A high-fat diet (HFD) is a well-established risk factor for coronary artery disease (CAD). Accumulating evidence indicates that maternal nutritional status before and during pregnancy critically influences long-term cardiovascular outcomes in offspring. This review systematically synthesizes current mechanistic, epidemiological, and clinical evidence regarding the impact of HFD on CAD while also examining its effects on broader cardiovascular phenotypes that are integral to CAD pathogenesis, such as endothelial dysfunction, cardiac remodeling, and metabolic derangements. A particular focus is placed on the potential effects of maternal pre-pregnancy HFD exposure on offspring CAD risk in adulthood. Existing studies suggest that HFD induces coronary injury primarily through metabolic dysregulation, endothelial dysfunction, and epigenetic reprogramming. Notably, maternal exposure to HFD during the perinatal period may predispose offspring to coronary artery disease via these mechanisms. Conversely, appropriate maternal nutritional interventions during pregnancy have shown promise in mitigating these adverse effects, although their long-term efficacy and underlying molecular mechanisms remain to be fully elucidated. Future research should prioritize large-scale prospective cohort studies with extended follow-up to determine the optimal timing, mechanisms, and efficacy of dietary interventions. Such evidence would provide a scientific foundation for developing preventive and therapeutic strategies aimed at reducing cardiovascular disease risk from the earliest developmental stages.

IntroductionThe molecular mechanisms underlying cardioprotection against doxorubicin (DOX)-induced myocardial injury are poorly understood. Histone deacetylase 2 (HDAC2) plays a significant role in oxidative stress, apoptosis, and mitochondrial dysfunction and is implicated in many human diseases, This study investigated the relationship between HDAC2 expression and DOX-induced myocardial injury using the in vivo rat model of DOX-induced cardiotoxicity and in vitro experiments with the H9c2 cardiomyocytes.MethodsThe rat model of DOX-induced myocardial injury was established by administering DOX via intraperitoneal injections. HDAC2 expression was suppressed by administering rats with sodium butyrate (SB) via intraperitoneal injections. Echocardiography measurements were performed at baseline and on day 15 post-treatment. The rats were euthanized on day 15 and cardiac tissues were harvested. The cardiac tissue samples were analyzed by hematoxylin and eosin H&E staining, immunohistochemistry, Masson staining, Sirius Red staining, TUNEL staining, and western blotting to determine the status of HDAC2 expression and myocardial apoptosis. In the vitro experiments, H9c2 cells were treated with DOX. HDAC2 expression was suppressed using sodium butyrate or transfected cells with the shRNA knockdown HDAC2 (shHDAC2). The H9c2 cells from different groups were analyzed by Rt-qPCR, CCK-8 cell viability assay, and western blotting to determine the status of HDAC2 expression and cardiomyocyte apoptosis.ResultsDOX treatment induced cardiac dysfunction in rats. The cardiac tissues of the DOX-treated rats and H9c2 cells showed significantly higher levels of HDAC2 compared to the corresponding controls. However, inhibition of HDAC2 significantly mitigated DOX-induced myocardial injury in rats. This suggested a strong association between HDAC2 expression and DOX-induced myocardial injury. In the H9c2 cells, HDAC2 knockdown by shHDAC2 alleviated DOX-induced apoptosis by enhacing AKT phosphorylation. These findings demonstrated that HDAC2 silencing protected against DOX-induced cardiomyocyte apoptosis by activating the PI3K/AKT signaling pathway.ConclusionSuppressing HDAC2 protected against DOX-induced cardiomyocyte apoptosis by activating the PI3K/AKT signaling pathway. Therefore, HDAC2 is a promising therapeutic target for mitigating DOX-induced myocardial injury.

Introduction:Transducin beta-like 1 X-linked receptor 1 (TBL1XR1) is significantly upregulated in the peripheral blood of patients with coronary artery disease (CAD). This study aimed to validate the differential expression of TBL1XR1 in CAD and investigate its role in CAD progression using RNA interference. Methods:The expression of TBL1XR1 at the mRNA and protein levels was detected in patients with CAD and controls using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. Additionally, the effects of TBL1XR1 gene silencing in human liver cells through RNA interference on PPARα expression and intracellular triglyceride (TG) levels were determined. Results:TBL1XR1 expression was significantly higher in the peripheral blood of CAD patients compared to controls at both mRNA (1.71 ± 0.96 vs. 1.00 ± 0.34, p < 0.01) and protein levels (0.41 ± 0.19 vs. 0.13 ± 0.07, p = 0.038). Logistic regression analysis revealed that high TBL1XR1 expression is an independent risk factor for CAD. Relative TBL1XR1 expression positively correlated with serum TG levels (rs = 0.56, p < 0.01) and Gensini score (rs = 0.53, p < 0.01), indicating an association with CAD severity. In human liver cells, TBL1XR1 silencing significantly increased peroxisome proliferator-activated receptor alpha (PPARα) expression at both mRNA (p < 0.05) and protein levels (p < 0.01) while reducing intracellular TG levels (0.24 ± 0.16 vs. 0.51 ± 0.09, p < 0.01). Conclusion:TBL1XR1 is a key factor for risk assessment, diagnosis, and evaluating coronary lesion severity in patients with CAD. Its role in promoting atherosclerosis initiation and development may be associated with regulation of TG metabolism via the PPARα pathway.

BackgroundThe transmembrane protein Notch1 is associated with cell growth, development, differentiation, proliferation, apoptosis, adhesion, and the epithelial mesenchymal transition. Proteomics, as a research method, uses a series of sequencing techniques to study the composition, expression levels, and modifications of proteins. Here, the association between Notch1 and acute myocardial infarction (AMI) was investigated using proteomics, to assess the possibility of using Notch1 as a biomarker for the disease.MethodsFifty-five eligible patients with AMI and 74 with chronic coronary syndrome (CCS) were enrolled, representing the experimental and control groups, respectively. The mRNA levels were assessed using RT-qPCR and proteins were measured using ELISA, and the results were compared and analyzed.ResultsNotch1 mRNA levels were 0.52 times higher in the peripheral blood mononuclear cells of the AMI group relative to the CCS group (p < 0.05) while Notch1 protein levels were 0.63 times higher in peripheral blood plasma in AMI patients (p < 0.05). Notch1 levels were not associated with older age, hypertension, smoking, high abdominal-blood glucose, high total cholesterol, and high LDL in AMI. Logistic regression indicated associations between AMI and reduced Notch1 expression, hypertension, smoking, and high fasting glucose.ConclusionsNotch1 expression was reduced in the peripheral blood of patients with AMI relative to those with CCS. The low expression of Notch1 was found to be an independent risk factor for AMI and may thus be an indicator of the disease.

Atherosclerosis refers to a disease characterized by the formation of lipid plaque deposits within arterial walls, leading to reduced blood flow or blockage of blood outflow. The process of endothelial injury induced by oxidized low‐density lipoprotein (ox‐LDL) is considered the initial stage of atherosclerosis. Ferroptosis is a form of iron‐dependent, non‐apoptotic cell death, and current research suggests its association with coronary artery disease (CAD). In this study, we observed a correlation between reduced expression of SREBP‐1 and the occurrence of stable CAD. Additionally, during the process of endothelial injury induced by ox‐LDL, we also noted decreased expression of the SREBP‐1/SCD1/FADS2 and involvement in the ferroptosis process. Mechanistically, ox‐LDL induced endothelial injury by inhibiting the lipid biosynthesis process mediated by the SREBP‐1/SCD1/FADS2, thereby inducing lipid peroxidation and ferroptosis. On the contrary, overexpression of SREBP‐1 or supplementation with monounsaturated fatty acids counteracted iron accumulation, mitochondrial damage, and lipid peroxidation‐induced ferroptosis, thereby improving endothelial injury. Our study indicated that the decreased expression of peripheral blood SREBP‐1 mRNA is an independent risk factor for stable CAD. Furthermore, in endothelial cells, the lipid biosynthesis process mediated by SREBP‐1 could ameliorate endothelial injury by resisting ferroptosis. The study has been registered with the Chinese Clinical Trial Registry, which serves as a primary registry in the World Health Organization International Clinical Trials Registry Platform (ChiCTR2300074315, August 3rd, 2023).

The phenomenon of polypharmacy is a common occurrence among older people with multiple health conditions due to the rapid increase in population aging and the popularization of clinical guidelines. The prevalence of metabolic syndrome is growing quickly, representing a serious threat to both the public and the worldwide healthcare systems. In addition, it enhances the risk of cardiovascular disease as well as mortality and morbidity. Sterol regulatory element binding proteins (SREBPs) are basic helix-loop-helix leucine zipper transcription factors that transcriptionally modulate genes that regulate lipid biosynthesis and uptake, thereby serving an essential role in biological systems regulation. In this article, we have described the structure of SREBPs and explored their activation and regulation of signals. We also reveal that SREBPs are intricately involved in the modulation of metabolic diseases and thus have tremendous potential as the novel target for single-drug therapy for multiple diseases.

Objective To explore the predictive value of serum amyloid A1(SAA1)in acute myocardial infarction(AMI).Methods A total of 139 patients with AMI and 146 patients with non coronary atherosclerotic heart disease admitted to the China-Japan Union Hospital of Jilin University from September 2017 to April 2019 were selected as the research objects.Enzyme linked immunosorbent assay(ELISA)was used to determine the level of SAA1 in plasma.Logistic regression was used to analyze the independent influencing factors of AMI,and receiver operating characteristic(ROC)curve was used to analyze the value of SAA1 in the diagnosis of AMI.Results The level of SAA1 in the AMI group was lower than that in the control group[2.62(2.08,3.21)ng/mL vs 5.18(3.24,8.27)ng/mL,Z=10.169,P＜0.05].The decrease in SAA1 level was correlated with high-density lipoprotein cholesterol,white blood cell count,and neutrophils/lymphocytes.Multi variate logistic regression analysis showed that the decreased SAA1 level was an independent risk factor for AMI occurrence.The ROC curve indicated that the cut-off value of SAA1 for diagnosing AMI was 3.14 ng/mL,and the AUC was 0.847,and the sensitivity and specificity were 76.1％and 80.1％,respectively.Conclusion The plasma levels of SAA1 decrease in AMI patients,and SAA1 levels may serve as an independent predictor of AMI.

Pneumatosis of the portal vein is considered a rare imaging sign rather than a disease. It usually occurs in patients with digestive tract diseases such as intestinal obstructive diseases, mesenteric vascular diseases, closed abdominal trauma, and liver transplantation. Because of its high mortality rate, it is also termed the “sign of death.” Hawthorn contains tannic acid, and seafood is rich in calcium, iron, carbon, iodine, and other minerals and proteins. Thus, consuming both hawthorn and seafood together can result in the formation of an indigestible complex in the body, acting as the main pathogenic factor in patients with intestinal obstruction. We herein describe a patient with duodenal obstruction caused by hawthorn who developed the hepatic portal venous gas sign and was cured by nonsurgical treatment.

Abnormal or excessive accumulation of adipose tissue leads to a condition called obesity. Long-term positive energy balance arises when energy intake surpasses energy expenditure, which increases the risk of metabolic and other chronic diseases, such as atherosclerosis. In industrialized countries, the prevalence of coronary heart disease is positively correlated with the human development index. Atherosclerotic cardiovascular disease (ACD) is among the primary causes of death on a global scale. There is evidence to support the notion that individuals from varied socioeconomic origins may experience varying mortality effects as a result of high blood pressure, high blood sugar, raised cholesterol levels, and high body mass index (BMI). However, it is believed that changes in the concentration of trace elements in the human body are the main contributors to the development of some diseases and the transition from a healthy to a diseased state. Metal trace elements, non-metal trace elements, and the sampling site will be examined to determine whether trace elements can aid in the diagnosis of atherosclerosis. This article will discuss whether trace elements, discussed under three sections of metal trace elements, non-metal trace elements, and the sampling site, can participate in the diagnosis of atherosclerosis.

Purpose ZCCHC9 is a zinc finger protein with a CCHC zinc finger structure and has important roles in several cellular processes. This study was conducted on an expanded number of samples to evaluate The usefulness of ZCCHC9 gene expression in peripheral blood as a molecular marker for the prediction of AMI (acute myocardial infarction) risk. Patients and Methods Peripheral blood samples were collected from 117 patients with stable CAD (coronary atherosclerotic disease) and 126 patients with AMI. The mRNA level of the ZCCHC9 gene was assessed by qRT-PCR, and its protein level was determined by Western blotting. Results The AMI group exhibited reduced expression of the ZCCHC9 gene, at both transcript and protein levels, than the stable CAD group. The low expression of the ZCCHC9 gene was not related to blood glucose level (P=0.635), blood lipid level, and troponin level (P=0.715), and may cause AMI through the MAPK signaling pathway. Compared with other patients, patients with low ZCCHC9 gene expression in their peripheral blood have a 2.597-fold higher risk of AMI. Conclusion ZCCHC9 gene expression in peripheral blood was significantly lower in patients with AMI than in stable CAD patients. Individuals with low expression of ZCCHC9 in peripheral blood have higher a probability to develop AMI than those with stable CAD. Thus, lowered ZCCHC9 gene expression can act as an independent risk factor for AMI.

Coronary atherosclerosis is a potentially chronic circulatory condition that endangers human health. The biological cause underpinning cardiovascular disease is coronary atherosclerosis, and acute cardiovascular events can develop due to thrombosis, platelet aggregation, and unstable atherosclerotic plaque rupture. Coronary atherosclerosis is progressive, and three specific changes appear, with fat spots and stripes, atherosclerosis and thin-walled fiber atherosclerosis, and then complex changes in arteries. The progression and severity of cardiovascular disease are correlated with various levels of calcium accumulation in the coronary artery. The therapy and diagnosis of coronary atherosclerosis benefit from the initial assessment of the size and degree of calcification. This article will discuss the new progress in the early diagnosis of coronary atherosclerosis in terms of three aspects: imaging, gene and protein markers, and trace elements. This study intends to present the latest methods for diagnosing patients with early atherosclerosis through a literature review.

Background: Previous microarray analysis on peripheral blood leukocytes from three patients with acute myocardial infarction (AMI) showed that elevated expression of membrane bound o-acyltransferase domain containing 7(MBOAT7) relative to control. To further verify these findings, we investigated more patients and explored the possible mechanisms in vitro. Objective: To study alterations in MBOAT7 expression in leukocytes after AMI, and to explore the relationship between MBOAT7 and lipid metabolism pathways in hepatocytes in vitro. Methods: Ninety patients with AMI and 90 controls were recruited from the Han population in Northeast China. RT-fluorescent PCR was used to measure MBOAT7 mRNA levels. MBOAT7 interference and overexpression vectors were constructed and transfected into L-02 hepatocytes and expression was examined by RT-qPCR and western blotting. The expression of SCAP, LDLR, HMGCR, ACAT1, ABCA1, SREBP1, ACC, FAS, SCD, and PPARγ in the lipid metabolism pathway were investigated by RT-qPCR. Triglyceride and cholesterol levels were measured by ELISA. Results: It was found that MBOAT7 mRNA levels were elevated in the leukocytes of patients with AMI. Hepatocytes were successfully transfected, shown by attenuated MBOAT7 mRNA levels in the silenced group (0.41±0.04 vs 1.01±0.07 for control, P=0.0019 <0.01) and raised levels in the overexpressing cells (23.29±0.39 vs 1.00±0.06 for control, P <0.0001). These results were confirmed by western blotting. Expression of the lipid metabolism-related genes was altered in response to MBOAT7 expression. Triglyceride levels increased after MBOAT7 silencing (118.40 ± 2.26 vs 70.54 ± 0.25 for control, P<0.0001), as did those of cholesterol (628.30 ± 8.89 vs 544.70 ± 11.04, P = 0.0041) but were not altered on MBOAT7 overexpression. Conclusion: MBOAT7 did not affect the metabolism of triglycerides in hepatocytes through fatty acid synthesis and decomposition pathways. The MBOAT7 level in the peripheral blood can be used as a marker for acute myocardial infarction but cannot be used as a single therapeutic target to regulate lipid metabolism.

This study aimed to determine the amount of expression of the ATP-binding cassette subfamily B member 1 (ABCB1) gene chip as a prospective diagnostic marker for acute myocardial infarction (AMI) in a wide population . In the AMI and control groups, 113 patients with AMI and 83 persons with non-coronary artery disease were selected for peripheral venous leukocyte collection. Western blot and real-time polymerase chain reaction (RT-PCR) were employed to detect relative ABCB1 expression in both groups. The results showed that the ABCB1 transcription and protein levels in the AMI group were higher than in the control. The relative mRNA expression of ABCB1 was 0.26 (0.03-0.79) in the AMI group and 0.13 (0.01-0.52) in the control group (P < 0.05). The expression of the ABCB1 gene at the protein level in the AMI group was 1.65 times that in the control (P < 0.05). Further, the subjects in the AMI group were older (P < 0.001), had lower levels of high-density lipoprotein cholesterol (P = 0.038), and had higher incidence of type II diabetes mellitus (P = 0.003) compared with the control. Logistic regression analysis showed that the expression of ABCB1 in peripheral blood was correlated with the occurrence of AMI (P = 0.003). High ABCB1 expression, type II diabetes, and advanced age were found to serve as potential independent risk factors for AMI, with a 4.88-fold, 2.99-fold, and 2.63-fold increased risk of AMI. Overall, the high expression of ABCB1 in peripheral blood might be related to the occurrence of AMI.

(1) Background: Obesity and diabetes continue to reach epidemic levels in the population with major health impacts that include a significantly increased risk of coronary atherosclerosis. The imbalance of trace elements in the body caused by nutritional factors can lead to the progression of coronary atherosclerosis. (2) Methods: We measured the concentrations of sodium (Na), potassium (K), magnesium (Mg), calcium (Ca), Zinc (Zn), and iron (Fe) in peripheral blood samples from 4243 patients and performed baseline analysis and propensity matching of the patient datasets. The patients were grouped into acute myocardial infarction (AMI, 702 patients) and stable coronary heart disease (SCAD1, 253 patients) groups. Both of these groups were included in the AS that had a total of 1955 patients. The control group consisted of 2288 patients. The plasma concentrations of calcium, magnesium, and iron were measured using a colorimetric method. For comparison, 15 external quality assessment (EQA) samples were selected from the Clinical Laboratory Center of the Ministry of Health of China. SPSS software was used for statistical analysis. The average values and deviations of all of the indicators in each group were calculated, and a p-value threshold of <0.05 was used to indicate statistical significance. (3) Results: The iron ion concentrations of the acute myocardial infarction (AMI) group were significantly lower than the control group (p < 0.05, AUC = 0.724, AUC = 0.702), irrespective of tendency matching. Compared to the data from the stable coronary artery disease (SCAD) group, the concentration of iron ions in the acute myocardial infarction group was significantly lower (p < 0.05, AUC = 0.710, AUC = 0.682). Furthermore, the iron ion concentrations in the (AMI + SCAD) group were significantly lower (p < 0.05) than in the control group. (4) Conclusions: The data presented in this study strongly indicate that the concentration of iron ions in the peripheral blood is related to coronary atherosclerosis. Decreases in the levels of iron ions in the peripheral blood can be used as a predictive biomarker of coronary atherosclerosis.

BACKGROUND:Thrombospondin (THBS) 3 is an adhesive glycoprotein involved in cell-cell and cell-matrix interactions. The purpose of this study is to determine whether THBS3 expression in peripheral blood can be used as a biomarker to predict the risk of acute myocardial infarction (AMI).METHODS:The peripheral blood of 111 patients with stable coronary artery disease (SCAD) and 112 patients with AMI was obtained. The experimental and the control cohorts were the AMI and SCAD groups, respectively. The expression of THBS3 mRNA and protein in both groups was determined using reverse-transcription polymerase chain reaction and enzyme-linked immunosorbent assay.RESULTS:THBS3 expression (range) in the peripheral plasma of patients in the AMI group was lower than that of patients in the SCAD group (4.526 (3.748-5.521), 5.511 (4.726-6.334), respectively), which was 0.82 times lower than the control (p < 0.001). Furthermore, THBS3 mRNA level in the peripheral blood mononuclear cells of patients with AMI was 0.47 times lower than that in patients with SCAD (p < 0.05). AMI was associated with fasting blood glucose levels, platelet counts and low THBS3 expression. Logistic regression analysis revealed that decreased expression of THBS3 protein increased the probability of AMI by 4.076 times (p < 0.01). Additionally, high fasting blood glucose and high platelet counts increased the risk of AMI by 2.819 and 6.515 times, respectively (p < 0.05).CONCLUSIONS:THBS3 mRNA and protein levels in the peripheral blood of patients in the AMI group were much lower compared with those of patients in the SCAD group. Low THBS3 expression in peripheral blood was related to AMI and was an independent risk factor for AMI. Thus, low THBS3 expression in peripheral blood may be a novel, suitable molecular marker for the early detection of AMI.

The COVID-19 pandemic can be seen as a traumatic event during which time medical students have been required to perform dual roles both as students and as medical workers. In this study, we aimed to use the Perceived Stress Scale (PSS-14) to judge the pressures on medical students and to identify effective ways to relieve these pressures. In this cross-sectional study, the subjects were recruited under informed consent according to the Declaration of Helsinki. Students undertaking Masters degrees at the China-Japan Union Hospital of Jilin University were randomly selected and data were collected through questionnaire surveys. Our data showed significant differences in the levels of pressure experienced by Masters students (p < 0.05). In the student population that showed increased pressure, females were significantly more stressed than males (p < 0.05). In addition, the pressures persisted after a holiday period (p < 0.05) but were reduced by undertaking recreational activities. The psychological pressures resulting from the COVID-19 pandemic were higher in female medical students compared to males. We showed that recreational activities including chatting with friends reduced psychological pressures in female medical students.

Objective: Coronary heart disease (CHD) is a complex disease caused by multifaceted interaction between genetic and environmental factors, which makes identification of the most likely disease candidate proteins and their associated risk markers a big challenge. Atherosclerosis is presented by a broad spectrum of heart diseases, including stable coronary artery disease (SCAD) and acute myocardial infarction (AMI), which is the progressive stage of SCAD. As such, the correct and prompt diagnosis of atherosclerosis turns into imperative for precise and prompt disease diagnosis, treatment and prognosis.Methods: The current work aims to look for specific protein markers for differential diagnosis of coronary atherosclerosis. Thirty male patients between 45 and 55 years diagnosed with atherosclerosis were analyzed by tandem mass tag (TMT) mass spectrometry. The study excluded those who were additionally diagnosed with hypertension and type 1 and 2 diabetes. The Mufuzz analysis was applied to select target proteins for precise and prompt diagnosis of atherosclerosis, most of which were most related to high lipid metabolism. The parallel reaction monitoring (PRM) was used to verify the selected target proteins. Finally, The receiver operating characteristic curve (ROC) was calculated by a random forest experiment.Results: One thousand one hundred and forty seven proteins were identified in the TMT mass spectrometry, 907 of which were quantifiable. In the PRM study, six proteins related to lipid metabolism pathway were selected for verification and they were ALB, SHBG, APOC2, APOC3, APOC4, SAA4.Conclusion: Through the detected specific changes in these six proteins, our results provide accuracy in atherosclerosis patients' diagnosis, especially in cases with varying types of the disease.

Rationale: In recent decades, the incidence of advanced syphilis has declined due to early recognition and the application of effective antibiotics. Advanced syphilis often manifests in the cardiovascular system as simple aortitis, aortic valve insufficiency, coronary artery stenosis or obstruction, Aortic aneurysm and mucinous myocarditis. In most case reports on the subject, acute myocardial infarction caused by syphilis was reported to be due to aortic valve insufficiency and coronary stenosis as a result of the involvement of the aorta. Patient concerns: The patient was a 48-year-old woman. She was admitted to our hospital because of intermittent upper abdominal pain with chest tightness for 3 hours. The patient reported a past syphilis infection, when she was hospitalized for hysteromyoma surgery four years ago, and had no related treatment. Diagnosis: According to the characteristics of coronary angiography and results of lab tests and echocardiography, she was finally diagnosed with myocardial infarction associated with syphilis. Interventions: At the first diagnosis of syphilis, the patient did not received antibiotics treatment. After the diagnosis of myocardial infarction, she received the percutaneous coronary intervention (PCI) operation assisted by extracorporeal membrane oxygenation (ECMO) technology, successfully got drug -eluted stents in right coronary artery ostium and left main ostium. Then the patient received penicillin to treat the syphilis infection. Outcomes: After coronary revascularization, the cardiac function of the patients was gradually improved, and the left ventricular ejection fraction was gradually improved after combined with optimized drug therapy. Lessons: The cardiovascular system is often involved in the stages of advanced syphilis with severe complications like myocardial infarction. Standard treatment should be given as soon as syphilis is diagnosis. For stenosis of coronary ostium, the PCI assisted by ECMO technology did not only ensure the effectiveness of the treatment, but also reduce the surgical risk of the patient. This case indicated the effectiveness of ECMO-assisted PCI, and thus may provide a reference for future patient treatment.