Objective:To observe the effect of Icariin on diabetic myocardial hypertrophy and explore its molecular mechanism.Methods:C57BL/6 mice were randomly divided into Ctrl group(normal control group),DM group(STZ intraperi...Objective:To observe the effect of Icariin on diabetic myocardial hypertrophy and explore its molecular mechanism.Methods:C57BL/6 mice were randomly divided into Ctrl group(normal control group),DM group(STZ intraperitoneal injection model),and DM+ICA group(diabetic C57BL/6 mice by intragastric Icariin solution 80mg/kg/d,for 3 consecutive weeks).Real-time quantitative PCR was used to detect myocardial hypertrophy markers BNP andβ-MHC.Western blotting was used to detect myocardial AMPK,p-AMPK,mTOR,p-mTOR,LC3B and Beclin1 protein expression.Echocardiogram was used to detect left ventricular mass and ejection fraction.Results:Compared with the normal control group,the expression of myocardial hypertrophy markers BNP andβ-MHC mRNA in diabetic mice were significantly increased;the expression of phosphorylated AMPK protein,autophagy-related protein LC3B and Beclin1 were significantly increased,and the expression of phosphorylated mTOR protein is significantly reduced;the left ventricular mass is significantly increased.The above changes can be reversed after treatment with Icariin,but the effect of Icariin is blocked by the autophagy inhibitor rapamycin.Conclusion:Icariin may inhibit autophagy and reduce diabetic myocardial hypertrophy through AMPK-mTOR signaling pathway.展开更多
Objective:To study the correlation between expression of Wnt and NCXl and cardiomyocyte apoptosis in mouse with myocardial hypertrophy.Methods:C57B/16 male mice were given the subcutaneous injection of 1 mg/kg isopren...Objective:To study the correlation between expression of Wnt and NCXl and cardiomyocyte apoptosis in mouse with myocardial hypertrophy.Methods:C57B/16 male mice were given the subcutaneous injection of 1 mg/kg isoprenaline to build the myocardial hypertrophy model.After 14 d of model building,mice were executed by cervical vertebra luxation.The ratio of heart weight/body weight(HW/BW) and heart weight/tibia length(HW/TL) was observed and proved using HE staining mat detected the size of eaidiomyocytes.40 male C57B/16 mice were randomly divided into the sham group(normal saline) and model group(isoprenaline),with 20 mice in each group.The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling was applied to detect the cardiomyocyte apoptosis;while Western blot and immunohistochemistry were employed to detect the expression of Wnt and NCX1.Meanwhile,the correlation between these two proteins and cardiomyocyte apoptosis was explored.Results:Compared with the sham group,the ratio of HW/BW and HW/TL was increased in the model group,as well as the bigger and hypertrophied cardiomyocytes,decreased number and increased apoptosis of eaidiomyocytes,and increased positive expression of Wnt3 a,WntSa and NCXl in the cardiac muscle tissue.Besides,there was positive correlation between the expression of Wnt and NCXl and the cardiomyocyte apoptosis.Conclusions:The expression of Wnt3 a,Wnt5a and NCXl in mouse with myocardial hypertrophy is increased and positively correlated with the cardiomyocyte apoptosis.展开更多
This study was aimed to establish a stable animal model of left ventricular hypertrophy(LVH) to provide theoretical and experimental basis for understanding the development of LVH. The abdominal aorta of male Wistar r...This study was aimed to establish a stable animal model of left ventricular hypertrophy(LVH) to provide theoretical and experimental basis for understanding the development of LVH. The abdominal aorta of male Wistar rats(80–100 g) was constricted to a diameter of 0.55 mm between the branches of the celiac and anterior mesenteric arteries. Echocardiography using a linear phased array probe was performed as well as pathological examination and plasma B-type natriuretic peptide(BNP) measurement at 3, 4 and 6 weeks after abdominal aortic constriction(AAC). The results showed that the acute mortality rate(within 24 h) of this modified rat model was 8%. Animals who underwent AAC demonstrated significantly increased interventricular septal(IVS), LV posterior wall(LVPWd), LV mass index(LVMI), cross-sectional area(CSA) of myocytes, and perivascular fibrosis; the ejection fraction(EF), fractional shortening(FS), and cardiac output(CO) were consistently lower at each time point after AAC. Notably, differences in these parameters between AAC group and sham group were significant by 3 weeks and reached peaks at 4th week. Following AAC, the plasma BNP was gradually elevated compared with the sham group at 3rd and 6th week. It was concluded that this modified AAC model can develop LVH, both stably and safely, by week four post-surgery; echocardiography is able to assess changes in chamber dimensions and systolic properties accurately in rats with LVH.展开更多
Aim The present study aims to investigate whether BMSCs transplantation may inhibit hypertrophic hearts and its underlying mechanisms. Background There is no evidence so far that Bone marrow-derived mesenchy- mal stem...Aim The present study aims to investigate whether BMSCs transplantation may inhibit hypertrophic hearts and its underlying mechanisms. Background There is no evidence so far that Bone marrow-derived mesenchy- mal stem cells （BMSCs） can heal pathological myocardial hypertrophy. Methods To observe the antihypertrophic actions, BMSCs was indirectly cocultured with NRVCs in vitro, or intramyocardially transplanted into hypertrophic hearts in vivo. Results ISO-induced typical hypertrophic characteristics of cardiomyocytes were obviously preven- ted by BMSCs in the co-culture model in vitro and after BMSCs transplantation in vivo. Furthermore, the activation of the Ca2＋/calcineurin/NFATc3 hypertrophic pathway was shown abrogated in the presence of BMSCs both in vitro and in vivo. Interestingly, blockage of VEGF release from BMSCs but not bFGF and IGF-1 can abolish the protec- tive effects of BMSCs on cardiomyocytes hypertrophy. Consistently, VEGF administration attenuated ISO-induced BNP and β-MHC expression and the activation of Ca2＋/cal- the enlargement of cellular size, the augment of ANP, cineurin/NFATc3 hypertrophic pathway, and these can be abrogated by blocking VEGFR-1, indicating VEGFR-1 is involved in the antihypertrophic role of VEGF. We further find that the ample VEGF secretion contributing to the anti-hypertrophic effects of BMSCs originates from BMSCs interplay with cardiac cells but not BMSCs or cardiomyo- cytes alone. Conclusions Thus, mesenchymal stem cells are able to inhibit myocardial hypertrophy via interacting with cardiomyocytes so as to promote VEGF release which inhibits the activation of the Ca2＋/calcineurin/NFATc3 hypertrophic signaling pathway in cardiac cells, in addition to its well-recognized ability to ameliorate myocardial injuries by replacing dead cells.展开更多
Objective:To investigate the effects of cagliazin,a sodium-glucose cotransporter 2 inhibitor(SGLT-2I),on ventricular remodeling in spontaneously hypertensive rats(SHR)through renin angiotensin system(RAS)and transform...Objective:To investigate the effects of cagliazin,a sodium-glucose cotransporter 2 inhibitor(SGLT-2I),on ventricular remodeling in spontaneously hypertensive rats(SHR)through renin angiotensin system(RAS)and transforming growth factor-β1(TGF-β1).Methods:The experiment was divided into 4 groups:normal blood pressure control group,SHR group,cagliet net low-dose group(30mg/kg),cagliet net high-dose group(60mg/kg),once a day for 8 weeks.Normal blood pressure rats(WKY)were used as the control group to measure blood pressure with tail sleeve sphygmomanometer(BP)and blood glucose level was measured with glucose meter Cardiac function was evaluated by echocardiography,cell area of left ventricle was evaluated by histomorphology,real-time quantitative polymerase chain reaction and protein imprinting hybridization were used to detect TGF-β1 Smad4 renin from type I collagen(Col1a)type III collagen(Col3a)matrix metalloproteinase 2(MMP-2)Expression results of angiotensin II1 type receptor 1(AGTR1)and Angiotensin II2 type receptor 2(AGTR2).Results:After 8 weeks of administration,the cardiac weight/body weight ratio(HW/BW)of left ventricular weight/heart weight ratio(LVW/HW)of kaglinet low-dose group and high-dose group was statistically significant compared with that of spontaneous hypertensive rats(P<);Compared with SHRs,the expression of Col1a,Col3a,MMP2,TGF-β1,Smad4,Renin AGTR1 was significantly down-regulated and the expression of AGTR2 was up-regulated in cagliet net low-dose and high-dose groups Conclusions:Cagliazin can improve hypertension-induced cardiac remodeling by regulating RAS and TGF-β1/Smad signaling pathways.Conclusion:From the results,canaglifozin was found to ameliorate pressure overload-induced cardiac remodeling by regulating the RAS and TGF-β1/Smad signaling pathway.展开更多
Objective. In a model of rat cardiac hypertrophy, the changes in the distribution of ET- 1 receptors in two subcellular fractions, the sarcolemma and the light vesicles during myocardial hypertrophy were studied. Meth...Objective. In a model of rat cardiac hypertrophy, the changes in the distribution of ET- 1 receptors in two subcellular fractions, the sarcolemma and the light vesicles during myocardial hypertrophy were studied. Methods. Cardiac hypertrophy was produced by placing a constricting clip around the suprarenal abdominal aorta of rats, and ET- 1 receptor was assayed with radioactive analysis method. Results. It was found that plasma and ventricular ET- 1 levels increased significantly on week 2 and week 4 of pressure overload. ET- 1 binding studies showed that during myocardial hypertrophy, the maximum binding capacity (Bmax) was increased by 41％ (P< 0.01) and 65％ (P< 0.01) in sarcolemma in H- 2 week and H- 4 week groups, but was decreased by 24％ (P< 0.01) and 21％ (P< 0.01) in light vesicles. The sum of Bmax of sarcolemmal and light vesicle fractions was increased by 33％ (P< 0.01) and 57％ (P< 0.01) in group H- 2 week and H- 4 week, respectively. Conclusion. ET- 1 receptors in rat heart were externalized from light vesicles to sarcolemma, which may contribute to the development of myocardial hypertrophy.展开更多
Objective:To explore the therapeutic efficacy of L-carvone from Mentha spicata L.leaf extracts against isoproterenol-induced cardiac hypertrophy in rats.Methods:Isoproterenol(5 mg/kg)was injected intraperitoneally int...Objective:To explore the therapeutic efficacy of L-carvone from Mentha spicata L.leaf extracts against isoproterenol-induced cardiac hypertrophy in rats.Methods:Isoproterenol(5 mg/kg)was injected intraperitoneally into rats for one month to induce cardiac hypertrophy.L-carvone(25 and 100 mg/kg)was administered orally to treat cardiac hypertrophy.The cardioprotective activity of L-carvone was evaluated by electrocardiogram,histopathological analysis as well as determination of biochemical parameters and enzymatic markers.Results:L-carvone from Mentha spicata L.at 25 and 100 mg/kg ameliorated isoproterenol-induced cardiac hypertrophy,as evidenced by reduced QRS interval on electrocardiogram,and decreased heart weight and heart index.In addition,both doses of L-carvone markedly lowered the levels of glucose,total protein,low-density lipoprotein cholesterol,aspartate transaminase,alanine transaminase,lactate dehydrogenase,creatine kinase MB,troponin-Ⅰ,N-terminal pro-B type natriuretic peptide and triglycerides while increasing high-density lipoprotein cholesterol and lipase level(P<0.05).Moreover,L-carvone alleviated contraction band necrosis,and reorganized the myofibrils with normal striations and myocytes as well as normal nuclei in cardiac histoarchitecture of rats with isoproterenol-induced cardiac hypertrophy.Conclusions:L-carvone from Mentha spicata L.leaf extract can restore abnormal cardiac function and may be further explored as a therapeutic agent against the deleterious effects of cardiac hypertrophy after further evaluation.展开更多
The incidence of acute myocardial infarction (AMI) is increasing year by year, which seriously endangers human health around the world. The preferred treatment strategy for AMI patients is the use of drug-eluting sten...The incidence of acute myocardial infarction (AMI) is increasing year by year, which seriously endangers human health around the world. The preferred treatment strategy for AMI patients is the use of drug-eluting stents (DES), as there is ample evidence to suggest that stent implantation can reduce major adverse cardiovascular events (MACEs). With the application of drug-coated balloons (DCBs) and the enhancement of the concept of interventional without implantation, the question is whether DCBs can be safely and effectively used in patients with AMI? The purpose of this study was to investigate the safety and effectiveness of DCBs in the treatment of AMI. A retrospective review of clinical data was conducted on 55 AMI patients who underwent primary percutaneous coronary intervention (PCI) from January 2020 to December 2021. Of these patients, 25 were treated with DCBs and 30 were treated with DESs. Optical coherence tomography (OCT) was used to measure the minimum lumen diameter, lumen stenosis, and coronary artery dissection before and after surgery, and angina pectoris attacks and various MACEs were recorded at 1, 6, and 12 months after surgery. The results showed that there were no significant differences in clinical baseline data between the two groups. However, the minimum lumen diameter of the DCB group immediately after the operation was smaller than that of the DES group, and the stenosis degree of the lumen in the DCB group was higher than that in the DES group. The incidence of coronary artery dissection in the DCB group was significantly higher than that in the DES group, but the majority of them were type B. At 1, 6, and 12 months after treatment, there was no significant difference in the occurrence of MACEs between the two groups. In conclusion, DCBs is a safe and effective treatment for AMI. However, the incidence of coronary artery dissection in DCB patients is higher than that in DES patients, but the majority of them are type B. .展开更多
Medical history summary: Male, 47 years old, was admitted to the hospital due to “dizziness accompanied by chest tightness and pain for more than 8 days”. One week ago, the patient experienced chest tightness, chest...Medical history summary: Male, 47 years old, was admitted to the hospital due to “dizziness accompanied by chest tightness and pain for more than 8 days”. One week ago, the patient experienced chest tightness, chest pain accompanied by profuse sweating for 3 hours and underwent emergency percutaneous coronary intervention (PCI) at a local hospital. The procedure revealed left main stem occlusion with subsequent left main stem to left anterior descending artery percutaneous transluminal coronary angioplasty (PTCA). After the procedure, the patient experienced hemodynamic instability, recurrent ventricular fibrillation, and critical condition, thus transferred to our hospital for further treatment. Symptoms and signs: The patient is in a comatose state, unresponsive to stimuli, with bilateral dilated pupils measuring 2.0 mm, exhibiting reduced sensitivity to light reflex, and recurrent fever. Coarse breath sounds can be heard in both lungs, with audible moist rales. Irregular breathing pattern is observed, and heart sounds vary in intensity. No pathological murmurs are auscultated in any valve auscultation area. Diagnostic methods: Coronary angiography results at the local hospital showed complete occlusion of the left main stem, and left main stem to left anterior descending artery percutaneous transluminal coronary angioplasty (PTCA) was performed. However, the distal guidewire did not pass through. After admission, blood tests showed a Troponin T level of 1.44 ng/ml and a Myoglobin level of 312 ng/ml. The platelet count was 1390 × 10<sup>9</sup>/L. Von Willebrand factor (vWF) activity was measured at 201.9%. Bone marrow aspiration biopsy showed active bone marrow proliferation and platelet clustering. The peripheral blood smear also showed platelet clustering. JAK-2 gene testing was positive, confirming the diagnosis of primary thrombocytosis. Treatment methods: The patient is assisted with mechanical ventilation and intra-aortic balloon counterpulsation to improve coronary blood flow. Electrolyte levels are closely monitored, especially maintaining plasma potassium levels between 4.0 and 4.5 mmol/l. Hydroxyurea 500 mg is administered for platelet reduction. Anticoagulants and antiplatelet agents are used rationally to prevent further infarction or bleeding. Antiarrhythmic, lipid-lowering, gastroprotective, hepatoprotective, and heart failure treatment are also provided. Clinical outcome: The family members chose to withdraw treatment and signed for discharge due to a combination of reasons, including economic constraints and uncertainty about the prognosis due to the long disease course. Acute myocardial infarction has gradually become one of the leading causes of death in our country. As a “green channel” disease, corresponding diagnostic and treatment protocols have been established in China, and significant progress has been made in emergency care. There are strict regulations for the time taken from the catheterization lab to the cardiac intensive care unit, and standardized treatments are provided to patients once they enter the intensive care unit. Research results show that the incidence of acute myocardial infarction in patients with primary thrombocythemia within 10 years is 9.4%. This type of disease is rare and difficult to cure, posing significant challenges to medical and nursing professionals. In order to benefit future patients, we have documented individual cases of treatment and nursing care for these patients. The research results show that these patients exhibit resistance to traditional oral anticoagulant drugs and require alternative anticoagulants. Additionally, there are significant differences in serum and plasma potassium levels among patients. Therefore, when making clinical diagnoses, it is necessary to carefully distinguish between the two. Particularly, nursing personnel should possess dialectical thinking when supplementing potassium levels in patients in order to reduce the incidence of malignant arrhythmias and mortality rates.展开更多
BACKGROUND Metastatic cardiac tumors are known to occur more frequently than primary cardiac tumors,however,they often remain asymptomatic and are commonly dis-covered on autopsy.Malignant tumors with a relatively hig...BACKGROUND Metastatic cardiac tumors are known to occur more frequently than primary cardiac tumors,however,they often remain asymptomatic and are commonly dis-covered on autopsy.Malignant tumors with a relatively high frequency of cardiac metastasis include mesothelioma,melanoma,lung cancer,and breast cancer,whereas reports of esophageal cancer with cardiac metastasis are rare.CASE SUMMARY The case of a 60-year-old man who complained of dysphagia is presented.Upper gastrointestinal endoscopy showed a submucosal tumor-like elevated lesion in the esophagus causing stenosis.Contrast-enhanced computed tomography showed left atrial compression due to the esophageal tumor,multiple liver and lung metastases,and a left pleural effusion.Pathological examination of a biopsy speci-men from the esophageal tumor showed spindle-shaped cells,raising suspicion of esophageal sarcoma.The disease progressed rapidly,and systemic chemotherapy was deemed necessary,however,due to his poor general condition,adminis-tration of cytotoxic agents was considered difficult.Given his high Combined Positive Score,nivolumab was administered,however,the patient soon died from the disease.The autopsy confirmed spindle cell carcinoma(SCC)of the esophagus and cardiac metastasis with similar histological features.Cancer stem cell markers,ZEB1 and TWIST,were positive in both the primary tumor and the cardiac metastasis.CONCLUSION To the best of our knowledge,there have been no prior reports of cardiac metastasis of esophageal SCC.This case highlights our experience with a patient with esophageal SCC who progressed rapidly and died from the disease,with the autopsy examination showing cardiac metastasis.展开更多
BACKGROUND Acute myocardial infarction(AMI)is a severe cardiovascular disease caused by the blockage of coronary arteries that leads to ischemic necrosis of the myocardium.Timely medical contact is critical for succes...BACKGROUND Acute myocardial infarction(AMI)is a severe cardiovascular disease caused by the blockage of coronary arteries that leads to ischemic necrosis of the myocardium.Timely medical contact is critical for successful AMI treatment,and delays increase the risk of death for patients.Pre-hospital delay time(PDT)is a significant challenge for reducing treatment times,as identifying high-risk patients with AMI remains difficult.This study aims to construct a risk prediction model to identify high-risk patients and develop targeted strategies for effective and prompt care,ultimately reducing PDT and improving treatment outcomes.AIM To construct a nomogram model for forecasting pre-hospital delay(PHD)likelihood in patients with AMI and to assess the precision of the nomogram model in predicting PHD risk.METHODS A retrospective cohort design was employed to investigate predictive factors for PHD in patients with AMI diagnosed between January 2022 and September 2022.The study included 252 patients,with 180 randomly assigned to the development group and the remaining 72 to the validation group in a 7:3 ratio.Independent risk factors influencing PHD were identified in the development group,leading to the establishment of a nomogram model for predicting PHD in patients with AMI.The model's predictive performance was evaluated using the receiver operating characteristic curve in both the development and validation groups.RESULTS Independent risk factors for PHD in patients with AMI included living alone,hyperlipidemia,age,diabetes mellitus,and digestive system diseases(P<0.05).A characteristic curve analysis indicated area under the receiver operating characteristic curve values of 0.787(95%confidence interval:0.716–0.858)and 0.770(95%confidence interval:0.660-0.879)in the development and validation groups,respectively,demonstrating the model's good discriminatory ability.The Hosmer–Lemeshow goodness-of-fit test revealed no statistically significant disparity between the anticipated and observed incidence of PHD in both development and validation cohorts(P>0.05),indicating satisfactory model calibration.CONCLUSION The nomogram model,developed with independent risk factors,accurately forecasts PHD likelihood in AMI individuals,enabling efficient identification of PHD risk in these patients.展开更多
Myeloproliferative neoplasms(MPN)are a group of diseases characterized by the clonal proliferation of hematopoietic progenitor or stem cells.They are clinically classifiable into four main diseases:chronic myeloid leu...Myeloproliferative neoplasms(MPN)are a group of diseases characterized by the clonal proliferation of hematopoietic progenitor or stem cells.They are clinically classifiable into four main diseases:chronic myeloid leukemia,essential thrombocythemia,polycythemia vera,and primary myelofibrosis.These pathologies are closely related to cardio-and cerebrovascular diseases due to the increased risk of arterial thrombosis,the most common underlying cause of acute myocardial infarction.Recent evidence shows that the classical Virchow triad(hypercoagulability,blood stasis,endothelial injury)might offer an explanation for such association.Indeed,patients with MPN might have a higher number and more reactive circulating platelets and leukocytes,a tendency toward blood stasis because of a high number of circulating red blood cells,endothelial injury or overactivation as a consequence of sustained inflammation caused by the neoplastic clonal cell.These abnormal cancer cells,especially when associated with the JAK2V617F mutation,tend to proliferate and secrete several inflammatory cytokines.This sustains a pro-inflammatory state throughout the body.The direct consequence is the induction of a pro-thrombotic state that acts as a determinant in favoring both venous and arterial thrombus formation.Clinically,MPN patients need to be carefully evaluated to be treated not only with cytoreductive treatments but also with cardiovascular protective strategies.展开更多
Objective:To reveal the molecular mechanism underlying the compatibility of Salvia miltiorrhiza Bge(S.miltiorrhiza,Dan Shen)and C.tinctorius L.(C.tinctorius,Hong Hua)as an herb pair through network pharmacology and su...Objective:To reveal the molecular mechanism underlying the compatibility of Salvia miltiorrhiza Bge(S.miltiorrhiza,Dan Shen)and C.tinctorius L.(C.tinctorius,Hong Hua)as an herb pair through network pharmacology and subsequent experimental validation.Methods:Network pharmacology was applied to construct an active ingredient-efficacy target-disease protein network to reveal the unique regulation pattern of s.miltiorrhiza and C.tinctorius as herb pair.Molecular docking was used to verify the binding of the components of these herbs and their potential targets.An H9c2 glucose hypoxia model was used to evaluate the efficacy of the components and their synergistic effects,which were evaluated using the combination index.Western blot was performed to detect the protein expression of these targets.Results:Network pharmacology analysis revealed 5 pathways and 8 core targets of s.miltiorrhiza and C.tinctorius in myocardial protection.Five of the core targets were enriched in the hypoxia-inducible factor-1(HIF-1)signaling pathway.S.miltiorrhiza-C.tinctorius achieved vascular tone mainly by regulating the target genes of the HIF-1 pathway.As an upstream gene of the HIF-1 pathway,STAT3 can be activated by the active ingredients cryptotanshinone(Ctan),salvianolic acid B(Sal.B),and myricetin(Myric).Cell experiments revealed that Myric,Sal.B,and Ctan also exhibited synergistic myocardial protective activity.Molecular docking verified the strong binding of Myric,Sal.B,and Ctan to STAT3.Western blot further showed that the active ingredients synergistically upregulated the protein expressionof STAT3.Conclusion:The pharmacodynamic transmission analysis revealed that the active ingredients of S.miltiorrhiza and C.tinctorius can synergistically resist ischemia through various targets and pathways.This study provides a methodological reference for interpreting traditional Chinese medicine compatibility.展开更多
BACKGROUND Presently,there is no established standard anti-blood clot therapy for patients facing acute myocardial infarction(AMI)complicated by left ventricular thrombus(LVT).While vitamin K antagonists are the prefe...BACKGROUND Presently,there is no established standard anti-blood clot therapy for patients facing acute myocardial infarction(AMI)complicated by left ventricular thrombus(LVT).While vitamin K antagonists are the preferred choice for oral blood thinning,determining the best course of blood-thinning medication remains challenging.It is unclear if non-vitamin K antagonist oral blood thinners have different effectiveness in treating LVT.This study significantly contributes to the medical community.CASE SUMMARY The blood-thinning treatment of a patient with AMI and LVT was analyzed.Triple blood-thinning therapy included daily enteric-coated aspirin tablets at 0.1 g,daily clopidogrel hydrogen sulfate at 75 mg,and dabigatran etexilate at 110 mg twice daily.After 15 d,the patient’s LVT did not decrease but instead increased.Clinical pharmacists comprehensively analyzed the cases from the perspective of the patient’s disease status and drug interaction.The drug regimen was reformulated for the patient,replacing dabigatran etexilate with warfarin,and was administered for six months.The clinical pharmacist provided the patient with professional and standardized pharmaceutical services.The patient’s condition was discharged after meeting the international normalized ratio value(2-3)criteria.The patient fully complied with the follow-up,and the time in the therapeutic range was 78.57%,with no serious adverse effects during pharmaceutical monitoring.CONCLUSION Warfarin proves to be an effective drug for patients with AMI complicated by LVT,and its blood-thinning course lasts for six months.展开更多
Introduction:Myocardial ischemia-reperfusion(IR)injury has received widespread attention due to its damaging effects.Electroacupuncture(EA)pretreatment has preventive effects on myocardial IR injury.SLC26A4 is a Na+in...Introduction:Myocardial ischemia-reperfusion(IR)injury has received widespread attention due to its damaging effects.Electroacupuncture(EA)pretreatment has preventive effects on myocardial IR injury.SLC26A4 is a Na+independent anion reverse transporter and has not been reported in myocardial IR injury.Objectives:Tofind potential genes that may be regulated by EA and explore the role of this gene in myocardial IR injury.Methods:RNA sequencing and bioinformatics analysis were performed to obtain the differentially expressed genes in the myocardial tissue of IR rats with EA pretreatment.Myocardial infarction size was detected by TTC staining.Serum CK,creatinine kinase-myocardial band,Cardiac troponin I,and lactate dehydrogenase levels were determined by ELISA.The effect of SLC26A4 on cardiomyocyte apoptosis was explored by TUNEL staining and western blotting.The effects of SLC26A4 on inflammation were determined by HE staining,ELISA,and real-time PCR.The effect of SLC26A4 on the NF-κB pathway was determined by western blotting.Results:SLC26A4 was up-regulated in IR rats but downregulated in IR rats with EA pretreatment.Compared with IR rats,those with SLC26A4 knockdown exhibited improved cardiac function according to decreased myocardial infarction size,reduced serum LDH/CK/CK-MB/cTnI levels,and elevated left ventricular ejection fraction and fractional shortening.SLC26A4 silencing inhibited myocardial inflammation,cell apoptosis,phosphorylation,and nuclear translocation of NF-κB p65.Conclusion:SLC26A4 exhibited promoting effects on myocardial IR injury,while the SLC26A4 knockdown had an inhibitory effect on the NF-κB pathway.These results further unveil the role of SLC26A4 in IR injury.展开更多
BACKGROUND Myocardial infarction is a high-risk condition prevalent among the elderly population,often leading to adverse clinical manifestations such as reduced cardiopulmonary function,anxiety,and depression post-su...BACKGROUND Myocardial infarction is a high-risk condition prevalent among the elderly population,often leading to adverse clinical manifestations such as reduced cardiopulmonary function,anxiety,and depression post-surgery.Consequently,cardiac rehabilitation holds immense importance in mitigating these complications.AIM To evaluate the effect of individualized cardiac rehabilitation on blood pressure variability(BPV)and baroreflex sensitivity(BRS)in elderly patients with myocardial infarction.METHODS A cohort of 74 elderly patients diagnosed with myocardial infarction and admitted to our hospital between January 2021 and January 2022 were subjected to random selection.Subsequently,all patients were divided into two groups,namely the research group(n=37)and the control group(n=37),utilizing the number table method.The control group received conventional drug treatment and nursing guidance intervention,while the study group underwent individualized cardiac rehabilitation in addition to the interventions received by the control group.All patients were continuously intervened for 12 wk,and the BPV of these two groups in the 1st wk(T0),the 4th wk(T1)and the 12th wk(T2)were compared,BRS,changes in cardiopulmonary function measures,and adverse cardiovascular events.RESULTS Of 24 h diastolic BPV,24 h systolic BPV,carbon dioxide ventilation equivalent slope of the research group were lower than those of the control group at T1 and T2,BRS,peak heart rate and systolic blood pressure product,1 min heart rate recovery were higher than those of the control group,and the incidence of adverse events in the research group was lower than that of the control group,the difference was statistically significant(P<0.05).CONCLUSION In this study,we found that after individualized cardiac rehabilitation in elderly patients with myocardial infarction,BPV and BRS can be effectively improved,cardiac function is significantly enhanced,and a better prognosis is obtained.展开更多
BACKGROUND Cardiovascular disease,particularly myocardial infarction(MI)profound impact on patients'quality of life and places a substantial burden on the healthcare and economy systems.Developments in medical tec...BACKGROUND Cardiovascular disease,particularly myocardial infarction(MI)profound impact on patients'quality of life and places a substantial burden on the healthcare and economy systems.Developments in medical technology have led to the emer-gence of coronary intervention as an essential method for treating MI.AIM To assess the effects of cardiac rehabilitation care on cardiac function recovery and negative emotions in MI after coronary intervention.METHODS This study included a total of 180 patients with MI during the period from June 2022 to July 2023.Selected patients were divided into two groups:An observation group,which receiving cardiac rehabilitation care;a control group,which re-ceiving conventional care.By comparing multiple observation indicators such as cardiac function indicators,blood pressure,exercise tolerance,occurrence of adverse cardiac events,and negative emotion scores between the two groups of patients.All the data were analyzed and compared between two groups.RESULTS There were 44 males and 46 females in the observation group with an average age of 36.26±9.88 yr;there were 43 males and 47 females in the control group,with an average age of 40.87±10.5 yr.After receiving the appropriate postoperative nursing measures,the results of the observation group showed significant improvement in several indicators compared with the control group.Indicators of cardiac function,such as left ventricular end-diastolic internal diameter and left ventricular ejection fraction were significantly better in the observation group than in the control group(P<0.05).Exercise endurance assessment showed that the 6-minute walking test distance was significantly increased in the patients of the observation group(P<0.01).In addition,the incidence of adverse cardiac events was significantly lower in the observation group,and negative mood scores were significantly reduced(P<0.05).CONCLUSION Cardiac rehabilitation care after coronary intervention has a significant positive impact on functional recovery.This emphasizes the importance of cardiac rehabilitation care to improve patient recovery.展开更多
Objective:Myocardial ischemia-reperfusion injury(MIRI)is one of the leading causes of death from cardiovascular disease in humans,especially in individuals exposed to cold environments.Long non-coding RNAs(lncRNAs)reg...Objective:Myocardial ischemia-reperfusion injury(MIRI)is one of the leading causes of death from cardiovascular disease in humans,especially in individuals exposed to cold environments.Long non-coding RNAs(lncRNAs)regulate MIRI through multiple mechanisms.This study explored the regulatory effect of lncRNA-AK138945 on myocardial ischemia-reperfusion injury and its mechanism.Methods:In vivo,8-to 12-weeks-old C57BL/6 male mice underwent ligation of the left anterior descending coronary artery for 50 minutes followed by reperfusion for 48 hours.In vitro,the primary cultured neonatal mouse ventricular cardiomyocytes(NMVCs)were treated with 100μmol/L hydrogen peroxide(H_(2)O_(2)).The knockdown of lncRNA-AK138945 was evaluated to detect cardiomyocyte apoptosis,and a glucose-regulated,endoplasmic reticulum stress-related protein 94(GRP94)inhibitor was used to detect myocardial injury.Results:We found that the expression level of lncRNA-AK138945 was reduced in MIRI mouse heart tissue and H2O2-treated cardiomyocytes.Moreover,the proportion of apoptosis in cardiomyocytes increased after lncRNA-AK138945 was silenced.The expression level of Bcl2 protein was decreased,and the expression level of Bad,Caspase 9 and Caspase 3 protein was increased.Our further study found that miR-1a-3p is a direct target of lncRNA-AK138945,after lncRNA-AK138945 was silenced in cardiomyocytes,the expression level of miR-1a-3p was increased while the expression level of its downstream protein GRP94 was decreased.Interestingly,treatment with a GRP94 inhibitor(PU-WS13)intensified H2O2-induced cardiomyocyte apoptosis.After overexpression of FOXO3,the expression levels of lncRNA-AK138945 and GRP94 were increased,while the expression levels of miR-1a-3p were decreased.Conclusion:LncRNA-AK138945 inhibits GRP94 expression by regulating miR-1a-3p,leading to cardiomyocyte apoptosis.The transcription factor Forkhead Box Protein O3(FOXO3)participates in cardiomyocyte apoptosis induced by endoplasmic reticulum stress through up-regulation of lncRNA-AK138945.展开更多
基金Project of Medical and Health Research,Gansu Province(No.GSWSKY2020-13)。
文摘Objective:To observe the effect of Icariin on diabetic myocardial hypertrophy and explore its molecular mechanism.Methods:C57BL/6 mice were randomly divided into Ctrl group(normal control group),DM group(STZ intraperitoneal injection model),and DM+ICA group(diabetic C57BL/6 mice by intragastric Icariin solution 80mg/kg/d,for 3 consecutive weeks).Real-time quantitative PCR was used to detect myocardial hypertrophy markers BNP andβ-MHC.Western blotting was used to detect myocardial AMPK,p-AMPK,mTOR,p-mTOR,LC3B and Beclin1 protein expression.Echocardiogram was used to detect left ventricular mass and ejection fraction.Results:Compared with the normal control group,the expression of myocardial hypertrophy markers BNP andβ-MHC mRNA in diabetic mice were significantly increased;the expression of phosphorylated AMPK protein,autophagy-related protein LC3B and Beclin1 were significantly increased,and the expression of phosphorylated mTOR protein is significantly reduced;the left ventricular mass is significantly increased.The above changes can be reversed after treatment with Icariin,but the effect of Icariin is blocked by the autophagy inhibitor rapamycin.Conclusion:Icariin may inhibit autophagy and reduce diabetic myocardial hypertrophy through AMPK-mTOR signaling pathway.
基金supported by National Natural Science Foundation of China(81070655)
文摘Objective:To study the correlation between expression of Wnt and NCXl and cardiomyocyte apoptosis in mouse with myocardial hypertrophy.Methods:C57B/16 male mice were given the subcutaneous injection of 1 mg/kg isoprenaline to build the myocardial hypertrophy model.After 14 d of model building,mice were executed by cervical vertebra luxation.The ratio of heart weight/body weight(HW/BW) and heart weight/tibia length(HW/TL) was observed and proved using HE staining mat detected the size of eaidiomyocytes.40 male C57B/16 mice were randomly divided into the sham group(normal saline) and model group(isoprenaline),with 20 mice in each group.The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling was applied to detect the cardiomyocyte apoptosis;while Western blot and immunohistochemistry were employed to detect the expression of Wnt and NCX1.Meanwhile,the correlation between these two proteins and cardiomyocyte apoptosis was explored.Results:Compared with the sham group,the ratio of HW/BW and HW/TL was increased in the model group,as well as the bigger and hypertrophied cardiomyocytes,decreased number and increased apoptosis of eaidiomyocytes,and increased positive expression of Wnt3 a,WntSa and NCXl in the cardiac muscle tissue.Besides,there was positive correlation between the expression of Wnt and NCXl and the cardiomyocyte apoptosis.Conclusions:The expression of Wnt3 a,Wnt5a and NCXl in mouse with myocardial hypertrophy is increased and positively correlated with the cardiomyocyte apoptosis.
基金supported by grants from the National Natural Science Foundation of China(No.30440053)the Natural Science Foundation of Guangdong Province(Nos.S2011010004269 and 9151018201000029)the PhD Start-up Fund of Guangzhou Medical University(No.2012C57)
文摘This study was aimed to establish a stable animal model of left ventricular hypertrophy(LVH) to provide theoretical and experimental basis for understanding the development of LVH. The abdominal aorta of male Wistar rats(80–100 g) was constricted to a diameter of 0.55 mm between the branches of the celiac and anterior mesenteric arteries. Echocardiography using a linear phased array probe was performed as well as pathological examination and plasma B-type natriuretic peptide(BNP) measurement at 3, 4 and 6 weeks after abdominal aortic constriction(AAC). The results showed that the acute mortality rate(within 24 h) of this modified rat model was 8%. Animals who underwent AAC demonstrated significantly increased interventricular septal(IVS), LV posterior wall(LVPWd), LV mass index(LVMI), cross-sectional area(CSA) of myocytes, and perivascular fibrosis; the ejection fraction(EF), fractional shortening(FS), and cardiac output(CO) were consistently lower at each time point after AAC. Notably, differences in these parameters between AAC group and sham group were significant by 3 weeks and reached peaks at 4th week. Following AAC, the plasma BNP was gradually elevated compared with the sham group at 3rd and 6th week. It was concluded that this modified AAC model can develop LVH, both stably and safely, by week four post-surgery; echocardiography is able to assess changes in chamber dimensions and systolic properties accurately in rats with LVH.
文摘Aim The present study aims to investigate whether BMSCs transplantation may inhibit hypertrophic hearts and its underlying mechanisms. Background There is no evidence so far that Bone marrow-derived mesenchy- mal stem cells （BMSCs） can heal pathological myocardial hypertrophy. Methods To observe the antihypertrophic actions, BMSCs was indirectly cocultured with NRVCs in vitro, or intramyocardially transplanted into hypertrophic hearts in vivo. Results ISO-induced typical hypertrophic characteristics of cardiomyocytes were obviously preven- ted by BMSCs in the co-culture model in vitro and after BMSCs transplantation in vivo. Furthermore, the activation of the Ca2＋/calcineurin/NFATc3 hypertrophic pathway was shown abrogated in the presence of BMSCs both in vitro and in vivo. Interestingly, blockage of VEGF release from BMSCs but not bFGF and IGF-1 can abolish the protec- tive effects of BMSCs on cardiomyocytes hypertrophy. Consistently, VEGF administration attenuated ISO-induced BNP and β-MHC expression and the activation of Ca2＋/cal- the enlargement of cellular size, the augment of ANP, cineurin/NFATc3 hypertrophic pathway, and these can be abrogated by blocking VEGFR-1, indicating VEGFR-1 is involved in the antihypertrophic role of VEGF. We further find that the ample VEGF secretion contributing to the anti-hypertrophic effects of BMSCs originates from BMSCs interplay with cardiac cells but not BMSCs or cardiomyo- cytes alone. Conclusions Thus, mesenchymal stem cells are able to inhibit myocardial hypertrophy via interacting with cardiomyocytes so as to promote VEGF release which inhibits the activation of the Ca2＋/calcineurin/NFATc3 hypertrophic signaling pathway in cardiac cells, in addition to its well-recognized ability to ameliorate myocardial injuries by replacing dead cells.
基金National Natural Science Foundation of China(No.31570949)。
文摘Objective:To investigate the effects of cagliazin,a sodium-glucose cotransporter 2 inhibitor(SGLT-2I),on ventricular remodeling in spontaneously hypertensive rats(SHR)through renin angiotensin system(RAS)and transforming growth factor-β1(TGF-β1).Methods:The experiment was divided into 4 groups:normal blood pressure control group,SHR group,cagliet net low-dose group(30mg/kg),cagliet net high-dose group(60mg/kg),once a day for 8 weeks.Normal blood pressure rats(WKY)were used as the control group to measure blood pressure with tail sleeve sphygmomanometer(BP)and blood glucose level was measured with glucose meter Cardiac function was evaluated by echocardiography,cell area of left ventricle was evaluated by histomorphology,real-time quantitative polymerase chain reaction and protein imprinting hybridization were used to detect TGF-β1 Smad4 renin from type I collagen(Col1a)type III collagen(Col3a)matrix metalloproteinase 2(MMP-2)Expression results of angiotensin II1 type receptor 1(AGTR1)and Angiotensin II2 type receptor 2(AGTR2).Results:After 8 weeks of administration,the cardiac weight/body weight ratio(HW/BW)of left ventricular weight/heart weight ratio(LVW/HW)of kaglinet low-dose group and high-dose group was statistically significant compared with that of spontaneous hypertensive rats(P<);Compared with SHRs,the expression of Col1a,Col3a,MMP2,TGF-β1,Smad4,Renin AGTR1 was significantly down-regulated and the expression of AGTR2 was up-regulated in cagliet net low-dose and high-dose groups Conclusions:Cagliazin can improve hypertension-induced cardiac remodeling by regulating RAS and TGF-β1/Smad signaling pathways.Conclusion:From the results,canaglifozin was found to ameliorate pressure overload-induced cardiac remodeling by regulating the RAS and TGF-β1/Smad signaling pathway.
基金the National Major Basic Research Program(No.G2000056905)
文摘Objective. In a model of rat cardiac hypertrophy, the changes in the distribution of ET- 1 receptors in two subcellular fractions, the sarcolemma and the light vesicles during myocardial hypertrophy were studied. Methods. Cardiac hypertrophy was produced by placing a constricting clip around the suprarenal abdominal aorta of rats, and ET- 1 receptor was assayed with radioactive analysis method. Results. It was found that plasma and ventricular ET- 1 levels increased significantly on week 2 and week 4 of pressure overload. ET- 1 binding studies showed that during myocardial hypertrophy, the maximum binding capacity (Bmax) was increased by 41％ (P< 0.01) and 65％ (P< 0.01) in sarcolemma in H- 2 week and H- 4 week groups, but was decreased by 24％ (P< 0.01) and 21％ (P< 0.01) in light vesicles. The sum of Bmax of sarcolemmal and light vesicle fractions was increased by 33％ (P< 0.01) and 57％ (P< 0.01) in group H- 2 week and H- 4 week, respectively. Conclusion. ET- 1 receptors in rat heart were externalized from light vesicles to sarcolemma, which may contribute to the development of myocardial hypertrophy.
文摘Objective:To explore the therapeutic efficacy of L-carvone from Mentha spicata L.leaf extracts against isoproterenol-induced cardiac hypertrophy in rats.Methods:Isoproterenol(5 mg/kg)was injected intraperitoneally into rats for one month to induce cardiac hypertrophy.L-carvone(25 and 100 mg/kg)was administered orally to treat cardiac hypertrophy.The cardioprotective activity of L-carvone was evaluated by electrocardiogram,histopathological analysis as well as determination of biochemical parameters and enzymatic markers.Results:L-carvone from Mentha spicata L.at 25 and 100 mg/kg ameliorated isoproterenol-induced cardiac hypertrophy,as evidenced by reduced QRS interval on electrocardiogram,and decreased heart weight and heart index.In addition,both doses of L-carvone markedly lowered the levels of glucose,total protein,low-density lipoprotein cholesterol,aspartate transaminase,alanine transaminase,lactate dehydrogenase,creatine kinase MB,troponin-Ⅰ,N-terminal pro-B type natriuretic peptide and triglycerides while increasing high-density lipoprotein cholesterol and lipase level(P<0.05).Moreover,L-carvone alleviated contraction band necrosis,and reorganized the myofibrils with normal striations and myocytes as well as normal nuclei in cardiac histoarchitecture of rats with isoproterenol-induced cardiac hypertrophy.Conclusions:L-carvone from Mentha spicata L.leaf extract can restore abnormal cardiac function and may be further explored as a therapeutic agent against the deleterious effects of cardiac hypertrophy after further evaluation.
文摘The incidence of acute myocardial infarction (AMI) is increasing year by year, which seriously endangers human health around the world. The preferred treatment strategy for AMI patients is the use of drug-eluting stents (DES), as there is ample evidence to suggest that stent implantation can reduce major adverse cardiovascular events (MACEs). With the application of drug-coated balloons (DCBs) and the enhancement of the concept of interventional without implantation, the question is whether DCBs can be safely and effectively used in patients with AMI? The purpose of this study was to investigate the safety and effectiveness of DCBs in the treatment of AMI. A retrospective review of clinical data was conducted on 55 AMI patients who underwent primary percutaneous coronary intervention (PCI) from January 2020 to December 2021. Of these patients, 25 were treated with DCBs and 30 were treated with DESs. Optical coherence tomography (OCT) was used to measure the minimum lumen diameter, lumen stenosis, and coronary artery dissection before and after surgery, and angina pectoris attacks and various MACEs were recorded at 1, 6, and 12 months after surgery. The results showed that there were no significant differences in clinical baseline data between the two groups. However, the minimum lumen diameter of the DCB group immediately after the operation was smaller than that of the DES group, and the stenosis degree of the lumen in the DCB group was higher than that in the DES group. The incidence of coronary artery dissection in the DCB group was significantly higher than that in the DES group, but the majority of them were type B. At 1, 6, and 12 months after treatment, there was no significant difference in the occurrence of MACEs between the two groups. In conclusion, DCBs is a safe and effective treatment for AMI. However, the incidence of coronary artery dissection in DCB patients is higher than that in DES patients, but the majority of them are type B. .
文摘Medical history summary: Male, 47 years old, was admitted to the hospital due to “dizziness accompanied by chest tightness and pain for more than 8 days”. One week ago, the patient experienced chest tightness, chest pain accompanied by profuse sweating for 3 hours and underwent emergency percutaneous coronary intervention (PCI) at a local hospital. The procedure revealed left main stem occlusion with subsequent left main stem to left anterior descending artery percutaneous transluminal coronary angioplasty (PTCA). After the procedure, the patient experienced hemodynamic instability, recurrent ventricular fibrillation, and critical condition, thus transferred to our hospital for further treatment. Symptoms and signs: The patient is in a comatose state, unresponsive to stimuli, with bilateral dilated pupils measuring 2.0 mm, exhibiting reduced sensitivity to light reflex, and recurrent fever. Coarse breath sounds can be heard in both lungs, with audible moist rales. Irregular breathing pattern is observed, and heart sounds vary in intensity. No pathological murmurs are auscultated in any valve auscultation area. Diagnostic methods: Coronary angiography results at the local hospital showed complete occlusion of the left main stem, and left main stem to left anterior descending artery percutaneous transluminal coronary angioplasty (PTCA) was performed. However, the distal guidewire did not pass through. After admission, blood tests showed a Troponin T level of 1.44 ng/ml and a Myoglobin level of 312 ng/ml. The platelet count was 1390 × 10<sup>9</sup>/L. Von Willebrand factor (vWF) activity was measured at 201.9%. Bone marrow aspiration biopsy showed active bone marrow proliferation and platelet clustering. The peripheral blood smear also showed platelet clustering. JAK-2 gene testing was positive, confirming the diagnosis of primary thrombocytosis. Treatment methods: The patient is assisted with mechanical ventilation and intra-aortic balloon counterpulsation to improve coronary blood flow. Electrolyte levels are closely monitored, especially maintaining plasma potassium levels between 4.0 and 4.5 mmol/l. Hydroxyurea 500 mg is administered for platelet reduction. Anticoagulants and antiplatelet agents are used rationally to prevent further infarction or bleeding. Antiarrhythmic, lipid-lowering, gastroprotective, hepatoprotective, and heart failure treatment are also provided. Clinical outcome: The family members chose to withdraw treatment and signed for discharge due to a combination of reasons, including economic constraints and uncertainty about the prognosis due to the long disease course. Acute myocardial infarction has gradually become one of the leading causes of death in our country. As a “green channel” disease, corresponding diagnostic and treatment protocols have been established in China, and significant progress has been made in emergency care. There are strict regulations for the time taken from the catheterization lab to the cardiac intensive care unit, and standardized treatments are provided to patients once they enter the intensive care unit. Research results show that the incidence of acute myocardial infarction in patients with primary thrombocythemia within 10 years is 9.4%. This type of disease is rare and difficult to cure, posing significant challenges to medical and nursing professionals. In order to benefit future patients, we have documented individual cases of treatment and nursing care for these patients. The research results show that these patients exhibit resistance to traditional oral anticoagulant drugs and require alternative anticoagulants. Additionally, there are significant differences in serum and plasma potassium levels among patients. Therefore, when making clinical diagnoses, it is necessary to carefully distinguish between the two. Particularly, nursing personnel should possess dialectical thinking when supplementing potassium levels in patients in order to reduce the incidence of malignant arrhythmias and mortality rates.
文摘BACKGROUND Metastatic cardiac tumors are known to occur more frequently than primary cardiac tumors,however,they often remain asymptomatic and are commonly dis-covered on autopsy.Malignant tumors with a relatively high frequency of cardiac metastasis include mesothelioma,melanoma,lung cancer,and breast cancer,whereas reports of esophageal cancer with cardiac metastasis are rare.CASE SUMMARY The case of a 60-year-old man who complained of dysphagia is presented.Upper gastrointestinal endoscopy showed a submucosal tumor-like elevated lesion in the esophagus causing stenosis.Contrast-enhanced computed tomography showed left atrial compression due to the esophageal tumor,multiple liver and lung metastases,and a left pleural effusion.Pathological examination of a biopsy speci-men from the esophageal tumor showed spindle-shaped cells,raising suspicion of esophageal sarcoma.The disease progressed rapidly,and systemic chemotherapy was deemed necessary,however,due to his poor general condition,adminis-tration of cytotoxic agents was considered difficult.Given his high Combined Positive Score,nivolumab was administered,however,the patient soon died from the disease.The autopsy confirmed spindle cell carcinoma(SCC)of the esophagus and cardiac metastasis with similar histological features.Cancer stem cell markers,ZEB1 and TWIST,were positive in both the primary tumor and the cardiac metastasis.CONCLUSION To the best of our knowledge,there have been no prior reports of cardiac metastasis of esophageal SCC.This case highlights our experience with a patient with esophageal SCC who progressed rapidly and died from the disease,with the autopsy examination showing cardiac metastasis.
文摘BACKGROUND Acute myocardial infarction(AMI)is a severe cardiovascular disease caused by the blockage of coronary arteries that leads to ischemic necrosis of the myocardium.Timely medical contact is critical for successful AMI treatment,and delays increase the risk of death for patients.Pre-hospital delay time(PDT)is a significant challenge for reducing treatment times,as identifying high-risk patients with AMI remains difficult.This study aims to construct a risk prediction model to identify high-risk patients and develop targeted strategies for effective and prompt care,ultimately reducing PDT and improving treatment outcomes.AIM To construct a nomogram model for forecasting pre-hospital delay(PHD)likelihood in patients with AMI and to assess the precision of the nomogram model in predicting PHD risk.METHODS A retrospective cohort design was employed to investigate predictive factors for PHD in patients with AMI diagnosed between January 2022 and September 2022.The study included 252 patients,with 180 randomly assigned to the development group and the remaining 72 to the validation group in a 7:3 ratio.Independent risk factors influencing PHD were identified in the development group,leading to the establishment of a nomogram model for predicting PHD in patients with AMI.The model's predictive performance was evaluated using the receiver operating characteristic curve in both the development and validation groups.RESULTS Independent risk factors for PHD in patients with AMI included living alone,hyperlipidemia,age,diabetes mellitus,and digestive system diseases(P<0.05).A characteristic curve analysis indicated area under the receiver operating characteristic curve values of 0.787(95%confidence interval:0.716–0.858)and 0.770(95%confidence interval:0.660-0.879)in the development and validation groups,respectively,demonstrating the model's good discriminatory ability.The Hosmer–Lemeshow goodness-of-fit test revealed no statistically significant disparity between the anticipated and observed incidence of PHD in both development and validation cohorts(P>0.05),indicating satisfactory model calibration.CONCLUSION The nomogram model,developed with independent risk factors,accurately forecasts PHD likelihood in AMI individuals,enabling efficient identification of PHD risk in these patients.
文摘Myeloproliferative neoplasms(MPN)are a group of diseases characterized by the clonal proliferation of hematopoietic progenitor or stem cells.They are clinically classifiable into four main diseases:chronic myeloid leukemia,essential thrombocythemia,polycythemia vera,and primary myelofibrosis.These pathologies are closely related to cardio-and cerebrovascular diseases due to the increased risk of arterial thrombosis,the most common underlying cause of acute myocardial infarction.Recent evidence shows that the classical Virchow triad(hypercoagulability,blood stasis,endothelial injury)might offer an explanation for such association.Indeed,patients with MPN might have a higher number and more reactive circulating platelets and leukocytes,a tendency toward blood stasis because of a high number of circulating red blood cells,endothelial injury or overactivation as a consequence of sustained inflammation caused by the neoplastic clonal cell.These abnormal cancer cells,especially when associated with the JAK2V617F mutation,tend to proliferate and secrete several inflammatory cytokines.This sustains a pro-inflammatory state throughout the body.The direct consequence is the induction of a pro-thrombotic state that acts as a determinant in favoring both venous and arterial thrombus formation.Clinically,MPN patients need to be carefully evaluated to be treated not only with cytoreductive treatments but also with cardiovascular protective strategies.
基金supported by the National Natural Science Foundation of China(81703947)the Fundamental Research Funds for the Central Universities(2019-JYB-XJSJJ-011).
文摘Objective:To reveal the molecular mechanism underlying the compatibility of Salvia miltiorrhiza Bge(S.miltiorrhiza,Dan Shen)and C.tinctorius L.(C.tinctorius,Hong Hua)as an herb pair through network pharmacology and subsequent experimental validation.Methods:Network pharmacology was applied to construct an active ingredient-efficacy target-disease protein network to reveal the unique regulation pattern of s.miltiorrhiza and C.tinctorius as herb pair.Molecular docking was used to verify the binding of the components of these herbs and their potential targets.An H9c2 glucose hypoxia model was used to evaluate the efficacy of the components and their synergistic effects,which were evaluated using the combination index.Western blot was performed to detect the protein expression of these targets.Results:Network pharmacology analysis revealed 5 pathways and 8 core targets of s.miltiorrhiza and C.tinctorius in myocardial protection.Five of the core targets were enriched in the hypoxia-inducible factor-1(HIF-1)signaling pathway.S.miltiorrhiza-C.tinctorius achieved vascular tone mainly by regulating the target genes of the HIF-1 pathway.As an upstream gene of the HIF-1 pathway,STAT3 can be activated by the active ingredients cryptotanshinone(Ctan),salvianolic acid B(Sal.B),and myricetin(Myric).Cell experiments revealed that Myric,Sal.B,and Ctan also exhibited synergistic myocardial protective activity.Molecular docking verified the strong binding of Myric,Sal.B,and Ctan to STAT3.Western blot further showed that the active ingredients synergistically upregulated the protein expressionof STAT3.Conclusion:The pharmacodynamic transmission analysis revealed that the active ingredients of S.miltiorrhiza and C.tinctorius can synergistically resist ischemia through various targets and pathways.This study provides a methodological reference for interpreting traditional Chinese medicine compatibility.
文摘BACKGROUND Presently,there is no established standard anti-blood clot therapy for patients facing acute myocardial infarction(AMI)complicated by left ventricular thrombus(LVT).While vitamin K antagonists are the preferred choice for oral blood thinning,determining the best course of blood-thinning medication remains challenging.It is unclear if non-vitamin K antagonist oral blood thinners have different effectiveness in treating LVT.This study significantly contributes to the medical community.CASE SUMMARY The blood-thinning treatment of a patient with AMI and LVT was analyzed.Triple blood-thinning therapy included daily enteric-coated aspirin tablets at 0.1 g,daily clopidogrel hydrogen sulfate at 75 mg,and dabigatran etexilate at 110 mg twice daily.After 15 d,the patient’s LVT did not decrease but instead increased.Clinical pharmacists comprehensively analyzed the cases from the perspective of the patient’s disease status and drug interaction.The drug regimen was reformulated for the patient,replacing dabigatran etexilate with warfarin,and was administered for six months.The clinical pharmacist provided the patient with professional and standardized pharmaceutical services.The patient’s condition was discharged after meeting the international normalized ratio value(2-3)criteria.The patient fully complied with the follow-up,and the time in the therapeutic range was 78.57%,with no serious adverse effects during pharmaceutical monitoring.CONCLUSION Warfarin proves to be an effective drug for patients with AMI complicated by LVT,and its blood-thinning course lasts for six months.
基金This study was funded by the Joint Guidance Project of Heilongjiang Provincial Natural Science Foundation of China(LH2023H063)the Scientific Research Project of Academic Thought Inheritance of Chinese Medicine Great Master of Heilongjiang Provincial Administration of Traditional Chinese Medicine(ZHY2023-151).
文摘Introduction:Myocardial ischemia-reperfusion(IR)injury has received widespread attention due to its damaging effects.Electroacupuncture(EA)pretreatment has preventive effects on myocardial IR injury.SLC26A4 is a Na+independent anion reverse transporter and has not been reported in myocardial IR injury.Objectives:Tofind potential genes that may be regulated by EA and explore the role of this gene in myocardial IR injury.Methods:RNA sequencing and bioinformatics analysis were performed to obtain the differentially expressed genes in the myocardial tissue of IR rats with EA pretreatment.Myocardial infarction size was detected by TTC staining.Serum CK,creatinine kinase-myocardial band,Cardiac troponin I,and lactate dehydrogenase levels were determined by ELISA.The effect of SLC26A4 on cardiomyocyte apoptosis was explored by TUNEL staining and western blotting.The effects of SLC26A4 on inflammation were determined by HE staining,ELISA,and real-time PCR.The effect of SLC26A4 on the NF-κB pathway was determined by western blotting.Results:SLC26A4 was up-regulated in IR rats but downregulated in IR rats with EA pretreatment.Compared with IR rats,those with SLC26A4 knockdown exhibited improved cardiac function according to decreased myocardial infarction size,reduced serum LDH/CK/CK-MB/cTnI levels,and elevated left ventricular ejection fraction and fractional shortening.SLC26A4 silencing inhibited myocardial inflammation,cell apoptosis,phosphorylation,and nuclear translocation of NF-κB p65.Conclusion:SLC26A4 exhibited promoting effects on myocardial IR injury,while the SLC26A4 knockdown had an inhibitory effect on the NF-κB pathway.These results further unveil the role of SLC26A4 in IR injury.
文摘BACKGROUND Myocardial infarction is a high-risk condition prevalent among the elderly population,often leading to adverse clinical manifestations such as reduced cardiopulmonary function,anxiety,and depression post-surgery.Consequently,cardiac rehabilitation holds immense importance in mitigating these complications.AIM To evaluate the effect of individualized cardiac rehabilitation on blood pressure variability(BPV)and baroreflex sensitivity(BRS)in elderly patients with myocardial infarction.METHODS A cohort of 74 elderly patients diagnosed with myocardial infarction and admitted to our hospital between January 2021 and January 2022 were subjected to random selection.Subsequently,all patients were divided into two groups,namely the research group(n=37)and the control group(n=37),utilizing the number table method.The control group received conventional drug treatment and nursing guidance intervention,while the study group underwent individualized cardiac rehabilitation in addition to the interventions received by the control group.All patients were continuously intervened for 12 wk,and the BPV of these two groups in the 1st wk(T0),the 4th wk(T1)and the 12th wk(T2)were compared,BRS,changes in cardiopulmonary function measures,and adverse cardiovascular events.RESULTS Of 24 h diastolic BPV,24 h systolic BPV,carbon dioxide ventilation equivalent slope of the research group were lower than those of the control group at T1 and T2,BRS,peak heart rate and systolic blood pressure product,1 min heart rate recovery were higher than those of the control group,and the incidence of adverse events in the research group was lower than that of the control group,the difference was statistically significant(P<0.05).CONCLUSION In this study,we found that after individualized cardiac rehabilitation in elderly patients with myocardial infarction,BPV and BRS can be effectively improved,cardiac function is significantly enhanced,and a better prognosis is obtained.
文摘BACKGROUND Cardiovascular disease,particularly myocardial infarction(MI)profound impact on patients'quality of life and places a substantial burden on the healthcare and economy systems.Developments in medical technology have led to the emer-gence of coronary intervention as an essential method for treating MI.AIM To assess the effects of cardiac rehabilitation care on cardiac function recovery and negative emotions in MI after coronary intervention.METHODS This study included a total of 180 patients with MI during the period from June 2022 to July 2023.Selected patients were divided into two groups:An observation group,which receiving cardiac rehabilitation care;a control group,which re-ceiving conventional care.By comparing multiple observation indicators such as cardiac function indicators,blood pressure,exercise tolerance,occurrence of adverse cardiac events,and negative emotion scores between the two groups of patients.All the data were analyzed and compared between two groups.RESULTS There were 44 males and 46 females in the observation group with an average age of 36.26±9.88 yr;there were 43 males and 47 females in the control group,with an average age of 40.87±10.5 yr.After receiving the appropriate postoperative nursing measures,the results of the observation group showed significant improvement in several indicators compared with the control group.Indicators of cardiac function,such as left ventricular end-diastolic internal diameter and left ventricular ejection fraction were significantly better in the observation group than in the control group(P<0.05).Exercise endurance assessment showed that the 6-minute walking test distance was significantly increased in the patients of the observation group(P<0.01).In addition,the incidence of adverse cardiac events was significantly lower in the observation group,and negative mood scores were significantly reduced(P<0.05).CONCLUSION Cardiac rehabilitation care after coronary intervention has a significant positive impact on functional recovery.This emphasizes the importance of cardiac rehabilitation care to improve patient recovery.
基金This work was supported in part by the National Natural Science Foundation of China(82370417,81970320,82270273)the Certificate of China Postdoctoral Science Foundation Grant(2021M693826)+1 种基金the postdoctoral funding from Heilongjiang Province(21042230046)the Hai Yan Youth Fund from Harbin Medical University Cancer Hospital(JJQN2021-09).
文摘Objective:Myocardial ischemia-reperfusion injury(MIRI)is one of the leading causes of death from cardiovascular disease in humans,especially in individuals exposed to cold environments.Long non-coding RNAs(lncRNAs)regulate MIRI through multiple mechanisms.This study explored the regulatory effect of lncRNA-AK138945 on myocardial ischemia-reperfusion injury and its mechanism.Methods:In vivo,8-to 12-weeks-old C57BL/6 male mice underwent ligation of the left anterior descending coronary artery for 50 minutes followed by reperfusion for 48 hours.In vitro,the primary cultured neonatal mouse ventricular cardiomyocytes(NMVCs)were treated with 100μmol/L hydrogen peroxide(H_(2)O_(2)).The knockdown of lncRNA-AK138945 was evaluated to detect cardiomyocyte apoptosis,and a glucose-regulated,endoplasmic reticulum stress-related protein 94(GRP94)inhibitor was used to detect myocardial injury.Results:We found that the expression level of lncRNA-AK138945 was reduced in MIRI mouse heart tissue and H2O2-treated cardiomyocytes.Moreover,the proportion of apoptosis in cardiomyocytes increased after lncRNA-AK138945 was silenced.The expression level of Bcl2 protein was decreased,and the expression level of Bad,Caspase 9 and Caspase 3 protein was increased.Our further study found that miR-1a-3p is a direct target of lncRNA-AK138945,after lncRNA-AK138945 was silenced in cardiomyocytes,the expression level of miR-1a-3p was increased while the expression level of its downstream protein GRP94 was decreased.Interestingly,treatment with a GRP94 inhibitor(PU-WS13)intensified H2O2-induced cardiomyocyte apoptosis.After overexpression of FOXO3,the expression levels of lncRNA-AK138945 and GRP94 were increased,while the expression levels of miR-1a-3p were decreased.Conclusion:LncRNA-AK138945 inhibits GRP94 expression by regulating miR-1a-3p,leading to cardiomyocyte apoptosis.The transcription factor Forkhead Box Protein O3(FOXO3)participates in cardiomyocyte apoptosis induced by endoplasmic reticulum stress through up-regulation of lncRNA-AK138945.
