development in immunotherapy during the past decade. However, only a small percentage of cancer patients respond to checkpoint blockade, suggesting that a fundamental knowledge of the underlying processes of immune checkpoint receptor signaling remains elusive and that novel therapeutic medications are needed. Here, the programmed cell death protein 1(PD-1) expressing nanovesicles were developed to enhance T cell activity. Iguratimod (IGU) and Rhodium (Rh) nanoparticles (NPs) were loaded in PD-1 nanovesicles (NVs) for synergistic therapeutic antitumor effects against lung cancer and metastasis. For the first time, this study revealed that IGU exhibits an antitumor effect by inhibiting the phosphorylation of mammalian target of rapamycin (mTOR) and Rh-NPs provided a photothermal effect by improving reactive oxygen species (ROS)-dependent apoptosis in lung cancer cells. IGU-Rh-PD-1 NVs also reduced the migration ability through the epithelial-mesenchymal transition (EMT) pathway. Furthermore, IGU-Rh-PD-1 NVs reached the targeted site and inhibited tumor growth in vivo. This strategy could boost T cell performance and simultaneously possess chemotherapeutic and photothermal therapy to serve as a new combination therapy for lung cancer and potentially other aggressive cancer.

The first clinical data of the SAPIEN 3 aortic valve in the treatment of aortic stenosis in China.

Background: Data on outcomes following transcatheter aortic valve replacement with SAPIEN 3 in China is limited as it was approved by the National Medical Products since 2020. The present study was designed to collect clinical data on the SAPIEN 3 aortic valve in Chinese patients with bicuspid aortic valve and tricuspid aortic valve stenosis. Methods: We analyzed the patient characteristics, procedural features and procedural outcomes of the first 438 patients (223 for bicuspid aortic valve and 215 tricuspid aortic valve) from 21 provinces in 74 sites treated with the SAPIEN 3 valve system for transcatheter aortic valve replacement between September 2020 and May 2022. Results: Procedural mortality was 0.7%. 5 cases during the operation were converted to surgery. Among 438 cases, permanent pacemaker implantation was performed in a total of 12 cases (2.7%). The patient had severe leaflet calcification of the aortic valve, with moderate and severe calcification reaching 39.7% and 35.2% respectively. The size of the implanted valves was predominantly 26 mm and 23 mm, reaching 42.5% and 39.5% respectively. The incidence of moderate or severe perivalvular leak in the postoperative period was 0.5%, with a predominance of 90/10 and 80/20 valve deployment height. There was a significant difference in the deployment height of the valve between bicuspid aortic valve and tricuspid aortic valve, with the bicuspid aortic valve having a more deployment height of 90/10. Annulus size in bicuspid aortic valve group was significantly larger than tricuspid aortic valve group. Valve sizing for oversized, within size, and undersized were different between bicuspid aortic valve and tricuspid aortic valve. Conclusions: Procedural success rates were high, with similar and good results for bicuspid aortic valve and tricuspid aortic valve, low perivalvular leak for both valve types, and low permanent pacemaker implantation rates for both valve types. Annulus size, valve sizing and coronary artery height were significantly different in the BAV and TAV group.

The predictive value of prognosis and therapeutic response for STAT family in pancreatic cancer.

Background: Signal transducers and activators of transcription (STAT) proteins, well-known cytoplasmic transcription factors, were found to be abnormally expressed in various cancers and play essential parts in the initiation, progression and therapy resistance of cancer. Nevertheless, the functions of different STATs in pancreatic cancer (PC) and their relationship to the prognosis and immune infiltration as well as drug efficacy in PC patients have not been systematically elucidated. Methods: Expression, prognosis, genetic alterations and pathway enrichment analyses of the STAT family were investigated via Oncomine, GEPIA, Kaplan Meier-plotter, cBioPortal, Metascape and GSEA. Analysis of tumor immune microenvironment was conducted by ESTIMATE and TIMER. "pRRophetic" packages were used for analysis of chemotherapeutic response. Finally, the diagnostic and prognostic value of key STATs were further validated through public datasets and immunohistochemistry. Results: In this study, only STAT1 mRNA level was significantly increased in tumor tissues and highly expressed in PC cell lines via multiple datasets. PC patients with higher STAT1/4/6 expression had a worse overall survival (OS) and progression-free survival (PFS), while higher STAT5B expression was correlated with better prognosis in the TCGA cohort. The STATs-associated genes were enriched in pathways about the remodeling of tumor immune microenvironment. The STATs levels were significantly correlated with immune infiltration, except STAT6. The STAT1 was identified as a potential biomarker and its diagnostic and prognostic value were further validated at mRNA and protein levels. GSEA showed that STAT1 may be involved in the progression and immune regulations of PC. Moreover, STAT1 expression was significantly related to the level of immune checkpoint, and predicted immunotherapy and chemotherapy responses. Conclusion: STAT family members were comprehensively analyzed and STAT1 was identified as an effective biomarker for predicting the survival and therapeutic response, which could be beneficial to develop better treatment strategies.

Peripheral changes in T cells predict efficacy of anti-PD-1 immunotherapy in non-small cell lung cancer.

The application of programmed cell death protein 1 (PD-1) antibodies has brought great benefits to non-small cell lung cancer (NSCLC) patients. Nevertheless, not all patients respond to anti-PD-1 immunotherapy. This study aimed to find response markers to predict efficacy of anti-PD-1 immunotherapy in NSCLC patients. 80 patients with NSCLC who would accept anti-PD-1 immunotherapy were recruited, and peripheral blood was obtained before and after treatment. Flow cytometry was used to detect proportions of circulating cell subsets and expression of co-stimulatory molecules, co-inhibitory molecules and cytokines in T cells from pre- and post-treatment patients. Results showed that proportions of CD4+ and CD8+ T cells, NK, γδT and mucosal-associated invariant T (MAIT) cells were higher and regulatory T cells (Tregs) were lower in responders (n = 50) after treatment but no obvious difference was found in non-responders (n = 30). After treatment, responders showed an increase in the frequency of co-stimulatory and co-inhibitory molecules, as well as the production of cytokines in T cells. This study indicates that monitoring the alterations of immune markers in circulating cells from NSCLC patients may be helpful to discriminate responders and non-responders, which provides a potential novel way to assess efficacy of anti-PD-1 immunotherapy.

First-in-human evaluation of a novel ultrathin sirolimus-eluting iron bioresorbable scaffold: 3-year outcomes of the IBS-FIM trial.

BACKGROUND: The first-generation polymeric bioresorbable scaffolds resulted in higher than acceptable 3-year rates of device-related adverse outcomes. AIMS: We aimed to assess the intermediate-term safety and performance of a novel ultrathin-strut sirolimus-eluting iron bioresorbable scaffold (IBS) in non-complex coronary lesions. METHODS: The prospective, single-arm, open-label IBS first-in-human study enrolled 45 patients, each with a single de novo lesion. Enrolled patients were randomly assigned to 2 follow-up cohorts. Angiographic and imaging follow-up with intravascular ultrasound and optical coherence tomography (OCT) were conducted at 6 and 24 months in cohort 1 (n=30) and at 12 and 36 months in cohort 2 (n=15). Clinical follow-up was conducted at 1, 6 and 12 months, and annually thereafter up to 5 years. The coprimary outcomes were target lesion failure (TLF) and angiographic late lumen loss (LLL) at 6 months. RESULTS: A total of 45 patients were enrolled between April 2018 and January 2019. The mean age was 53.2 years, 77.8% were male, and 26.7% had diabetes. The TLF rates were 2.2% at 6 months and 6.7% at 3 years, which in all cases were due to clinically indicated target lesion revascularisation. No deaths, myocardial infarctions or stent thromboses occurred during 3-year follow-up. In-scaffold LLL was 0.33±0.27 mm at 6 months and 0.37±0.57 mm at 3 years. By OCT, the proportion of covered struts was 99.8% at 6 months and 100% after 1 year. The 3-year strut absorption rate was 95.4%. CONCLUSIONS: In this first-in-human experience, an ultrathin IBS was safe and effective for the treatment of de novo non-complex coronary lesions up to 3-year follow-up.

SLAMF7 regulates the inflammatory response in macrophages during polymicrobial sepsis.

Uncontrolled inflammation occurred in sepsis results in multiple organ injuries and shock, which contributes to the death of patients with sepsis. However, the regulatory mechanisms that restrict excessive inflammation are still elusive. Here, we identified an Ig-like receptor called signaling lymphocyte activation molecular family 7 (SLAMF7) as a key suppressor of inflammation during sepsis. We found that the expression of SLAMF7 on monocytes/macrophages was significantly elevated in patients with sepsis and in septic mice. SLAMF7 attenuated TLR-dependent MAPK and NF-κB signaling activation in macrophages by cooperating with Src homology 2-containing inositol-5'­phosphatase 1 (SHIP1). Furthermore, SLAMF7 interacted with SHIP1 and TNF receptor-associated factor 6 (TRAF6) to inhibit K63 ubiquitination of TRAF6. In addition, we found that tyrosine phosphorylation sites within the intracellular domain of SLAMF7 and the phosphatase domain of SHIP1 were indispensable for the interaction between SLAMF7, SHIP1, and TRAF6 and SLAMF7-mediated modulation of cytokine production. Finally, we demonstrated that SLAMF7 protected against lethal sepsis and endotoxemia by downregulating macrophage proinflammatory cytokines and suppressing inflammation-induced organ damage. Taken together, our findings reveal a negative regulatory role of SLAMF7 in polymicrobial sepsis, thus providing sights into the treatment of sepsis.

Simultaneous Hybrid Coronary Revascularization vs Conventional Strategies for Multivessel Coronary Artery Disease: A 10-Year Follow-Up.

BACKGROUND: Although evidence is sufficient to confirm that hybrid coronary revascularization (HCR) is safe and effective in the short term, its value in the long run is debatable. OBJECTIVES: This study sought to compare the long-term outcomes of HCR with coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) for multivessel disease. METHODS: Three groups of patients, 540 each, receiving HCR, CABG, or PCI between June 2007 to September 2018, were matched using propensity score matching. Patients were stratified by EuroSCORE (European System for Cardiac Operative Risk Evaluation) II (low ≤0.9; 0.9 < medium <1.5; high ≥1.5) and SYNTAX (Synergy Between Percutaneous Coronary Intervention With Taxus and Cardiac Surgery) score (low ≤22; 22 < medium <33; high ≥33). Major adverse cardiac and cerebrovascular events (MACCE) and Seattle Angina Questionnaire (SAQ) scores were compared among the 3 groups. RESULTS: In terms of MACCE and SAQ, HCR performed similarly to off-pump CABG but significantly outperformed PCI (P < 0.001). In the low-to-medium EuroSCORE II and medium-to-high SYNTAX score tertiles, MACCE rates in the HCR group were significantly lower than those in the PCI (EuroSCORE II: low, 30.7% vs 41.2%; P = 0.006; medium, 31.3% vs 41.7%; P = 0.013; SYNTAX score: medium, 27.6% vs 41.2%; P = 0.018; high, 32.4% vs 52.7%; P = 0.011) but were similar to those in the CABG group. In the high EuroSCORE II stratum, HCR had a lower MACCE rate than CABG (31.9% vs 47.0%; P = 0.041) and PCI (31.9% vs 53.7%; P = 0.015). CONCLUSIONS: Compared with conventional strategies, HCR provided satisfactory long-term outcomes in MACCE and functional status for multivessel disease.

Evaluation of the effect of simultaneous hybrid coronary revascularization on postoperative bleeding and renal function: A comparison study with minimally invasive direct off-pump coronary artery bypass grafting in patients with multivessel coronary artery disease.

OBJECTIVES: The present study sought to compare postoperative bleeding and renal function in patients with multivessel coronary artery disease undergoing simultaneous hybrid coronary revascularization (HCR) and minimally invasive direct off-pump coronary artery bypass grafting (MIDCABG). METHODS: The study retrospectively collected the data of 594 consecutive patients who underwent simultaneous HCR and 351 patients who underwent MIDCABG with planned staged HCR (MIDCABG first, then elective percutaneous coronary intervention) in Fuwai Hospital from June 2007 to December 2020. A total of 317 pairs of patients who were matched in a 1:1 ratio with propensity score matching were enrolled in this study. Bleeding and changes in renal function were compared between the 2 groups. RESULTS: Compared with patients who underwent MIDCABG, patients who underwent simultaneous HCR had significantly greater chest tube drainage on the day of the operation (492.7 ± 282.4 mL vs 441.0 ± 261.9 mL; P = .023), but no significant difference was detected in the total amount during the postoperative period (788.8 ± 458.9 mL vs 753.3 ± 409.8 mL; P = .74). The differences in re-exploration for bleeding (0.3% vs 1.6%; P = .13), blood transfusion (18.9% vs 16.4%; P = .13), acute kidney injury (23.3% vs 18.6%; P = .53), and in-hospital major adverse cardiovascular and cerebrovascular events (including all-cause death, myocardial infarction, stroke, and repeated revascularization) (2.5% vs 1.9%; P = .67) between the 2 groups did not reach statistical significance. CONCLUSIONS: Compared with MIDCABG, simultaneous HCR (MIDCABG first, instant percutaneous coronary intervention) did not increase postoperative bleeding or the incidence of acute kidney injury.

Prevalence, Predictors, and Impact of Coronary Artery Ectasia in Patients With Atherosclerotic Heart Disease.

The clinical relevance of coronary artery ectasia (CAE) is poorly understood. We investigated the prevalence, potential predictors, and prognostic significance of CAE in patients with atherosclerotic coronary artery disease. Consecutive patients undergoing percutaneous coronary intervention (PCI) from January 2016 to December 2018 were included and followed up for 1 year. CAE was diagnosed as an abnormal dilation >1.5-fold the diameter of adjacent normal segments on angiography. A total of 590 patients with CAE were identified from 36 790 patients undergoing PCI (overall rate of CAE: 1.6%). In multivariate analysis, variables including body mass index >30 kg/m2 (risk ratio, RR: 2.413, P = .018), ever-smoking (RR: 1.669, P < .001), hypertension (RR: 1.221, P = .025), acute myocardial infarction at admission (RR: 1.343, P = .004), no diabetes (RR: .810, P = .023), previous myocardial infarction (RR: 1.545, P < .001), no left main disease (RR: .632, P = .008) and multiple-vessel disease (RR: 1.326, P = .001), increased C-reactive protein (RR: 1.006, P = .012) were predictors of CAE. The incidence of adverse cardiovascular outcomes did not differ significantly between patients with or without CAE (P = .203). CAE is not uncommon among patients undergoing PCI in this cohort study. The presence of CAE vs its absence had no significant impact on 1-year clinical outcomes after PCI.

A New Risk Score for Predicting Postoperative Mortality in Suspected Heart Failure Patients Undergoing Valvular Surgery.

Background: Heart failure (HF) is one of the most important indications of the severity of valvular heart disease (VHD). VHD with HF is frequently associated with a higher surgical risk. Our study sought to develop a risk score model to predict the postoperative mortality of suspected HF patients after valvular surgery. Methods: Between January 2016 and December 2018, all consecutive adult patients suspected of HF and undergoing valvular surgery in the Chinese Cardiac Surgery Registry (CCSR) database were included. Finally, 14,645 patients (55.39 ± 11.6 years, 43.5% female) were identified for analysis. As a training group for model derivation, we used patients who had surgery between January 2016 and May 2018 (11,292 in total). To validate the model, patients who underwent surgery between June 2018 and December 2018 (a total of 3353 patients) were included as a testing group. In training group, we constructed and validated a scoring system to predict postoperative mortality using multivariable logistic regression and bootstrapping method (1000 re-samples). We validated the scoring model in the testing group. Brier score and calibration curves using bootstrapping with 1000 re-samples were used to evaluate the calibration. The area under the receiver operating characteristic curve (AUROC) was used to evaluate the discrimination. The results were also compared to EuroSCORE II. Results: The final score ranged from 0 to 19 points and involved 9 predictors: age ≥ 60 years; New York Heart Association Class (NYHA) IV; left ventricular ejection fraction (LVEF) < 35%; estimated glomerular filtration rate (eGFR) < 50 mL/min/1.73 m 2 ; preoperative dialysis; Left main artery stenosis; non-elective surgery; cardiopulmonary bypass (CPB) time > 200 minutes and perioperative transfusion. In training group, observed and predicted postoperative mortality rates increased from 0% to 45.5% and from 0.8% to 50.3%, respectively, as the score increased from 0 up to ≥ 10 points. The scoring model's Brier scores in the training and testing groups were 0.0279 and 0.0318, respectively. The area under the curve (AUC) values of the scoring model in both the training and testing groups were 0.776, which was significantly higher than EuroSCORE II in both the training (AUC = 0.721, Delong test, p < 0.001) and testing (AUC = 0.669, Delong test, p < 0.001) groups. Conclusions: The new risk score is an effective and concise tool that could accurately predict postoperative mortality rates in suspected HF patients after valve surgery.