Following the publication of the above paper, a concerned reader has drawn the Editor's attention to the fact that, regarding the western blot data shown in Fig. 4A and E on p. 612, the p‑p38 blots featured in these figure parts were strikingly similar, although the blots were rotated through 180° relative to each other. Upon investigating the data in this paper independently in the Editorial Office, it also came to light that β‑actin control blots featured in Fig. 1E, and p‑p38 blots featured in Fig. 5I, subsequently appeared in another paper written by the same research group in an article published in the journal PLoS One. Finally, control western blots appeared to have been re‑used in Fig. 4A and C, although the experimental conditions reported for the western blots in these figure parts were different. The authors have been contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in this paper, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of these potential problems while the Editorial Office continues to investigate this matter further.  [International Journal of Molecular Medicine 27: 607‑615, 2011; DOI: 10.3892/ijmm.2011.621].

Ferroptosis significantly contributes to myocardial injury in Type 2 Diabetes Mellitus (T2DM). Liver X Receptor (LXR) and Retinoid X Receptor (RXR) play crucial roles in lipid metabolism and inflammation, but their involvement in regulating ferroptosis in diabetic cardiomyocytes is not fully understood. High-fat diet/streptozotocin-induced T2DM mouse models and high glucose and high fat (HG)-exposed cardiomyocytes were used to assess the impact of LXR activation on myocardial injury and ferroptosis. The study also examined the role of the ROS/AMPK/Nrf2 pathway and the effect of LXR/RXR activation on Calpain1 and Calpastatin expression. Activation of LXR was shown to reduce myocardial injury susceptibility by protecting cardiomyocytes from ferroptosis. This protection occurs via relieving HG-induced ROS-mediated suppression of the AMPK/Nrf2 axis, preventing ferroptosis under hyperglycemic conditions. Moreover, pharmacological activation of LXR/RXR heterodimers was found to alleviate cardiomyocyte injury by downregulating Calpain1, a protein that induces ferroptosis through mitochondrial pathways. Mechanistically, LXR/RXR resulted in the transcriptional activation of Calpastatin, which in turn inhibited Calpain1 expression. This inhibition of Calpain1 led to reduction of mitochondrial ROS overproduction, thereby disinhibiting the AMPK/Nrf2 pathway, significantly reducing ferroptosis and myocardial injury. LXR activation protects against T2DM-induced myocardial injury by inhibiting ferroptosis, particularly through the LXR/RXR-Calpastatin-Calpain1 axis, offering a potential therapeutic strategy for T2DM-related heart damage.

Background:Coronary artery disease (CAD) is a leading cause of global mortality, primarily due to the accumulation of atheromatous plaques in coronary arteries. The current diagnostic standards include X-ray coronary angiography, which evaluates morphological features of the coronary arteries. The primary goal of this modality is to quantify stenosis severity, but variability and complexities in the resultant images make consistent interpretation challenging. This study developed a deep learning-based approach for segmenting and grading vessel stenosis via X-ray coronary angiography. Methods:Based on 383 angiographic images from 168 patients, we developed a dual-output deep convolutional neural network (CNN) to automatically diagnose stenosis. For clinical relevance, we manually annotated stenosis severity into five distinct levels: nonobstructive lesion (1-49%), intermediate lesion (50-70%), severe lesion (71-95%), sub-total occlusion (96-99%), and total occlusion (100%). Results:We built a coronary stenosis segmentation and grading method based on X-ray coronary angiography. The model achieved an average intersection over union (IoU) of 0.92, a Dice score of 0.95, a precision of 0.93, and a sensitivity of 0.96. Conclusions:We introduce an image-based vascular analysis method that localizes and grades stenosis in X-ray coronary angiography. This method can automatically identify clinically critical grades, especially within the 71-100% range. Deep learning methods can potentially facilitate the diagnosis of CAD and patient-centric treatment planning.

Backgroud: Acute myocardial infarction is mainly caused by a lack of blood flood in the coronary artery. Angiopoietin-like protein 2 (ANGPTL2) induces platelet activation and thrombus formation in vitro through binding with immunoglobulin-like receptor B, an immunoglobulin superfamily receptor. However, the mechanism by which it regulates platelet function in vivo remains unclear. Methods: In this study, we investigated the role of ANGPTL2 during thrombosis in relationship with ST-segment elevation myocardial infarction (STEMI) with spontaneous recanalization (SR). In a cohort of 276 male and female patients, we measured plasma ANGPTL2 protein levels. Using male Angptl2-knockout and wild-type mice, we examined the inhibitory effect of Angptl2 on thrombosis and platelet activation both in vivo and ex vivo. Results: We found that plasma and platelet ANGPTL2 levels were elevated in patients with STEMI with SR compared to those in non-SR (NSR) patients, and was an independent predictor of SR. Angptl2 deficiency accelerated mesenteric artery thrombosis induced by FeCL3 in Angptl2–/– compared to WT animals, promoted platelet granule secretion and aggregation induced by thrombin and collogen while purified ANGPTL2 protein supplementation reversed collagen-induced platelet aggregation. Angptl2 deficiency also increased platelet spreading on immobilized fibrinogen and clot contraction. In collagen-stimulated Angptl2–/– platelets, Src homology region 2 domain–containing phosphatase (Shp)1-Y564 and Shp2-Y580 phosphorylation were attenuated while Src, Syk, and Phospholipase Cγ2 (PLCγ2) phosphorylation increased. Conclusion: Our results demonstrate that ANGPTL2 negatively regulated thrombus formation by activating ITIM which can suppress ITAM signaling pathway. This new knowledge provides a new perspective for designing future antiplatelet aggregation therapies.

BACKGROUND:Myocardial ischemia-reperfusion injury (MIRI) poses a prevalent challenge in current reperfusion therapies, with an absence of efficacious interventions to address the underlying causes. AIM:To investigate whether the extracellular vesicles (EVs) secreted by adipose mesenchymal stem cells (ADSCs) derived from subcutaneous inguinal adipose tissue (IAT) under γ-aminobutyric acid (GABA) induction (GABA-EVsIAT) demonstrate a more pronounced inhibitory effect on mitochondrial oxidative stress and elucidate the underlying mechanisms. METHODS:We investigated the potential protective effects of EVs derived from mouse ADSCs pretreated with GABA. We assessed cardiomyocyte injury using terminal deoxynucleotidyl transferase dUTP nick end-labeling and Annexin V/propidium iodide assays. The integrity of cardiomyocyte mitochondria morphology was assessed using electron microscopy across various intervention backgrounds. To explore the functional RNA diversity between EVsIAT and GABA-EVsIAT, we employed microRNA (miR) sequencing. Through a dual-luciferase reporter assay, we confirmed the molecular mechanism by which EVs mediate thioredoxin-interacting protein (TXNIP). Western blotting and immunofluorescence were conducted to determine how TXNIP is involved in mediation of oxidative stress and mitochondrial dysfunction. RESULTS:Our study demonstrates that, under the influence of GABA, ADSCs exhibit an increased capacity to encapsulate a higher abundance of miR-21-5p within EVs. Consequently, this leads to a more pronounced inhibitory effect on mitochondrial oxidative stress compared to EVs from ADSCs without GABA intervention, ultimately resulting in myocardial protection. On a molecular mechanism level, EVs regulate the expression of TXNIP and mitigating excessive oxidative stress in mitochondria during MIRI process to rescue cardiomyocytes. CONCLUSION:Administration of GABA leads to the specific loading of miR-21-5p into EVs by ADSCs, thereby regulating the expression of TXNIP. The EVs derived from ADSCs treated with GABA effectively ameliorates mitochondrial oxidative stress and mitigates cardiomyocytes damage in the pathological process of MIRI.

Background The diameter of the ostial and proximal left main coronary artery can be greater than 5.0 mm. However, the diameters of the mostly available coronary drug-eluting stents (DESs) are ≤ 4.0 mm. Whether high-pressure dilatation can increase the diameter of stents from 4.0 to 5.0 mm and whether post-dilatation leads to longitudinal stent deformation (LSD) of 4.0-mm-diameter stents have rarely been studied. Therefore, this study aims to evaluate LSD and stent malapposition of six types of commercially available 4.0-mm-diameter stents in China in a 5.0-mm-diameter artificial blood vessel model by optical coherence tomography (OCT) in vitro. Methods The left main coronary artery was simulated by a truncated cone-shaped silicone tube. The internal diameters were 4.0 mm at one end of the silicone tube and 5.0 mm at the other end. Six different types of coronary stents widely used in China were selected for this study. Each stent was respectively implanted into the simulated blood vessel and dilated to a diameter of 4.2 mm according to the stent-balloon pressure compliance table. The stents were subjected to post-dilatation with a 5.0 × 15-mm noncompliant balloon. The LSD ratio of the longitudinal axis of each stent and stent malapposition were measured through OCT, and any fractures of the stents were determined. Results None of the six types of stents fractured following post-dilatation. The longitudinal axes of the BuMA and Excrossal stents were slightly shortened, while the other stents were elongated after high-pressure post-dilatation. All stents expanded to a diameter of 5.0 mm without incomplete stent apposition, except for the Nano Plus stent, which remained malapposed after high-pressure post-dilatation. Conclusion All 4.0-mm-diameter stents can be expanded to a diameter of 5.0 mm by noncompliant balloon post-dilatation without stent strut fracture. Most stents were found to be well apposed after high-pressure post-dilatation. However, LSD was observed after post-balloon dilatation. Stent malapposition might be positively correlated with the percentage change in stent length.

Abstract Background: Previous studies reached inconsistent conclusions about the relationship between alcohol or cigarette consumption and coronary artery calcification (CAC). We aim to explore the association between drinking and smoking with CAC in men. Methods: Male patients who underwent coronary angiography (CAG) and intravascular ultrasound (IVUS) and diagnosed with coronary heart disease (CHD) were retrospectively included. Maximum angle of calcified plaque (Arc) and calcium length were measured by IVUS to evaluate CAC severity. Drinking and smoking details were collected. Drinking and smoking were stratified to 4 layers according to weekly alcohol intake(g) and total smoking(package*years), respectively. Uni- and multivariable analysis were performed to explore the association between drinking and smoking with severe coronary artery calcification (SCAC). Results: Totally, 359 men with CHD were included, of whom 151 were regular drinkers and 275 were smokers. Compared with non-drinkers, calcium length in light drinkers decreased (P<0.05), both Arc and calcium length in moderate and heavy drinkers increased (all P<0.05). Weekly alcohol intake was positively correlated with Arc and calcium length (r=0.490, P<0.001; r=0.381, P<0.001). A negative association was found between light drinking and SCAC (OR: 0.492, 95%CI: 0.177-1.372, P=0.175), while moderate (OR: 5.244, 95%CI: 2.245-12.252, P＜0.001) and heavy drinking (OR: 15.238, 95%CI: 5.695-40.767, P＜0.001) were positively associated with SCAC. No associations were found between smoking and SCAC (P>0.05). Conclusions: Light drinking showed a slight negative association with SCAC, whereas moderate and heavy drinking were positively associated with SCAC in Chinese men. No associations were found between smoking and SCAC.

目的 探讨端粒重复因子2-P53(TRF2-P53)信号通路在糖尿病心肌病(DCM)中的作用.方法 体内研究予以链脲佐菌素(STZ)腹腔注射制造1型糖尿病小鼠模型,9周后超声检测明确DCM模型构建成功.小鼠心脏样本采用免疫印迹(WB)检测TRF2表达水平,采用免疫荧光检测P53表达水平.体外研究予以高糖刺激乳鼠心肌细胞,并采用WB检测TRF2表达水平,采用免疫荧光检测P53表达水平.TRF2 siRNA降低乳鼠心肌细胞TRF2的表达后,采用TUNEL检测凋亡情况,采用衰老相关-β-半乳糖苷酶(SA-β-gal)染色检测衰老情况,采用WB检测P53表达水平.结果 体内研究发现,与WT小鼠相比,DCM小鼠TRF2表达下降,P53表达增加.体外研究发现,高糖刺激引起乳鼠心肌细胞TRF2表达下降,P53表达增加.TRF2 siRNA转染降低乳鼠心肌细胞TRF2水平后可促进凋亡和衰老,增加P53表达.结论 TRF2-P53信号通路在DCM中起了重要的调控作用.

目的:分析老年代谢异常动脉粥样硬化性心血管疾病(ASCVD)风险等级及血脂达标的影响因素.方法:依据是否存在代谢异常,16305例60岁以上ASCVD患者被分为代谢异常组(14778例)与代谢正常组(1527例).比较两组一般临床资料,分析代谢异常因素与ASCVD风险等级的相关性及代谢异常ASCVD高危患者LDL-C水平达标的影响因素.结果:与代谢正常组比较,代谢异常组女性、城市居民比例,年龄、腰围、BMI、收缩压、舒张压、平均动脉压(MAP)、空腹血糖(FBG),总胆固醇、LDL-C、TG水平均显著升高,吸烟比例、HDL-C水平均显著降低(P＜0.05或＜0.01).Spearman相关性分析显示,ASCVD危险等级与FBG、TG呈显著正相关(r=0.206～0.365,P 均=0.001),与 HDL-C、MAP、腰围呈显著负相关(r=-0.051～-0.221,P均=0.001).多因素Logistic回归分析显示,代谢异常累积个数3、4、5种是代谢异常ASCVD高危患者的独立危险因素(OR=1.686～2.447,P＜0.05或＜0.01).结论:血脂、血糖水平等代谢异常是ASCVD的独立危险因素.

BACKGROUND Intermediate coronary lesions (40-70% stenosis) present a higher risk for future cardiovascular events for instability of plaques. Shortened telomere is an indicator of cellular senescence, which is associated with age-related diseases. However, the relationship between telomere length and severity of intermediate coronary lesions remains largely unknown. METHODS A total of 121 lesions of 121 patients with intermediate coronary disease that underwent intravascular optical coherence tomography were enrolled. These patients were retrospectively divided into two groups according to whether accept percutaneous coronary intervention (PCI) treatment: non-PCI group and PCI group. RESULTS Leukocyte telomere length (LTL) in patients of PCI group were significantly shorter (12.54±2.70 vs. 15.32±3.72 kb, P<0.001) than non-PCI group. The PCI group had longer lipid length (17.17±9.94 vs. 12.21±10.15 mm, P=0.01) and greater lipid index (4,286.82±3,012.54 vs. 2,444.87±2,677.59 °*mm, P<0.001). There was a significant difference in the prevalence of thin-cap fibroatheroma (36.6% vs. 16.0%, P=0.013), macrophages (56.3% vs. 38.0%, P=0.047), plaque rupture (23.9% vs. 6.0%, P=0.009), cholesterol crystal (49.3% vs. 30.0%, P=0.034), dissection (23.9% vs. 4.0%, P=0.003) between PCI and non-PCI group. Logistic regression revealed that LTL was independently associated with PCI after adjusting for confounding factors (OR 0.952, CI: 0.930-0.974, per 1unit increase, P<0.001). Receiver operating characteristic (ROC) analysis revealed a LTL area under the ROC curve (AUC) of 0.714 (95% CI: 0.619-0.808, P<0.001) in the study population. Furthermore, LTL was inversely correlated with lipid length (r =-0.190, P=0.037), lipid arc (r =-0.301, P=0.001), lipid index (r =-0.182, P=0.046), and positive correlation with FCT (r =0.213, P=0.034). CONCLUSIONS LTL was independently associated with possibility of receiving PCI in intermediate coronary lesion patients and LTL is also significantly related to plaque instability features that evaluated by optical coherence tomography. LTL may be as an indicator to assess the necessity of PCI in intermediate coronary lesion patients.

目的:探讨上海市60岁以上高血压患者动脉粥样硬化性心血管病(ASCVD)危险分层及血脂达标情况,和ASCVD高危患者LDL-C水平未达标的影响因素.方法:13735例60岁以上无ASCVD病史的体检者被分为非高血压组(7125例)与高血压组(6610例),比较两组一般资料.依据ASCVD危险分层评估,3925例LDL-C水平未达标的高血压患者被分为ASCVD低危组(554例)、中危组(42例)与高危组(3329例),比较各组间血脂水平.依据LDL-C水平是否达标,分析高血压ASCVD高危患者LDL-C水平未达标的影响因素.结果:与非高血压组比较,高血压组女性、吸烟、慢性肾脏病(CKD)比例,年龄、腰围、BMI、SBP、DBP、FBG、TC、TG水平均显著升高,农村人员、合并DM比例均显著降低(P均=0.001).与ASCVD低危组比较,ASCVD中危组、高危组TC、LDL-C、HDL-C水平均显著降低;与ASCVD中危组比较,ASCVD高危组上述血脂水平均显著升高(P<0.05或<0.01).多因素Lsgiotic回归分析显示,女性、农村人员、吸烟是ASCVD高危患者LDL-C水平未达标的独立危险因素(OR=2.169～3.643,P均=0.001),高龄、合并DM、合并CKD是其独立保护因素(OR=0.192～0.728,P<0.05或<0.01).结论:上海市60岁以上高血压ASCVD高危患者血脂达标率低、女性、农村人员、吸烟是此类患者LDL-C水平未达标的独立危险因素.

目的:调查社区全科医生对房颤的诊疗能力及继续教育对诊疗水平提升的效果.方法:随机选择962名社区全科医生,分别来自上海市的6个区域,组成6个组,比较各组调查问卷得分、培训前后对房颤认识的正确率.结果:社区全科医生对于房颤诊疗知识的掌握程度在不同区域、全科类别、年龄、学历、职称之间有显著差异,P＜0.05或＜0.01.与培训前比较,培训后全科医生对房颤主要并发症的认识(56.13％比86.63％)、抗凝治疗重要性认识(47.40％比77.01％)、CHA2DS2-VASC评分的认识(60.29％比78.40％)、抗凝治疗指征的认识(40.23％比60.69％)、抗凝药物的识别(42.83％比61.07％)、合并慢性心衰治疗的认识(3.22％比13.26％)、房颤出血评分系统的认识(43.04％比64.06％)、控制心室率药物的选择(49.06％比61.50％)和复律治疗认识的正确率(39.71％比75.19％)均显著升高(P均=0.001).结论:社区全科医生房颤诊疗水平存在不足,且受城市不同区域、学历、职称、年龄、全科类别影响;有针对性培训可显著提高诊疗能力.

BACKGROUND Extracellular vesicles (EVs) derived from hypoxia-preconditioned (HP) mesenchymal stem cells (MSCs) have better cardioprotective effects against myocardial infarction (MI) in the early stage than EVs isolated from normoxic (NC)-MSCs. However, the cardioprotective mechanisms of HP-EVs are not fully understood. AIM To explore the cardioprotective mechanism of EVs derived from HP MSCs. METHODS We evaluated the cardioprotective effects of HP-EVs or NC-EVs from mouse adipose-derived MSCs (ADSCs) following hypoxia in vitro or MI in vivo, in order to improve the survival of cardiomyocytes (CMs) and restore cardiac function. The degree of CM apoptosis in each group was assessed by the terminal deoxynucleotidyl transferase dUTP nick end-labeling and Annexin V/PI assays. MicroRNA (miRNA) sequencing was used to investigate the functional RNA diversity between HP-EVs and NC-EVs from mouse ADSCs. The molecular mechanism of EVs in mediating thioredoxin-interacting protein (TXNIP) was verified by the dual-luciferase reporter assay. Co-immunoprecipitation, western blotting, and immunofluorescence were performed to determine if TXNIP is involved in hypoxia-inducible factor-1 alpha (HIF-1α) ubiquitination and degradation via the chromosomal region maintenance-1 (CRM-1)-dependent nuclear transport pathway. RESULTS HP-EVs derived from MSCs reduced both infarct size (necrosis area) and apoptotic degree to a greater extent than NC-EVs from CMs subjected to hypoxia in vitro and mice with MI in vivo. Sequencing of EV-associated miRNAs showed the upregulation of 10 miRNAs predicted to bind TXNIP, an oxidative stress-associated protein. We showed miRNA224-5p, the most upregulated miRNA in HP-EVs, directly combined the 3’ untranslated region of TXNIP and demonstrated its critical protective role against hypoxia-mediated CM injury. Our results demonstrated that MI triggered TXNIP-mediated HIF-1α ubiquitination and degradation in the CRM-1-mediated nuclear transport pathway in CMs, which led to aggravated injury and hypoxia tolerance in CMs in the early stage of MI. CONCLUSION The anti-apoptotic effects of HP-EVs in alleviating MI and the hypoxic conditions of CMs until reperfusion therapy may partly result from EV miR-224-5p targeting TXNIP.

Objective: This retrospective cohort study aimed to evaluate the effect of post-dilation on coronary blood flow and MACE events during hospitalization and 1 year follow-up following primary PCI in patients with ST-segment. Methods: 419 eligible patients who underwent PPCI due to STEMI between January 2015 and October 2019 were enrolled. The CTFC, final QCA, and the incidence of no-reflow/slow-flow during different procedure moments were assayed. Study end points was to compare two groups of patients with clinical characteristics, compared two groups of patients with the incidence of no-reflow and slow-flow, and the incidence of MACE during hospitalization and 1-year follow-up. Results: The incidence of final no-reflow/slow-flow in the post-dilation group was not significantly higher than that in the non-post-dilation group (24.3％ vs.19.4％; p = 0.238).There was no significant statistical difference in MACE events during hospitalization, but for the 1-year follow-up, the incidence of Target vessel revascularization and Target lesion revascularization in the post-dilation group was lower than that in the non-post-dilation group. A multivariable logistic regression model revealed that age (OR=1.078, 95％CI=1.038-1.120; P <0.001), history of diabetes (OR=3.009, 95％CI=1.183-7.654; P =0.021), post-dilation (OR=0.192, 95％CI=0.067-0.549; P=0.002) were independently correlated with long-term follow-up of MACE.Conclusion: Post-dilation does not increase poor prognosis during hospitalization, and reduces the incidence of TVR and TLR events during long-term follow-up.

Background Telomere shortening, an indicator of aging, is associated with age-related diseases. This study aims to investigate the association between leukocyte telomere length (LTL) and thin-capped fibroatheromata (TCFA) and the impact of using LTL cutoff to determine the incidence of major adverse cardiovascular events (MACEs) in patients with angiographically intermediate coronary lesions. Methods This was a signal-center retrospective study focusing on patients who underwent coronary angiography and optical coherence tomography (OCT). The degree of coronary stenosis was assessed by angiography. The presence of TCFA was determined by OCT imaging. A total of 156 patients with angiographically intermediate coronary lesions were enrolled. Results Leukocyte telomere lengths were significantly shorter in the TCFA group compared with non-TCFA group [11.95 (10.56, 15.21) kb vs. 13.81 (12.06, 16.11) kb, p = 0.003]. The short-LTL group and long-LTL group were divided according to the optimal cut-off value which was determined by the receiver operating characteristic (ROC) curve analysis. Logistic regression model revealed that short-LTL was independently associated with TCFA incidence (odds ratio [OR] 4.387, 95% CI: 1.902–10.120, p = 0.001) after adjusting for confounding factors. Over a 24-months follow-up, the MACE incidence among patients with short-LTL was significantly higher than those in the long-LTL group (12.5 vs. 2.0%, p = 0.006 by log-rank test). Multivariable cox regression analysis indicated that short-LTL (hazard ratio [HR] 9.716, 95% CI: 1.995–47.319, p = 0.005) was an independent prognostic factor of MACE incidence in angiographically intermediate coronary lesions patients. Conclusions Short-LTL was independently associated with the incidence of TCFA and may serve as a prognostic factor for MACE risk on top of conventional risk factors.

Liver-X-receptor (LXR) has previously been shown to exert a cardioprotective effect against the development of diabetic cardiomyopathy (DCM) associated with a reduction in mitochondrial dysfunction. However, the underlying mechanism by which LXR activation attenuates the structural and functional mitochondrial impairments caused by high glucose (HG) stress remains unclear. We demonstrate here that LXR activation inhibits HG stress-induced mitochondrial dysfunction and ameliorates aberrant mitochondrial dynamics. Furthermore, LXR activation regulates mitochondrial dynamics by inhibiting HG stress-induced upregulation of Calpain1 expression. These data indicate that amelioration of Calpain1-mediated aberrant mitochondrial dynamics may be at least part of the mechanism underlying the cardioprotective effects of LXR against HG stress. Therefore, LXR is a potentially attractive molecular target for treating cardiac mitochondrial dysfunction in patients with diabetes.

Background Serum free fatty acid (FFA) concentrations are associated with coronary heart disease and diabetes mellitus (DM). Few studies focused on the relationship between serum FFA levels and coronary artery calcification (CAC). Methods This was a retrospective, single-centered study recruiting patients underwent FFA quantification, coronary angiography and intravascular ultrasound (IVUS). CAC severity was assessed with the maximum calcific angle (arc) of the calcified plaque scanned by IVUS. Patients with an arc ≥ 180° were classified into the severe CAC (SCAC) group, and those with an arc < 180° were classified into the non-SCAC group. Clinical characteristics, serum indices were compared between 2 groups. Logistic regression, receiver operating characteristic (ROC) curves and area under the curves (AUC) were performed. Results Totally, 426 patients with coronary artery disease were consecutively included. Serum FFA levels were significantly higher in the SCAC group than non-SCAC group (6.62 ± 2.17 vs. 5.13 ± 1.73 mmol/dl, p < 0.001). Logistic regression revealed that serum FFAs were independently associated with SCAC after adjusting for confounding factors in the whole cohort (OR 1.414, CI 1.237–1.617, p < 0.001), the non-DM group (OR 1.273, CI 1.087–1.492, p = 0.003) and the DM group (OR 1.939, CI 1.388–2.710, p < 0.001). ROC analysis revealed a serum FFA AUC of 0.695 (CI 0.641–0.750, p < 0.001) in the whole population. The diagnostic predictability was augmented (AUC = 0.775, CI 0.690–0.859, p < 0.001) in the DM group and decreased (AUC = 0.649, CI 0.580–0.718, p < 0.001) in the non-DM group. Conclusions Serum FFA levels were independently associated with SCAC, and could have some predictive capacity for SCAC. The association was strongest in the DM group.

Background: The contemporary incidence of heart failure (HF) in patients with coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI) remains unclear. This prospective cohort study was designed to study the incidence and predictors of new-onset HF in CAD patients after PCI (ChiCTR1900023033). Methods: From January 2014 to December 2018, 3,910 CAD patients without HF history undergoing PCI were prospectively enrolled. Demographics, medical history, cardiovascular risk factors, cardiac parameters, and medication data were collected at baseline. Multivariable adjusted competing-risk regression analysis was performed to examine the predictors of incident HF. Results: After a median follow-up of 63 months, 497 patients (12.7%) reached the primary endpoint of new-onset HF, of which 179, 110, and 208 patients (36.0, 22.1, and 41.9%) were diagnosed as having HF with reduced ejection fraction (EF) (HFrEF), HF with mid-range EF (HFmrEF), and HF with preserved EF (HFpEF), respectively. Higher B-type natriuretic peptide (BNP) or E/e′ level, lower estimated glomerular filtration rate (eGFR) level, and atrial fibrillation were the independent risk factors of new-onset HF. Gender (male) and angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker (ACEI/ARB) prescription were the negative predictors of new-onset HF. Moreover, it was indicated that long-term ACEI/ARB therapy, instead of beta-blocker use, was linked to lower risks of development of all three HF subtypes (HFrEF, HFmrEF and HFpEF). Conclusions: This prospective longitudinal cohort study shows that the predominant subtype of HF after PCI is HFpEF and ACEI/ARB therapy is accompanied with reduced risks of incident HF across three subtypes.

Our study was aimed to investigate the effects of lgals3a (Gal-3 encoding gene) on the development of zebrafish embryo and its underlying mechanisms. Morpholino (MO) technology was used to inhibit the expression of zebrafish lgals3a, and the effect of lgals3a gene knockdown on zebrafish embryo development and the number of monocyte macrophages was observed. Effect of lgals3a-e3i3-MO on apoptosis of zebrafish was detected by acridine orange staining. In addition, the mRNA expression levels of Wnt/β-catenin signaling pathway-related genes were detected by RT-qPCR. Compared with control-MO group, the zebrafish embryos injected with lgals3a-e3i3-MO had obvious defects in the head, eyes, and tail, and pericardial edema. Lgals3a-e3i3-MO significantly reduced the number of mononuclear macrophages in zebrafish embryos compared with the control-MO group. The results of acridine orange staining showed that compared with the control-MO group, lgals3a-e3i3-MO promoted cardiomyocyte apoptosis in zebrafish. Furthermore, lgals3a-e3i3-MO significantly up-regulated the expression of dkk1b, wnt9a, lrp5, fzd7a, β-catenin, Gsk-3β, mycn, myca in the Wnt/β-catenin pathway, and decreased the expression of lef1. These results indicate that lgals3a-e3i3-MO inhibits zebrafish embryo development, reduces the number of mononuclear macrophages, activates Wnt/β-catenin signaling pathway and promotes cardiomyocyte apoptosis.