The clinical effect of sacubitril valsartan combined with dapagliflozin in heart failure with reduced ejection fraction and non-diabetes patients / 西安交通大学学报(医学版)

【Objective】 To observe the clinical effect of combination therapy of sacubitril valsartan and dapagliflozin in heart failure with reduced ejection fraction (HFrEF) and non-diabetes patients. 【Methods】 This study involved 96 patients with HFrEF and non-diabetes. The patients were randomly divided into control group (50 cases) and observation group (46 cases). On the basis of routine treatment, the control group was treated with sacubitril valsartan, while the observation group was treated with sacubitril valsartan and dapagliflozin. After 1-month and 6-month treatment, we monitored blood pressure, N-terminal pro brain natriuretic peptide (NT-proBNP), high sensitivity troponin T (cTnT), fasting blood glucose (FBG), glycosylated hemoglobin (HbA1c), left ventricular ejection fraction (LVEF), left ventricular end diastolic diameter (LVEDd), left atrial diameter (LAD), left ventricular posterior wall thickness (LVPW), Minnesota soda heart failure life quality score (MLHFQ), the incidence of rehospitalization and death, and major adverse cardiovascular events (MACE) in the two groups. 【Results】 After 6 months, systolic blood pressure, cTnT, NT-proBNP, LVEDd, LVPW, and LAD of the observation group were significantly decreased compared with the control group (P0.05). 【Conclusion】 The combination treatment of sacubitril valsartan and dapagliflozin on HFrEF and non-diabetes patients can significantly improve cardiac function, inhibit myocardial remodeling, reduce the incidence of MACE, and improve the prognosis.

B lymphocytes promote angiotensin Ⅱ/phenylephrine induced cardiac hypertrophy by regulating inflammatory cell aggregation / 西安交通大学学报(医学版)

【Objective】 To explore B lymphocytes’ role and mechanisms in angiotensinⅡ/phenylephrine (AngⅡ/PE) induced cardiomyopathy so as to understand the role of inflammatory cells in myocardial injury. 【Methods】 AngⅡ/PE was administered to wild-type (WT) and B cells deficiency (μMT) mice for 14 days or 28 days. The mice were analyzed by blood pressure measurement, echocardiography imaging, flow cytometry, and histology. Cardiac fibrosis was evaluated by Masson staining. 【Results】 Compared with the control group, the left ventricular mass (P<0.01), heart mass/tibia length ratio (P<0.01) and cross-sectional area of cardiomyocytes in AngⅡ/PE group were significantly increased (P<0.01). After 2 weeks of AngⅡ/PE treatment, B lymphocytes (P<0.05), CD45+ leukocytes (P<0.05), CD64-Ly6C+ monocytes (P<0.05), CD64+Ly6C-macrophages (P<0.05) and Ly6g+ neutrophils (P<0.05) were recruited in myocardial tissue. Compared with WT_AngⅡ/PE group, the heart weight/tibia length ratio (P<0.05), left ventricular weight (P<0.05) and myocardial cell cross-sectional area (P<0.05) of μMT_AngⅡ/PE mice were significantly improved. CD45+Ly6C+CD64- monocytes (P<0.05) and CD45+Ly6C-CD64+ macrophages (P<0.05) were significantly decreased. 【Conclusion】 B lymphocytes deficiency improves AngⅡ/PE induced cardiac hypertrophy by reducing the infiltration of CD45+Ly6C+CD64- monocytes and CD45+Ly6C- CD64+ macrophages.

Effects of insulin on the QT interval and induced arrhythmias of human cardiomycytes / 西安交通大学学报(医学版)

【Objective】 To explore the effects of insulin on the QT interval and induced arrhythmias of cardiomyocytes derived from human induced pluripotent stem cells （hiPSC-CMs）. 【Methods】 Immunofluorescence staining and flow cytometry were used to analyze the purity of hiPSC-CMs. Microelectrode array （MEA） was utilized to detect the electrophysiological changes including heart rate （HR）， field potential duration （FPD， which is similar to QT interval in ECG）， FPDc （FPD corrected by HR）， conduction velocity （CV）， and spike amplitude before and after insulin treatment. The effects of E4031 on QT interval prolongation and induced arrhythmias of hiPSC-CMs were evaluated before and after treatment with insulin. 【Results】 hiPSC-CMs highly expressed myocardial specific marker cTnT. The purity of hiPSC-CMs was 97.1%. After 5-day insulin treatment of hiPSC-CMs， HR increased by （11.9±3.3）%， FPD shortened by （22.7±2.8）%， FPDc shortened by （15.6±1.6）%， and spike amplitude increased by （39.1±7.9）% when compared with untreated group， but CV remained unchanged. 10 nmol/L of E4031 could prolong the FPDc of hiPSC-CMs by （37.8±9.0）%， and 30 nmol/L of E4031 could induce arrhythmias. After insulin treatment， 10 nmol/L of E4031 prolonged the FPDc of hiPSC-CMs by （21.8±3.1）% （compared with the untreated group， insulin decreased FPDc prolongation by E4031， 37.8%±9.0% vs. 21.8%±3.1%， P<0.05）， while 30 nmol/L of E4031 did not induce arrhythmias. 【Conclusion】 Insulin can shorten the QT interval of hiPSC-CMs and significantly reduce the QT interval prolongation and the risk of arrhythmias induced by drugs.

Effect of bisoprolol on ICa,Lin volume overload combined with pressure overload heart failure in rabbits / 西安交通大学学报(医学版)

【Objective】 To explore the effect of bisoprolol on ICa，Lin volume overload combined with pressure overload heart failure in rabbits. 【Methods】 Totally 82 male New Zealand rabbits （2.5-3.0 kg） were randomly divided into three groups： SO （sham group）， HF （heart failure group）， and BF （heart failure with bisoprolol treatment group）. HF rabbits were duplicated by aortic valve insufficiency procedure combined with abdominal aorta constriction procedure. Real-time PCR and Western blot analysis were performed to detect the expression of ICa，L in left ventricular myocytes. Left ventricular myocytes were isolated； then the cell membrane capacitance， the current density， activation and inactivation of ICa，L were recorded by whole cell patch clamp. 【Results】 ① Bisoprolol could improve the heart function of heart failure rabbits according to the measurement of echocardiography and BNP. ② The expressions of ICa，L mRNA and protein decreased significantly in heart failing rabbits （P<0.01）， but remained unaltered after chronic bisoprolol treatment （P>0.05）. ③ Membrane capacitance was larger in heart failing groups than in sham group （P<0.01）. ICa，L current density decreased greatly in HF group （P<0.01）. Bisoprolol treatment could not change Cm or ICa，L density （P>0.05）. V1/2 of activation curve negative shift enlarged window currents in heart failure groups. Bisoprolol treatment caused window currents to decrease. 【Conclusion】 Bisoprolol could reverse the heart function of heart failure rabbits and also affect the function of ICa，L.

TNF Receptor 1/2 Predict Heart Failure Risk in Type 2 Diabetes Mellitus Patients.

Inflammation plays an important role in heart failure and diabetes mellitus. Traditional serum markers have limited predictive value in heart failure and diabetes. TNFR1 and TNFR2 (TNFR1/2) have been proven to be strongly associated with heart failure and diabetes complications. This study aimed to assess the association of sTNFR1 and sTNFR2 levels and incidental HF risk in diabetes patients.We detected the mRNA, protein, and serum expression of TNFR1/2, their downstream signaling pathway protein NF-kB, and JNK expression and some traditional serum inflammatory markers in a heart failure group without diabetes mellitus or abnormal glucose tolerance (n = 84), a diabetes mellitus group without heart failure (n = 86), and a heart failure with diabetes mellitus group (n = 86).TNFR1/2 were significantly higher in patients with heart failure and diabetes mellitus based on mRNA expression to protein expression and serum expression. However, there were no differences in mRNA, protein, and serum levels of TNFR1/2 between the HF group and DM group. Furthermore, there were no differences between the groups in some traditional serum inflammatory markers.This study demonstrated higher expressions of TNFR, NF-kB, and JNK in patients with heart failure and diabetes mellitus. Compared with traditional serum markers, TNFR1 and TNFR2 are associated with heart failure risk in type 2 diabetes mellitus patients.

TLR3 and TLR4 as potential clinical biomarkers for in-stent restenosis in drug-eluting stents patients.

In-stent restenosis is still a clinic trouble for percutaneous coronary intervention in drug-stent era. The molecular basis of restenosis is intensively associated with inflammation. TLR3 and TLR4 as innate immune factors have been proven to play a key role in atherosclerosis disease. The aim of this study is to study the TLR3 and TLR4 expressions and their downstream signaling proteins in the inflammatory process of restenosis after drug-stent therapy. mRNA and protein expression of TLR3 and TLR4 were detected in peripheral blood monocytes of primary group (n = 38), N-ISR group (n = 36) and ISR group (n = 33). Some inflammatory factors (including TLR3 and TLR4) were evaluated in serum of three groups. mRNA and protein expression of TLR3 and TLR4 and their downstream signaling proteins have shown a higher level in restenosis patients than non-restenosis patients and even primary patients who accepted first stent therapy. In serum, different from some nonspecific and downstream inflammatory factors, TLR3 and TLR4 also show a significantly higher level in ISR group compared with N-ISR group and primary group. This study provides a potential clinical biomarker for in-stent restenosis in drug-stent patients and some interesting data about the role of TLRs and their downstream signaling factors in the inflammatory process of in-stent restenosis. Compared with first stent therapy and non-restenosis patients, it is hopeful that TLR3 and TLR4 are potential noninvasive biomarkers in prognosis restenosis.

Clinical Feature Analysis of Papillary Muscle Hypertrophic Cardomyopathy in 21 Patients / 中国循环杂志

Objective: To explore the clinical and magnetic resonance imaging (MRI) features of papillary musclehypertrophic cardiomyopathy. Methods: Our research contained 2 groups: Papillary muscle hypertrophic cardiomyopathy group,n=21 patients treated in our hospital from 2013-01 to 2015-12 including 18 male and 3 female; Control group,n=50 subjects without cardiovascular disease those were conifrmed by our hospital at the same period of time. Clinical and MRI examinations were conducted in all patients, the ifndings were compared between 2 groups. Results: Compared with control subjects, papillary musclehypertrophic cardiomyopathy patients had the main symptoms of shortness of breath, chest tightness and pain; associated with systolic murmur; ECG could be normal or with T wave inversion; cardiac MRI showed that 1/2 papillary muscle diameter>1.1cm. Blood levels of triglyceride, left atrial diameter, inter-ventricular septum thickness, the values of E/A and EDT were statistically different between 2 groups, allP<0.05. Conclusion: Clinical features of papillary muscle hypertrophic cardiomyopathy were lack of speciifcity, the morbidity and clinical signiifcance should be further investigated.

GAPDH-silence preserves H9C2 cells from acute hypoxia and reoxygenation injury.

BACKGROUND: Acute hypoxia and reoxygenation injury, as a common environmental stress condition, is a basic condition of most pathophysiological processes. It has been approve that autophagy and oxidant stress could contribute to acute hypoxia and reoxygenation injury. This study is aimed to examine the effect of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) silence on cell injury with acute hypoxia and reoxygenation injury by autophagy and antioxidant stress pathway. METHODS: GAPDH expression was silenced by siRNA in H9C2 cardiomyoblasts with acute hypoxia and reoxygenation injury. Autophagy was detected by western blot for autophagy proteins and monodansylcadaverine (MDC) staining for acidic substances. Pro-apoptosis protein and flow cytometry were used to assess cell apoptosis and death and intracellular adenosine triphosphate (ATP) relative concentration was measured. Oxidant stress was assessed by measuring 2'-7'-dichlorodihydrofluorescein diacetate (DCFH-DA), thiobarbituric acid reactive substances (TBARS), glutathione (GSH) and super oxide dismutase (SOD). RESULTS: In this study, GAPDH-silence enhanced autophagy in H9C2 cells with acute hypoxia and reoxygenation injury, decreased oxidant stress and increased antioxidant pathways; and reduced cell apoptosis and death. However, GAPDH-silence had no significant effect on cell energy. CONCLUSION: GAPDH pre-silence by siRNA reduces H9C2 cell death occurring via autophagy and anti-oxidative stress pathway in acute hypoxia and reoxygenation injury. This study enriches the understanding of GAPDH pathophysiology role, and provides potential new therapeutic targets for cardiac disease states characterized by oxidative stress.

GAPDH-knockdown reduce rotenone-induced H9C2 cells death via autophagy and anti-oxidative stress pathway.

BACKGROUND: GAPDH, well known for its house-keeping functions, has also been shown to be involved in cell injury, apoptosis and death under conditions of stress such as starvation, chemical injury and oxidative stress. This study examines the effect of GAPDH knockdown on cell injury in response to Rotenone. METHODS: GAPDH was knocked down in H9C2 cardiomyoblasts using siRNA prior to exposure to rotenone (0 nM, 20 nM, 40 nM and 80 nM). Autophagy was detected by western blot for autophagy proteins (Beclin-1, Atg5, LC-3A/B and p62) and MDC staining for acidic substances. Pro-apoptosis protein and flow cytometry were used to assess cell apoptosis and death and intracellular ATP relative concentration was measured. Oxidant stress was assessed by measuring DCFH-DA, TBARS, GSH and SOD. RESULTS: In this study, GAPDH-knockdown enhanced autophagy in rotenone-induced H9C2 cells, decreased oxidant stress and increased antioxidant pathways; and reduced cell apoptosis and death. Furthermore, GAPDH-knockdown preserved cell energy. CONCLUSION: siRNA-mediated GAPDH knockdown reduced rotenone-induced H9C2 cell death occurring via autophagy and anti-oxidative stress pathway. This study enriches the understanding of GAPDH pathophysiology role, and provides potential new therapeutic targets for cardiac disease states characterized by oxidative stress.

Effect of adipose-derived mesenchymal stem cell transplantation on inflammatory response and ventricular remodeling after myocardial infarction / 中国组织工程研究

BACKGROUND:Whether adipose-derived mesenchymal stem cells are able to exert immunomodulatory effects in the treatment of myocardial infarction, as wel as the best time, is less reported. OBJECTIVE:To observe the effect of adipose-derived mesenchymal stem cells on inflammatory reaction and ventricular remodeling after myocardial infarction, and to explore the possible mechanisms of adipose-derived mesenchymal stem cells for the treatment of myocardial infarction. METHODS:Enzyme digestion method was employed to isolate and culture rat adipose-derived mesenchymal stem cells. By ligation of the left anterior descending coronary artery, we established animal models of myocardial infarction in 40 rats. The rats were randomly divided into four groups:sham group, control group (injected high-glucose Dulbecco’s modified Eagle’s medium), 3-hour transplantation group (transplanted adipose-derived mesenchymal stem cells after 3 hours of myocardial infarction), 7-day transplantation group (transplanted adipose-derived mesenchymal stem cells after 7 days of myocardial infarction). After 14 days of operation, the levels of tumor necrosis factor-αand interleukin-10 in the plasma were detected by enzyme linked immunosorbent assay. After 28 days of operation, the left ventricular end diastolic diameter, left ventricular end systolic diameter, left ventricular ejection fraction and left ventricular fractional shortening were measured by echocardiography. RESULTS AND CONCLUSION:Compared with the control group, in the 3-hour transplantation group and 7-day transplantation group, the levels of tumor necrosis factor-αwere significantly lower (P<0.01), and the levels of interleukin-10 were significantly higher (P<0.01) at postoperative 14 days;the left ventricular end diastolic diameter and left ventricular end systolic diameter in the two transplantation groups were also significantly smal er (P<0.05), but left ventricular ejection fraction and left ventricular fractional shortening were significantly elevated (P<0.05), which was more apparent in the 3-hour transplantation group than the 7-day transplantation group. Adipose-derived mesenchymal stem cells transplantation in acute phase of myocardial infarction can suppress the inflammatory response, regulate the cytokine network equilibrium, and thus delay ventricular remodeling and improve cardiac function.

Sodium channel blockers inhibit the differentiation of rat bone marrow mesenchymal stem cells into cardiac-like cells / 中国组织工程研究

10.3969/j.issn.2095-4344.2013.23.001

Improvement of cardiac function and reversal of gap junction remodeling by Neuregulin-1β in volume-overloaded rats with heart failure / 老年心脏病学杂志（英文版）

Objective We performed experiments using Neuregulin-1β (NRG-1β) treatment to determine a mechanism for the protective role derived from its beneficial effects by remodeling gap junctions (GJs) during heart failure (HF). Methods Rat models of HF were established by aortocaval fistula. Forty-eight rats were divided randomly into the HF (HF, n = 16), NRG-1β treatment (NRG, n = 16), and sham operation (S, n = 16) group. The rats in the NRG group were administered NRG-1β (10 μg/kg per day) for 7 days via the tail vein, whereas the other groups were injected with the same doses of saline. Twelve weeks after operation, Connexin 43 (Cx43) expression in single myocytes obtained from the left ventricle was determined by immunocytochemistry. Total protein was extracted from frozen left ventricular tissues for immunoblotting assay, and the ultrastructure of myocytes was observed by transmission electron microscopy. Results Compared with the HF group, the cardiac function of rats in the NRG group was markedly improved, irregular distribution and deceased Cx43 expression were relieved. The ultrastructure of myocytes was seriously damaged in HF rats, and NRG-1β reduced these pathological damages. Conclusions Short-term NRG-1β treatment can rescue pump failure in experimental models of volume overload-induced HF, which is related to the recovery of GJs structure and the improvement of Cx43 expression.

Vena cava thrombosis after vena cava filter placement:Incidence and risk factors / 老年心脏病学杂志（英文版）

Background The objective of this study was to assess the clinical safety and efficacy of vena cava filter (VCF) placement,with particular emphasis on the incidence and risk factors of inferior vena cava thrombosis (VCT) after VCF placement.Methods Clinical data of patients with venous thromboembolism (VTE),with or without placement of VCF,were analyzed in a retrospective single-center audit of medical records from January 2005 to June 2009.The collected data included demographics,procedural details,filter type,indications,and complications.Results A total of 168 cases of VTE (82 with VCF; 86 without VCF) were examined.Over a median follow-up of 24.2months,VCT occurred in 18 of 82 patients with VCFs (11 males,7 females,mean age 55.4 years).In 86 patients without VCFs,VCT occurred in only 6 individuals (4 males,2 females) during the study period.VCT was observed more frequently in patients fitted with VCFs than in those without VCFs (22% vs.7.0%).Conclusions The incidence of VCT in patients with VTE after VCF implantation was 22% approximately.Anticoagulation therapy should be continued for all patients with VCF placement,unless there is a specific contraindication.Almost all instances of VCT in patients with VCF implants in our study occurred after stopping anticoagulation treetment.The use of VCFs is increasing,and more trials are needed to confirm their benefit and accurately assess their safety.

Role of hepatocyte growth factor in diagnosing and predicting recurrence of stroke / 药物分析学报

Objective To research whether serum hepatocyte growth factor (HGF) level increases in ischemic stroke and hemorrhagic stroke, and explore the relationship between the serum HGF level and stroke recurrence. Methods We studied a total of 92 consecutive acute stroke patients who had been admitted to hospital within 24h of onset from 6 participating hospitals in Xi'an from January 2000 to May 2004. All patients were divided into ischemic stroke group and hemorrhagic stroke group according to the results of brain computed tomography (CT) scan or MRI on admission. Patients in stroke groups were divided into recurrent group and non-recurrent group. Healthy volunteers or patients without cerebrovascular diseases comprised the control group. Stroke and control groups were strictly matched with 1∶1 ratio. The patients were followed up for 4 years. Serum HGF was tested with enzyme-linked immunosorbent assay (ELISA). Results Serum HGF of stroke patients was significantly higher than that of control group (P<0.05). The serum HGF level in recurrent group was higher than that in non-recurrent group of ischemic patients, and there was no significant difference in hemorrhagic ones. Conclusion These results indicate that serum HGF may be used as a diagnostic marker for stroke, and serum HGF level is helpful in predicting the recurrence of ischemic stroke.

Oleanolic acid-induced apoptosis and its relation with intracellular calcium in human lung adenocarcinoma A549 cells / 药物分析学报

Objective To investigate the effect of oleanolic acid (OA) on apoptosis, correlation between apoptosis and intracellular calcium, and its mechanism in human lung adenocarcinoma cell line A549. Methods Human lung adenocarcinoma A549 cells were incubated in vitro and assigned with OA concentrations of 0, 10, 20 and 40μg/mL. The apoptosis status of A549 cell line was detected with Annexin V-FITC/PI by flow cytometry (FCM); fluorescence intensity (FI) of A549 cells was assessed and the level of intracellular calcium was calculated at 24 hour of OA intervention. The relation between apoptosis and calcium FI was illustrated by curve fitting. Results FCM showed that 10, 20 and 40μg/mL of OA could induce A549 cell apoptosis, which followed a concentration-effect pattern; 24-hour intervention with 20μg/mL and 40μg/mL OA showed increased A549 cell apoptosis, and was significantly different from that with 0μg/mL OA (P<0.01). The FI of intracellular calcium concentration in 10, 20 and 40μg/mL OA groups was significantly higher than that in 0μg/mL group after 24 hours' intervention, and the FI showed a trend of increase with increased OA concentration (P<0.01). Curve fitting showed a significant correlation between apoptosis rate and intracellular calcium concentration in A549 cells (r=0.981, P<0.01). Regression equation was Y=0.508X-1.627. Conclusion OA plays a role in inducing apoptosis of human lung adenocarcinoma cells in a concentration-dependent manner. The OA-induced apoptosis is responsible for intracellular calcium overload of the tumor.

Comparative study on ghrelin level change and its related factors in hypertensive elders with psychological distress / 药物分析学报

Objective To investigate the change of plasma ghrelin level and explore the related factors of ghrelin alteration in elderly hypertensive patients with psychological distress. Methods A total of 300 elders, who were screened with Hamilton Anxiety Scale (HAMA), Hamilton Rating Scale for Depression (HAMD), and the Symptom Checklist-90 (SCL-90) for psychological stress and somato-psychological manifestations respectively, were divided into hypertension group (n=148) and non-hypertension group (n=152). Their blood samples were collected to measure the plasma level of ghrelin and total cortisol on the same day. Results The incidences of anxiety and depression were 27.7% and 11.7%, respectively, in all the enrolled elders. However, the rates of psychological distress, particularly anxiety, were significantly higher in the hypertensive elders than in the non-hypertensive ones (43.2% vs. 12.5%). Anxiety was positively related to the cortisol level but negatively related to the plasma ghrelin level, and the latter two were negatively correlated with each other. Conclusion Chronic increase of plasma cortisol induced by long-term anxiety can lead to the reduction of ghrelin level, which then adversely affects blood pressure in elders with psychological distress. Therefore, ghrelin might be a selective antihypertensive medicine for hypertensive elders with anxiety.

Correlation between expression of lung resistance-related protein and angiogenesis in non-small cell lung cancer / 西安交通大学学报(医学版)

Objective To investigate the changes in lung resistance-related protein (LRP) and vascular endothelial growth factor (VEGF) expressions and micro-vessel density (MVD) in non-small cell lung cancer (NSCLC), and to elucidate their possible relationship and mechanism. Methods Immunohistochemistry was used to detect changes in LRP and VEGF expressions, and MVD level in lung tissues of 56 NSCLC cases and 27 normal controls. Results ① LRP expression (66.1%) was concentrated in the cytoplasm of cancer cells, which was significantly higher than that in lung tissues of control group (P<0.01); the significance was not related to the pathological type. There was no significant difference in LRP expression among gender, TNM stage, lymph node metastasis, and two-year survival in NSCLC (P>0.05). ② In comparison to the control group, NSCLC group had significantly increased VEGF expression (P<0.01), which was not related to the pathological type. VEGF expression in NSCLC group had a significant association with TNM stage and lymph node metastasis (P<0.05). ③ The NSCLC group had a significantly higher MVD than the control group (P<0.01), which was not affected by the pathological type or degree. MVD value (18.5±5.8) of stage Ⅲ and Ⅳ in NSCLC group was significantly higher than that (13.8±5.1) of stage Ⅰ (P<0.05); MVD value for patients with lymph node metastasis was higher than that without lymph node metastasis (P<0.05); MVD value for patients with two-year survival was less than those who died within two years (P<0.01). ④ NSCLC group with high VEGF and LRP expressions had a consistently increased MVD value (P<0.05). Conclusion There is a certain relationship between tumor angiogenesis and LRP expression in NSCLC. VEGF is responsible for the high expression of LRP through up-regulating LRP gene and augmenting tumor MVD. Inhibition of angiogenesis in tumor is expected to reduce or inhibit drug resistance to NSCLC.

Relationship of C-reactive protein and fibrinogen changes with left atrial size in atrial fibrillation and flatter patients / 西安交通大学学报(医学版)

Objective To compare the changes in fibrinogen (Fib), C-reactive protein (CRP) and left atrial (LA) size between patients with atrial flatter (AFL) and those with atrial fibrillation (AF) to explore the relations among them. Methods We selected 53 AF patients (including 16 cases of paroxymal AF, 13 of persistent AF and 24 of permanent AF) and 18 patients with AFL; the control group consisted of 32 cases of sinus rhythm (SR). In all the patients, ECG or Horter and UCG were conducted; Fib and CRP were measured. The levels of the above indexes in AF group, AFL group and subgroups were compared with each other, and with those in the control group. Correlation analysis between CRP and LA size was made. Results Fib, CRP and LA size in AF group were significantly different from those in AFL and SR groups, but did not differ between the latter two groups. So did other parameters among the three groups. CRP in persistent AF and permanent AF differed significantly from that in AFL, SR and paraxymal AF. LA size in the groups of persistent AF differed from that in SR group, but there was no difference between those in persistent AF and AFL groups. LA size in permanent AF was significantly different from that in AF, AFL and SR. Positive significant linear correlations were found between CRP and LA size in AF (r=0.33). Conclusion Hypercoagulable state exists in AF; the AF. Positive correlation exists between LA size and inflammatory reaction; there is no hypercoagulable state in AFL.

Red blood cell level is increased in obese but not in non-obese patients with coronary heart disease / 老年心脏病学杂志（英文版）

Objective To examine the changes of red blood cell levels in the obese and non-obese patients with coronary heart disease (CHD) and its clinical significance. Methods 230 cases of coronary heart disease were selected and divided into the obese group and the nonobese group. Obesity and non-obesity were defined based on the body mass index (BMI I (Y) 28.0kg/m2), or waist-hip ratio (men> 0.9, women> 0.85). In addition, 130 healthy subjects were recruited as controls. The pathological status of coronary lesions was quantitatively analyzed according to the Coronary Vascular Image Segmentation Evaluation Criteria (American Heart Association 1984) and the Gensini scoring system. Results of the changes of both the hemoglobin levels and the red blood cell count in the obese group, the nonobese group with CHD and the control group were compared. Besides, Multivariant Logistic Regression Analysis was applied to assess the correlation between the red blood cells and the coronary artery disease. Results The red blood cell count and the level of hemoglobin in the obese group with CHD was higher than that in the non-obese group with CHD [(4.35 ± 0.55) and (4.13 ± 0.56) 109/L; (136.71 ± 15.87) and (129.96 ± 16.23) g/L, P < 0.05 in both]; the proportion of acute coronary syndrome in the obese group with CHD was higher in the obese group with CHD than that in the non-obese group with CHD (P<0.05); Multivariant logistic regression analysis also showed that the red blood cell count was positively correlated with obesity with CHD.Conclusion The red blood cell count and the level of hemoglobin in the obese group were higher than those in the non-obese group; the increase of red blood cell count and hemoglobin level is one of the independent risk factors for the obese patients with CHD.

The coagulation factor VII gene polymorphisms in patients with myocardial infarction in Ningxia Hui and Han populations / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate the characteristics for activated coagulation factor VII(F VIIa) and the R353Q, -323 0/10 bp, HVR4 polymorphisms in the gene in patients with coronary heart disease (CHD) and myocardial infarction from Ningxia Hui and Han populations.</p><p><b>METHODS</b>Four hundred and twenty angiographically proven CHD patients in the Hui population, and 508 healthy blood donors were tested for their plasma levels of coagulation factor VII using recombinant tissue factor method. The coagulation factor VII gene R353Q, -323 0/10 bp and HVR4 genotypes were identified by polymerase chain reaction. In addition, 600 Han patients with CHD and 604 healthy Han control subjects were also investigated.</p><p><b>RESULTS</b>(1) The plasma F VIIa levels was significantly higher in patients with CHD and myocardial infarction than that in healthy control subjects and angor pectoris (P<0.01) in both Hui and Han populations. (2) There were significant differences in the distribution of genotypes and allelic frequencies of the R353Q between myocardial infarction and angor pectoris disease in the Hui population (P<0.05). So was the -323 0/10 bp locus in both the Hui and Han population. (3) The F VIIa level was significantly higher in individuals with RR genotype than those of Q allele carriers in the Hui population.</p><p><b>CONCLUSION</b>There are polymorphisms of the F VII gene R353Q, -323 0/10 bp and HVR4 in the Hui and Han populations. The Q allele might be a protective factor against myocardial infarction in the Hui, and the plasma F VIIa level may be influenced by the R353Q polymorphism of the F VII gene. The 10 allele may be a protective factor against myocardial infarction in both the Hui and Han populations.</p>