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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.
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Objective To evaluate the correlating clinical factors of coronary artery calcification score(CACS).Methods 141 patients suspected of coronary artery disease were included.They underwent multi-slice row computed tomography,pulse wave velocity ( PWV ),UCG and blood biochemistry within a period of 3 months.The subjects were divided into three groups according to CAC score:A(CACS =0-10),B ( CACS = 11-400),C ( CACS > 400).Results CACS was significantly associated with age,history of hypertension and diabetes mellitus.It was also associated with the presence of mitral annular calcification and aortic valve calcification,low ankel brachial pressure index(ABI) and high mean artery pressure(MAP) as well as high values of brachial ankel PWV (baPWV) and Upstroke time (UT).Muhifactorial logistic regression analysis showed that the presence of aortic valve calcification and mitral annular calcification,the history of diabetes mellitus and high value of UT were independently correlated with severe coronary artery calcification.Conclusions Aortic valve calcification,mitral annular calcification,history of diabetes mellitus,high value of UT were independently correlated with severe coronary artery calcification.Measurement of PWV and UCG should be performed before muhi-slicerow computed tomography,because the assessment of coronary artery lumen narrowing with multi-slice row computed tomography can not be carried out accurately in the presence of severe coronary artery calcification.
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ObjectiveTo analyze hospitalized death related factors in elderly patients with nonST-segment elevation myocardial infarction (NSTEMI). MethodsThree hundred and two patients (≥65 years old) with NSTEMI were included. Thirty-two patients of them died in hospital (death group). Their clinical data were retrospectively analyzed and correlated factors for in-hospital death were evaluated. ResultsCompared with survival group, patients in death group were more likely to have 3 or more chronic diseases,heart function killip grades Ⅲ- Ⅳ, heart rate＞ 100/min and peripheral blood WBC count＞10X 10＜'9＞/L on admission (all P＜:0.05). There was no significant difference in fasting plasma glucose level and serum creatinine on admission between the two groups (both P:＞0.05). But after glomerular filtration rate(eGFR) were estimated by the modified abbreviated MDRD equations based on the Chinese CKD patients, patients in death group were more likely to be with renal dysfunction and pulmonary infection (both P＜0.01 ). Multiple logistic regression analysis showed that heart function killip grades Ⅲ-Ⅳ, renal dysfunction evaluated by eGFR, pulmonary infection on admission were the independent predictors for in-hospital death in elderly patients with NSTEMI. ConclusionsCoexistence of 3 or more chronic diseases is a related factor of death and heart function killip grades Ⅲ-Ⅳ, renal dysfunction evaluated by eGFR and pulmonary infection are the independent predictors for in-hospital death in elderly patients with NSTEMI.
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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.