Objective To investigate the efficacy of infusion Diltiazem for patients with refractory angina pectoris. Methods　10 patients with refractory angina pectoris received continuous intravenous Diltiazem 40～150 μg/min (2.4～9 mg/h) for 48 hours after cessation of intravenous nitroglycerin and oral β-blokers. Results　With the single therapy of Diltiazem, 7 patients (70%) got satisfied results: 5 were free from and 2 were relieved of symptom; With the combination therapy of Diltiazem and intravenous nitroglycerin 60～120 μg/min after failed with Diltiazem alone, 3 (30%) patietns got satisfied results: 1 was free from and 2 were relieved of symptom. There is no severe side effects, including hypotension, bradycardia, cardiac function deterioration. Acute myocardial infarction, death and emergency interventional therapy did not occurred in all the 10 patients during the therapy period. Coronary angiography were performed in 8 patients within 1 week after the patients were stabled, 5 patients received PTCA and stent implantation and 3 patients received CABG. Conclusions　Continuous intravenous Diltiazem 40～150 μg/min (2.4～9 mg/h) or combination with intravenous nitroglycerin 60～120 μg/min is an efficient and safe therapy for patients with refractory angina pectoris.

Atherosclerosis ; Estrogens ; Female ; Humans ; Lipid Metabolism ; Postmenopause

Objective To assess the value of ECG in the diagnosis of acute pulmonary embolism (APE). Methods Twenty-eight patients with APE were included,with mean age of 56?16,and PaO 2,electrocardiogram (ECG),echocardiogram (ECHO) and ventilation/perfusion lung scan were performed. Results 96.4% patients had risk factors,and had different degree of hypoxia. 92.9% patients had ECG changes,most of whom (57.1%) showed ST-T changes. The ventilation/perfusion lung scan confirmed the diagnosis. Conclusion Considering the clinical symptom,arterial blood gas analysis,the early changes of ECG are useful in the diagnosis of the APE.

Objective To assess the clinical features and risk factors of coronary heart disease(CHD)in patients with systemic lupus erythematosus (SLE).Methods The clinical data of 32 lupus patients with CHD and 64 age and sex-matched lupus patients without CHD from a total of 1792 in-patients with lupus from January 1994 to December 2008 were collected and retrospectively analyzed.The traditional risk factors of atherosclemsis as well as their association with the characteristics of lupus were evaluated and compared between the two group of patients.Results The average age of CHD group was(51±12)years with an average disease duration of((8±6) years、.The most common coronary events were acute myocardial infaretio(53%)and non-stable,angina[34%).Among the 12 patients who accepted coronary angiography or computed tomography scan of coronary artery,11 patients had significant atheroselerosis lesions and 1 had thrombosis in coronary arteries.Their atheroselerosis lesions were severe,which manifested as diffuse stenosis and severe calcification.Compared to the control group,the CHD group patients had more traditional risk factors[(3.9±1.8)vs(2.0±1.6),P<0.01 j as well as higher prevalence of hypertension,hyperlipidemia,postmenopausal and smoking(P<0.05).Meanwhile,the CHD group patients had longer SLE duration[12.0(6.3~19.8)vs 2.0[O.8～9.0)years,P<0.01)J,higher C3 level[(750±364)vs(598±267)mg/L,P<0.05]and higher totalprednisone dose[28.8(0~49.8)vs 24.0(0~24.6)g,P<0.05]compared to patients without CHD.No significant differences were found in auto-antibodies,SLE disease activity,organ damage,average Drednisone dose and cyclophosI,hamide usage between the two groups of patients.Multi-variate analysls showed more traditional risk factors(OR:1.62)and longer SLE duration(OR=1.09)Were independent predictors of CHD.Condusion Atherosclerosis is a common pathological change of coronary in lupus patients with CHD.Traditional risk flactors of atherosclerosis and lupus duration are identified to be the independent risk factors of CHD in SLE patients.Early interventions for traditional risk factors and appropriate control of lupus arerecommended.

Objective To test the hypothesis that IL-10 may promoting left ventricular remodeling and cardiac function by modulating extracellular matrix after acute myocardial infarction. Methods Male adult rats were randomly divided into three groups:control group (n=6),MI/AAV2 group (n=16) and MI/AAV2-IL-10 group (n=16). Establishing animal modol of experimental myocardial infarction and recombinant adeno-associated virus type 2 (AAV)/IL-10 (AAV2-rhIL-10) and AAV2 were injected around the ischemic zone. Echocardiography parameters,hemodynamic parameters,left ventricular mass index (LVMI),collagen volume fraction (CVF),perivascular circumferential area (PVCA),collagen type Ⅰ&Ⅲ volume fraction and mRNA levels of collagen type Ⅰ&Ⅲ,matrix metalloproteinases-2 (MMP-2) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were compared among the three groups. Results Improved cardiac function was observed in MI/AAV2-IL-10 group shown by echocardiography and hemodynamic examination. Four weeks after myocardial infarction,thickness of different parts of LV was not different in MI/AAV2-IL-10 group and MI/AAV2 group. Nevertheless CVF,PVCA and collagen type Ⅰ volume fraction was significantly descending in remote zone of MI/AAV2-IL-10 group compared with that of MI/AAV2 group. The mRNA expression of collagen type I and MMP-2 was lower in MI/AAV2-IL-10 group than that in MI/AAV2 group. Conclusion Recombinant IL-10 expression mediated by AAV2-rhIL-10 transfection of rats' myocardium promotes LV remodeling and cardiac function after acute myocardial infarction. The promotion was partially achieved by inhibition myocardium collagen deposition.

Objective To test the hypothesis that IL-10 may promoting left ventricular remodeling and cardiac function by modulating extracellular matrix after acute myocardial infarction. Methods Male adult rats were randomly divided into three groups: control group (n=6) , MI/AAV2 group (n=16) and MI/AAV2-IL-10 group (n=16). Establishing animal modol of experimental myocardial infarction and recombinant adeno-associated virus type 2 (AAV)/IL-10 (AAV2-rhIL-10) and AAV2 were injected around the ischemic zone. Echocardiography parameters, hemodynamic parameters, left ventricular mass index (LVMI) , collagen volume fraction (CVF) , perivascu-lar circumferential area (PVCA) , collagen type Ⅰ & Ⅲ volume fraction and mRNA levels of collagen type Ⅰ & Ⅲ , matrix metalloproteinases-2 ( MMP-2 ) and tissue inhibitor of metalloproteinase-1 ( TIMP-1) were compared among the three groups. Results Improved cardiac function was observed in MI/AAV2-IL-10 group shown by echocardiography and hemodynamic examination. Four weeks after myocardial infarction, thickness of different parts of LV was not different in MI/AAV2-IL-10 group and MI/AAV2 group. Nevertheless CVF, PVCA and collagen type Ⅰ volume fraction was significantly descending in remote zone of MI/AAV2-IL-10 group compared with that of MI/ AAV2 group. The mRNA expression of collagen type I and MMP-2 was lower in MI/AAV2-IL-10 group than that in MI/AAV2 group. Conclusion Recombinant IL-10 expression mediated by AAV2-rhIL-10 transfection of rats' myocardium promotes LV remodeling and cardiac function after acute myocardial infarction. The promotion was partially achieved by inhibition myocardium collagen deposition.

SUMMARY Left ventricular noncompaction(LVNC)is a rare congenital disorder of endomyocardial morphogenesis.Since the knowledge of aetiology and pathology is accumulating,the 2006 AHA cardiomyopathy classification sorts LVNC as one of the primary genetic cardiomyopathies.The clinical features of LVNC,however,is not as clear as its aetiology.We summarized the manifestation,hemodynamics,natural course,diagnosis,therapy and prognosis of LVNC by analyzing its clinical features of 2 cases and reviewing the latest related articles.

Objective To conduct a systematic review on the need and experience of patients in end of life and provide evidence-based guidance for delivery of end-of-life care in hospital and community settings. Methods Two Chinese (CBM and CNKI) and four English relevant databases (PsycINFO,MEDLINE,EMbase and CINAHL) were in-cluded to retrieve literatures on Chinese dying patients' needs and experience between inception and August 2016. The JBI Critical Appraisal Tool for qualitative studies in Australia was used to evaluate the quality of studies. The searching results were synthesized by employing Integrating Methods. Results Seventy-five findings were extracted from 9 qualified studies. The 75 findings were sequently integrated into 5 categories and finally 2 synthesized re-sults were summarized from the 5 categories. Integration result 1:under the sufferings from both physical and psy-chological aspects,dying patients require support from both family and society. Integration result 2:although death is acceptable for patients,they still hope for dignity and goals of life. Conclusion Needs of patients in end-of-life should be understood and respected. Reasonable and effective measures need to be taken to meet their needs and improve their quality of life.

Objective To examine the effects of IL-10 on cardiac fibroblasts ( CFBs) proliferation and phenotype transformation to myofibroblasts (MyoFbs) induced by transforming growth factor-β1 (TGF-β1);and to investigate the regulating pathways .Methods Cardiac fibroblasts were isolated from cardiac ventricles of neonatal SD rats . The passage 2~4 were used and divided into the following groups for treatment:1) control group, 2) IL-10 reac-tion group, 3) TGF-β1 reaction group, and 4) IL-10 plus TGF-β1 reaction group (TGF-β1 treatment followed with IL-10 pretreatment ) .Cells proliferation was assessed by MTT assay and immunocytochemistry staining for prolifera-ting cell nuclear antigen (PCNA);the phenotype transformation into MyoFbs was assessed by immunocytochemistry of α-smooth muscle actin (α-SMA);extracellular signal related kinase ( ERK1/2) and P38 kinase pathways were assessed by western-blot.Results TGF-β1 (10 μg/L) treatment boosted the proliferation and the expression ofα-SMA significantly (P<0.01), while IL-10 (10, 50 or 100 μg/L) plus TGF-β1 co-treatment induced lower cell proliferation and expression of α-SMA than treating with TGF-β1 alone ( P<0.05 ) , with the inhibitory effect of IL-10 being concentration dependent .TGF-β1 could significantly stimulate the ERK 1/2 and P38 kinase phospho-rylation ( P<0.01 ) , however IL-10 (100 μg/L) plus TGF-β1 co-treatment failed to down-regulated the phospho-rylation of ERK1/2 and P38 kinase compared with TGF-β1 alone ( ERK1/2:P<0.05;P38:P<0.01 ) .Conclu-sions IL-10 can attenuate TGF-β1-induced CFBs proliferation and phenotype transformation to MyoFbs .The in-hibitory effects may explained by a mechanism of inhibiting the activation of ERK 1/2 and P38 kinase .