m6A methyltransferase WTAP regulates myocardial ischemia reperfusion injury through YTHDF1/FOXO3a signaling.

N6-methyladenosine (m6A) is emerging as an essential regulator in the progression of myocardial ischemia reperfusion (I/R) injury. However, the in-depth functions and mechanisms for m6A are still unclear. This work aimed to explore the potential functions and mechanisms for myocardial I/R injury. In this study, m6A methyltransferase WTAP and m6A modification level elevated in the hypoxia/reoxygenation (H/R) induced rat cardiomyocytes (H9C2) and I/R injury rat model. Bio-functional cellular experiments demonstrated that knockdown of WTAP remarkably released the proliferation and reduced the apoptosis and inflammatory cytokines induced by H/R. Moreover, exercise training alleviated WTAP level in exercise-trained rats. Mechanistically, methylated RNA immunoprecipitation sequencing (MeRIP-Seq) revealed that a remarkable m6A modification site was found in the 3'-UTR of FOXO3a mRNA. Moreover, WTAP triggered the installation of m6A modification on FOXO3a mRNA through m6A reader YTHDF1, thereby enhancing the stability of FOXO3a mRNA. Collectively, WTAP/YTHDF1/m6A/FOXO3a axis regulates the myocardial I/R injury progression, which provides new insights for the treatment of myocardial injury.

A framework of myocardial bridge detection with x-ray angiography sequence.

BACKGROUND: Myocardial bridges are congenital anatomical abnormalities in which myocardium covers a segment of coronary arteries, leading to stenocardia, myocardial ischemia, and sudden cardiac death in severe cases. However, automatic diagnosis of myocardial bridge presents significant challenges. METHOD: A novel framework of myocardial bridge detection with x-ray angiography sequence is proposed, which can realize automatic detection of vessel stenosis and myocardial bridge. Firstly, we employ a novel neural network model for coronary vessel segmentation, which consists of both CNNs and transformer structures to effectively extract both local and global information of the vessels. Secondly, we describe the vessel segment information, establish the vessel tree in the image, and fuse the vessel tree information between sequences. Finally, based on vessel stenosis detection, we realize automatic detection of the myocardial bridge by querying the blood vessels between the image sequence information. RESULTS: In experiment, we evaluate the segmentation results using two metrics, Dice and ASD, and achieve scores of 0.917 and 1.39, respectively. In the stenosis detection, we achieve an average accuracy rate of 92.7% in stenosis detection among 262 stenoses. In multi-frame image processing, vessels in different frames can be well-matched, and the accuracy of myocardial bridge detection achieves 75%. CONCLUSIONS: Our experimental results demonstrate that the algorithm can automatically detect stenosis and myocardial bridge, providing a new idea for subsequent automatic diagnosis of coronary vessels.

Liraglutide promotes the angiogenic ability of human umbilical vein endothelial cells through the JAK2/STAT3 signaling pathway.

Liraglutide is a glucagon-like peptide-1 receptor (GLP-1R) agonist and incretin mimetic used for the treatment of Type 2 diabetes mellitus. It has also been shown to have a beneficial role in the cardiovascular system. Here, we investigated the mechanism by which liraglutide promotes angiogenesis using human umbilical vein endothelial cells (HUVECs). HUVECs were treated with various concentrations of liraglutide, and assessed by wound healing assay and tube formation assay as measures of angiogenesis. We found that liraglutide at 10 and 100 nmol/L greatly promoted the angiogenic ability of HUVECs. Next, we examined the JAK2/STAT3 signaling pathway and found that liraglutide treatment led to JAK2/STAT3 activation and significant increase in the angiogenic mediator expressions, including vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and endothelial nitric oxide synthase (eNOS) in HUVECs. Treatment with JAK2 inhibitor, AG490, in HUVECs successfully reduced the observed effects of liraglutide. We conclude that liraglutide promotes the angiogenic ability of HUVECs by activating the JAK2/STAT3 signaling pathway and upregulating its downstream factors, VEGF, bFGF and eNOS. Thus, liraglutide may provide ischemic relief for diabetic patients with cardiovascular diseases in addition to glycemic control.

Application and observation of artificial intelligence in clinical practice of fundus screening for diabetic retinopathy with non-mydriatic fundus photography: a retrospective observational study of T2DM patients in Tianjin, China.

Objective: To observe the consistency of a preliminary report of artificial intelligence (AI) in the clinical practice of fundus screening for diabetic retinopathy (DR) using non-mydriatic fundus photography. Methods: Patients who underwent DR screening in the Metabolic Disease Management Center (MMC) of our hospital were selected as research participants. The degree of coincidence of the AI preliminary report and the ophthalmic diagnosis was compared and analyzed, and the kappa value was calculated. Fundus fluorescein angiography (FFA) was performed in patients referred to the out-of-hospital ophthalmology department, and the consistency between fluorescein angiography and AI diagnosis was evaluated. Results: In total, 6146 patients (12,263 eyes) completed the non-mydriasis fundus examination. The positive DR screening rate was 24.3%. When considering moderate nonproliferative retinopathy as the cut-off point, the kappa coefficient was 0.75 (p < 0.001), the sensitivity was 0.973, and the precision was 0.642, which was shown in the precision-recall curve. Fifty-nine patients referred to receive FFA were compared with non-mydriatic AI diagnoses. The kappa coefficient was 0.53, and the coincidence rate was 66.9%. Conclusion: Non-mydriasis fundus examination combined with AI has a medium-high consistency with ophthalmologists in DR diagnosis, conducive to early DR screening. Combining diagnosis and treatment modes with the Internet can promote the development of telemedicine, alleviate the shortage of ophthalmology resources, and promote the process of blindness prevention and treatment projects.

The Relationship of Hyperferritinemia to Metabolism and Chronic Complications in Type 2 Diabetes.

AIM: Elevated serum ferritin has been found to be closely related to type 2 diabetes mellitus. This study aimed to explore the relationship of high serum ferritin to metabolism and chronic complications in type 2 diabetes. METHODS: This was a cross-sectional study. A total of 330 type 2 diabetes patients who visited an endocrine clinic were included for the analysis. Serum ferritin and metabolic parameters were recorded. The prevalence of chronic diabetic complications was evaluated. Based on serum ferritin, participants were divided into hyperferritinemia and normal-ferritin groups. Metabolic parameters and prevalence of chronic diabetic complications were compared. The relationship between hyperferritinemia and chronic diabetic complications was explored with multivariate logistic regression models. Data were statistically analyzed by sex. RESULTS: Compared with the normal-ferritin group, the hyperferritinemia group showed higher levels of the serum inflammatory marker CRP and higher prevalence of diabetic retinopathy (DR) and coronary heart disease (CHD), regardless of sex (p<0.05). Moreover, male patients with hyperferritinemia had increased serum triglyceride, alanine transferase, γ-glutamyltranspeptidase, urea nitrogen, creatinine, and uric acid and higher prevalence of microalbuminuria (p<0.01). After controlling for demographics and metabolic profiles, hyperferritinemia remained an independent risk factor of DR (male OR 3.957, 95% CI 1.559-10.041, p=0.004; female OR 2.474, 95% CI 1.127-5.430, p=0.024) and CHD (male OR 2.607, 95% CI 1.087-6.257, p=0.032; female OR 2.293, 95% CI 1.031-5.096, p=0.042). CONCLUSION: This study found that hyperferritinemia was associated with increased CRP and higher prevalence of DR and CHD in type 2 diabetes. In men, high serum ferritin was also associated with dyslipidemia, hepatic dysfunction, and microalbuminuria.

Establishment and Evaluation of a Rat Model of Medial Malleolar Fracture with Vascular Injury.

OBJECTIVE: A stable animal model was needed to study bone non-union caused by insufficient blood supply, the main object of this paper is to develop a medial malleolar fracture model with controllable arterial vascular injuries in rats for revealing the biochemical mechanism of non-union by insufficient blood supply. METHODS: A total of 18 rats were randomly divided into three equal groups: the Sham group, the Fracture group, and the Fracture + Vascular group. The animals were subjected to unilateral medial malleolar bone fracture and vascular injury using customized molding equipment. The fracture site was scanned by micro-CT, and vascular injury was evaluated by laser Doppler flowmetry (LDF) 24 h after modeling. Histological examination (HE), alkaline phosphatase (ALP) and tartrate-resistant acid phosphatase (TRAP) staining, immunohistochemistry and immunofluorescence were conducted on the medial malleolar fracture tissues of three rats randomly selected from each group 24 h after modeling. Subsequently, to further confirm the success of fracture modeling, the fracture sites of three other rats in each group underwent micro-CT scanning again 6 weeks after surgery. RESULTS: The results of a 24 h micro-CT showed that all rats used to create the fracture models showed controlled injury of the medial malleolus. The model was stable, and the satisfaction of the homemade equipment agreed with the expectation. LDF showed that the blood flow of rats in the Fracture + Vascular group decreased significantly 24 h after fracture injury, while collateral blood flow perfusion increased by 50% on average. The results of HE, ALP and TRAP staining in the medial malleolus showed that the number of osteoblasts (OBs) and osteoclasts (OCs) in the Fracture group increased significantly, but the number of OBs and OCs in the Fracture + Vascular group decreased sharply relative to the number in the Sham group 24 h later. Furthermore, immunohistochemistry and immunofluorescence results showed that the number of neovessels in the Fracture group was significantly increased, while the number of neovessels in the Fracture + Vascular group was significantly decreased, which was consistent with the above results. After 6 weeks of modeling, the micro-CT results showed that the fractures in the Fracture group had healed substantially, while those in the Fracture + Vascular group had not. CONCLUSION: This study provided a reproducible and stable experimental animal model for medial malleolar fractures with arterial injury.

Educational Attainment and Ischemic Stroke: A Mendelian Randomization Study.

Observational studies have evaluated the potential association of socioeconomic factors such as higher education with the risk of stroke but reported controversial findings. The objective of our study was to evaluate the potential causal association between higher education and the risk of stroke. Here, we performed a Mendelian randomization analysis to evaluate the potential association of educational attainment with ischemic stroke (IS) using large-scale GWAS datasets from the Social Science Genetic Association Consortium (SSGAC, 293,723 individuals), UK Biobank (111,349 individuals), and METASTROKE consortium (74,393 individuals). We selected three Mendelian randomization methods including inverse-variance-weighted meta-analysis (IVW), weighted median regression, and MR-Egger regression. IVW showed that each additional 3.6-year increase in years of schooling was significantly associated with a reduced IS risk (OR = 0.54, 95% CI: 0.41-0.71, and p = 1.16 × 10-5). Importantly, the estimates from weighted median (OR = 0.49, 95% CI: 0.33-0.73, and p = 1.00 × 10-3) and MR-Egger estimate (OR = 0.18, 95% CI: 0.06-0.60, and p = 5.00 × 10-3) were consistent with the IVW estimate in terms of direction and magnitude. In summary, we provide genetic evidence that high education could reduce IS risk.

Berberine Attenuates Cerebral Ischemia-Reperfusion Injury Induced Neuronal Apoptosis by Down-Regulating the CNPY2 Signaling Pathway.

Berberine (BBR) has a neuroprotective effect against ischemic stroke, but its specific protective mechanism has not been clearly elaborated. This study explored the effect of BBR on the canopy FGF signaling regulator 2 (CNPY2) signaling pathway in the ischemic penumbra of rats. The model of cerebral ischemia-reperfusion injury (CIRI) was established by the thread embolization method, and BBR was gastrically perfused for 48 h or 24 h before operation and 6 h after operation. The rats were randomly divided into four groups: the Sham group, BBR group, CIRI group, and CIRI + BBR group. After 2 h of ischemia, followed by 24 h of reperfusion, we confirmed the neurologic dysfunction and apoptosis induced by CIRI in rats (p < 0.05). In the ischemic penumbra, the expression levels of CNPY2-regulated endoplasmic reticulum stress-induced apoptosis proteins (CNPY2, glucose-regulated protein 78 (GRP78), double-stranded RNA-activated protein kinase-like ER kinase (PERK), C/EBP homologous protein (CHOP), and Caspase-3) were significantly increased, but these levels were decreased after BBR treatment (p < 0.05). To further verify the inhibitory effect of BBR on CIRI-induced neuronal apoptosis, we added an endoplasmic reticulum-specific agonist and a PERK inhibitor to the treatment. BBR was shown to significantly inhibit the expression of apoptotic proteins induced by endoplasmic reticulum stress agonist, while the PERK inhibitor partially reversed the ability of BBR to inhibit apoptotic protein (p < 0.05). These results confirm that berberine may inhibit CIRI-induced neuronal apoptosis by downregulating the CNPY2 signaling pathway, thereby exerting a neuroprotective effect.

A Five-lncRNAs Signature-Derived Risk Score Based on TCGA and CGGA for Glioblastoma: Potential Prospects for Treatment Evaluation and Prognostic Prediction.

Accumulating studies have confirmed the crucial role of long non-coding RNAs (ncRNAs) as favorable biomarkers for cancer diagnosis, therapy, and prognosis prediction. In our recent study, we established a robust model which is based on multi-gene signature to predict the therapeutic efficacy and prognosis in glioblastoma (GBM), based on Chinese Glioma Genome Atlas (CGGA) and The Cancer Genome Atlas (TCGA) databases. lncRNA-seq data of GBM from TCGA and CGGA datasets were used to identify differentially expressed genes (DEGs) compared to normal brain tissues. The DEGs were then used for survival analysis by univariate and multivariate COX regression. Then we established a risk score model, depending on the gene signature of multiple survival-associated DEGs. Subsequently, Kaplan-Meier analysis was used for estimating the prognostic and predictive role of the model. Gene set enrichment analysis (GSEA) was applied to investigate the potential pathways associated to high-risk score by the R package "cluster profile" and Wiki-pathway. And five survival associated lncRNAs of GBM were identified: LNC01545, WDR11-AS1, NDUFA6-DT, FRY-AS1, TBX5-AS1. Then the risk score model was established and shows a desirable function for predicting overall survival (OS) in the GBM patients, which means the high-risk score significantly correlated with lower OS both in TCGA and CGGA cohort. GSEA showed that the high-risk score was enriched with PI3K-Akt, VEGFA-VEGFR2, TGF-beta, Notch, T-Cell pathways. Collectively, the five-lncRNAs signature-derived risk score presented satisfactory efficacies in predicting the therapeutic efficacy and prognosis in GBM and will be significant for guiding therapeutic strategies and research direction for GBM.

Application of non-mydriatic fundus examination and artificial intelligence to promote the screening of diabetic retinopathy in the endocrine clinic: an observational study of T2DM patients in Tianjin, China.

BACKGROUND: We aimed to determine the role of non-mydriatic fundus examination and artificial intelligence (AI) in screening diabetic retinopathy (DR) in patients with diabetes in the Metabolic Disease Management Center (MMC) in Tianjin, China. METHODS: Adult patients with type 2 diabetes mellitus who were first treated by MMC in Tianjin First Central Hospital and Tianjin 4th Center Hospital were divided into two groups according to the time that MMC was equipped with the non-mydriatic ophthalmoscope and AI system and could complete fundus examination independently (the former was the control group, the latter was the observation group). The observation indices were as follows: the incidence of DR, the fundus screening rate of the two groups, and fundus screening of diabetic patients with different course of disease. RESULTS: A total of 5039 patients were enrolled in this study. The incidence rate of DR was 18.6%, 29.8%, and 49.6% in patients with diabetes duration of ⩽1 year, 1-5 years, and >5 years, respectively. The screening rate of fundus in the observation group was significantly higher compared with the control group (81.3% versus 28.4%, χ 2 = 1430.918, p < 0.001). The DR screening rate of the observation group was also significantly higher compared with the control group in patients with diabetes duration of ⩽1 year (77.3% versus 20.6%; χ 2 = 797.534, p < 0.001), 1-5 years (82.5% versus 31.0%; χ 2 = 197.124, p < 0.001) and ⩾5 years (86.9% versus 37.1%; χ2 = 475.609, p < 0.001). CONCLUSIONS: In the case of limited medical resources, MMC can carry out one-stop examination, treatment, and management of DR through non-mydratic fundus examination and AI assistance, thus incorporating the DR screening process into the endocrine clinic, so as to facilitate early diagnosis.

Discovery and comparison of serum biomarkers for diabetes mellitus and metabolic syndrome based on UPLC-Q-TOF/MS.

INTRODUCTION: Diabetes mellitus (DM) and metabolic syndrome (MetS) are systemic metabolic disorders, which have risk factors for diabetic cardiovascular and cerebral microvascular disease. It is very important to screen the metabolic biomarkers between DM and MetS patients, which can make patients benefit to a greater extent and prevent the occurrence of disease in advance. OBJECTIVES: Diabetes mellitus (DM) and metabolic syndrome are a complex, chronic illness with a pronounced impact on the quality of life of many people. However, understanding the metabolic changes in patients and identifying high-risk individuals is crucial for prevention and disease management strategies. METHODS: In this study, a nontargeted metabolomics approach based on UPLC-Q-TOF/MS was used to find the differential metabolites in serum samples from patients with DM and MetS. RESULTS: Metabonomic analysis reveals metabolic differences between DM and HC with significant differences more than 60 metabolites. While, more than 65 metabolites have significant differences between MetS and HC. The independent disturbed pathway in the DM group was the FoxO signaling pathway. The independent disturbed pathways in the MetS group were the alpha-linolenic acid metabolism, glycerophospholipid metabolism and pyrimidine metabolism. The independent disturbed metabolites and the logistic regression result showed that betaine, alpha-linolenic acid, d-mannose, l-glutamine and methylmalonic acid can be used as a combinatorial biomarker to distinguish DM from healthy control. L-isoleucine, l-glutamine, PC(16:0/16:0), alpha-d-glucose, ketoisocaproic acid, d-mannose, uridine can be used as a combinatorial biomarker in MetS. CONCLUSION: Our findings, on one hand, provide critical insight into the pathological mechanism of DM and MetS. On the other hand, supply a combinatorial biomarker to aid the diagnosis of diseases in clinical usage.

Analysis of factors related to diabetic retinopathy in patients with newly diagnosed type 2 diabetes: a cross-sectional study.

AIM: To investigate the related factors of diabetic retinopathy (DR) and explore the correlation between smoking and DR in patients with newly diagnosed type 2 diabetes mellitus (T2DM). DESIGN: A single-centre cross-sectional study. SETTING: Tianjin 4th Central Hospital. PARTICIPANTS: Patients with newly diagnosed T2DM who visited the outpatient department of the hospital from December 2018 to April 2019. METHODS: A total of 947 patients were enrolled in the study. They were divided into two groups according to whether they were diagnosed with DR (diabetic retinopathy group, DR group; non-diabetic retinopathy group, NDR group). The smoking index (SI) was calculated to assess smoking status. Factors such as sex, age, hypertension, T2DM diagnosed age, family history of diabetes, drinking history, haemoglobin A1c (HbA1c), body mass index (BMI) and smoking status were compared between the two groups. Logistic regression was used to analyse the relationship between DR and the above factors. RESULTS: There was no statistically significant difference between the two groups in sex, age, hypertension, DM diagnosed age, family history of diabetes, drinking history and HbA1c. BMI was significantly higher in DR patients (27.7±4.2 vs 26.7±4.4, p=0.004). Smoking status was also different between the two groups (χ2=6.350, p=0.042). BMI was shown to be a related factor for DR in patients with newly diagnosed diabetes (OR=0.592, p=0.004). When BMI was ≥28 kg/m2, heavy smoking was significantly associated with DR (OR=2.219, p=0.049), and there was a negative correlation between DR and the age of diagnosis of diabetes ≥60 years (OR=0.289, p=0.009). CONCLUSIONS: Heavy smoking was an important related factor for DR in patients with newly diagnosed diabetes mellitus when BMI was ≥28 kg/m2. Delaying the age of diabetes might prevent the occurrence of DR. To elucidate the correlation, long-term cohort studies with large samples are needed.

CaSR activates PKCδ to induce cardiomyocyte apoptosis via ER stress­associated apoptotic pathways during ischemia/reperfusion.

Endoplasmic reticulum (ER) stress can be activated by ischemia/reperfusion (I/R) injury in cardiomyocytes. Persistent ER stress, with an increase in intracellular Ca2+ ([Ca2+]i) concentration, leads to apoptosis. Protein kinase C (PKC) has a key role in myocardial damage by elevation of [Ca2+]i. The calcium­sensing receptor (CaSR), a G protein­coupled receptor, can increase the release of [Ca2+]i from the ER through the inositol triphosphate receptor (IP3R). Intracellular calcium overload has been demonstrated to cause cardiac myocyte apoptosis during I/R. However, the associations between PKC, CaSR and ER stress are not clear. The present study examined the hypothesis that activation of PKCδ by CaSR participates in ER stress­associated apoptotic pathways within myocardial I/R. Rat hearts were subjected to 30 min of ischemia in vivo, followed by reperfusion for 120 min. GdCl3 (a CaSR activator) was used to elevate the intracellular Ca2+ concentration, but the Ca2+ concentration in the ER was significantly decreased during I/R. Following exposure to GdCl3, expression levels of CaSR, glucose­regulated protein 78 (GRP78), Caspase­12, phosphorylated JNK and Caspase­3 were increased, and the ratios of apoptotic myocardial cells were significantly increased. By contrast, following exposure to rottlerin, a PKCδ inhibitor, the expression levels of these proteins and the ratio of apoptotic myocardial cells were significantly reduced. The present study also demonstrated that PKCδ translocated into the ER to induce an ER stress response and participate in the ER stress­related apoptosis pathway. These results confirmed that CaSR activated PKCδ to induce cardiomyocyte apoptosis through ER stress­associated apoptotic pathways during I/R in vivo.

Liraglutide Increases VEGF Expression via CNPY2-PERK Pathway Induced by Hypoxia/Reoxygenation Injury.

Liraglutide (Lir) is a glucagon-like peptide-1 receptor agonist that lowers blood sugar and reduces myocardial infarct size by improving endothelial cell function. However, its mechanism has not yet been clarified. Unfolded protein response (UPR) plays an important role in the pathogenesis of myocardial ischemia-reperfusion injury. It determines the survival of cells. Endoplasmic reticulum position protein homologue 2 (CNPY2) is a novel initiator of UPR that also participates in angiogenesis. To this extent, the current study further explored whether Lir regulates angiogenesis through CNPY2. In our article, a hypoxia/reoxygenation (H/R) injury model of human umbilical vein endothelial cells (HUVECs) was established and the effect of Lir on HUVECs was first evaluated by the Cell Counting Kit-8. Endothelial tube formation was used to analyze the ability of Lir to induce angiogenesis. Subsequently, the effect of Lir on the concentrations of hypoxia-inducible factor 1α (HIF1α), vascular endothelial growth factor (VEGF), and CNPY2 was detected by enzyme-linked immunosorbent assay. To assess whether Lir regulates angiogenesis through the CNPY2-initiated UPR pathway, the expression of UPR-related pathway proteins (CNPY2, GRP78, PERK, and ATF4) and angiogenic proteins (HIF1α and VEGF) was detected by reverse transcription-polymerase chain reaction and Western blot. The results confirmed that Lir significantly increased the expression of HIF1α and VEGF as well as the expression of CNPY2-PERK pathway proteins in HUVECs after H/R injury. To further validate the experimental results, we introduced the PERK inhibitor GSK2606414. GSK2606414 was able to significantly decrease both the mRNA and protein expression of ATF4, HIF1α, and VEGF in vascular endothelial cells after H/R injury. The effect of Lir was also inhibited using GSK2606414. Therefore, our study suggested that the CNPY2-PERK pathway was involved in the mechanism of VEGF expression after H/R injury in HUVECs. Lir increased the expression of VEGF through the CNPY2-PERK pathway, which may promote endothelial cell angiogenesis and protect HUVEC from H/R damage.

[A clinical efficacy and safety study on coronary heart disease and angina treatment with Puerarin Injection].

OBJECTIVE: To observe the clinical efficacy and safety of Puerarin Injection treatment on angina pectoris. METHODS: 388 patients with angina pectoris, enrolled to Tianjin Fourth Central Hospital during January 2009 and February 2011 were selected and randomly divided into treatment or control groups with 194 patients of each. Based on the conventional therapy program, one group was given Puerarin Injection as treatment group while, the other was given with Danshen Injection as control group. Clinical efficacy, the attack rate of angina pectoris, oxygen consumption, indices on electrocardiogram, haemorheology and other adverse reactions among the two groups were compared. RESULTS: The total efficacy of the treatment group (88.14%, 171/194) was significantly higher than the control group (61.86%, 120/194) and the difference was statistically significant (P < 0.05). During the treatment, no significant adverse events were noticed in both of the two groups of patients. CONCLUSION: The Puerarin Injection treatment program on angina pectoris seemed effective and safe.

[Clinical studies on different coronary artery interventional therapies through femoral artery or radial artery approaches].

OBJECTIVE: To compare the clinical efficacies regarding femoral artery or radial artery approaches on coronary artery interventional therapies. METHODS: 360 patients were randomly divided into intervention group via femoral artery (TFI) or transradial coronary intervention (TRI) group. Postoperative observation on the two said groups of patients with vascular lesion characteristics, feasibility factors (success rate of interventional therapy puncture, time of operation and hospitalization) and complications, were made. RESULTS: There were no significant differences between the two groups on the characteristics of vascular lesion (P>0.05). Success rates of the two groups were 97.78% and 96.67% respectively. The differences on success rate, time of operation were not statistically significant (P>0.05) while the average time of puncture, the mean duration of hospitalization and the rates of complications were significantly different (P<0.05). CONCLUSION: The two methods under comparison had similar success rate and feasibility. However, the complications related to radial artery interventional therapy were much less than the femoral artery interventional therapy. As having better safety, radial artery interventional therapy seemed to have applicable value on clinical practice.