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The dose-related beneficial effects of carvedilol on survival in heart failure have been verified, however, the effects on left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) have not been defined. This experiment was designed to compare the effects of low, middle, and high doses of carvedilol (LD-car, MD-car, and HD-car) with metoprolol (Meto) in preventing postinfarction LVRM in rats. After the left coronary artery was ligated, 177 surviving female SD rats were randomized to: (1) AMI (n = 35), (2) LD-car (0.1 mg x kg(-1) x d(-1), n = 35), (3) MD-car (1 mg x kg(-1) x d(-1), n = 35), (4) HD-car (10 mg x kg(-1) x d(-1), n = 37) and (5) Meto (2 mg x kg(-1) x d(-1), n = 35) groups. A sham-operated group (n = 16) was also randomly selected. Gastric gavage therapy lasted for 4 weeks. After hemodynamic studies, the rat hearts were fixed and pathologically analyzed. After exclusion of rats which died or had an infarct size35% or55%, complete data were obtained in 69 rats, comprising AMI (n = 11), LD-car (n = 11), MD-car (n = 12), HD-car (n = 12), Meto (n = 11) and sham (n = 12) groups. There were no significant differences in MI size among the five AMI groups (44.5-46.3%, all P0.05). Compared with the sham group, left ventricular (LV) end-diastolic pressure (LVEDP), volume (LVV), weight (LVW) and septal thickness (STh) were all significantly increased, while +/- dp/dt was significantly decreased in the AMI group (all P0.001). Compared with the AMI group, heart rate was significantly decreased in all except the LD-car treatment groups (P0.05-0.01); LVEDP, LVV, LVW, and STh in the four treatment groups were also significantly decreased (P0.05-0.001) except LVW and STh in the Meto group (both P0.05)(LVEDP: 14.5 +/- 4.6, 12.1 +/- 2.4, 7.7 +/- 1.9 and 13.0 +/- 6.7 mmHg vs 24.1 +/- 5.2 mmHg; LVV: 0.82 +/- 0.1, 0.79 +/- 0.1, 0.72 +/- 0.1 and 0.72 +/- 0.1 mL vs 0.92 +/- 0.1 mL; LVW: 666 +/- 57, 622 +/- 70, 589 +/- 57 and 699 +/- 78 mg vs 730 +/- 79 mg; STh: 1.14 +/- 0.12, 1.18 +/- 0.21, 1.19 +/- 0.15 and 1.35 +/- 0.20 mm vs 1.33 +/- 0.29 mm; P0.05-0.001); while +/- dp/dt was significantly increased in each therapy group (P0.05-0.001). There were dose-effect relations in LVEDP and LVV in the carvedilol groups. The results indicate that low, middle and high dose carvedilol has dose-related effects in the prevention of postinfarction LVRM with respect to volume expansion and segmental hypertrophy in rats, while metoprolol prevents only LV dilatation but not hypertrophy.

To evaluate the gender differences on the short-term outcomes of patients with acute myocardial infarction in the real world.A total of 471 consecutive patients [male 368(78.1%) and female 103(21.9%)] with acute myocardial infarction72 hours in cardiac care unit were included. The clinical data, death and major adverse cardiac and cerebrovascular events at 30 days post hospitalization were analyzed.Female patients were older (66.8 ± 10.1 vs. 56.9 ± 12.0, P0.001), TIMI score (5.1 ± 2.3 vs. 3.9 ± 2.1, P0.001) and GRACE score (162 ± 39 vs. 142 ± 35, P0.001) in female patients were higher than in male patients. Female patients had lower proportion of stent implantation (P = 0.038) while higher percentage of complex lesions and contraindications to PCI (P = 0.015) compared to male patients. Proportion of cardiac rupture, mitral regurgitation, malignant arrhythmia, post-infarction angina pectoris, contrast-induced nephropathy and minor gastrointestinal bleeding were also higher in female patients tan in male patients (P0.05). Thirty-day mortality was significantly higher in female patients than in male patients [5.8% (6/103) vs. 1.9% (7/368), P = 0.032], MACCE [10.7% (11/103) vs. 5.4% (20/368), P = 0.058] also tended to be higher in female patients than in male patients. Multi-logistic regression analysis showed that female gender was not an independent predictor for thirty-day mortality (P = 0.141) or MACCE (P = 0.426) while systolic blood pressure (OR = 1.072, 95%CI:1.016-1.130, P = 0.010) and pericardial effusion after myocardial infarction (OR = 40.518, 95%CI:1.098-1495.702, P = 0.044) were independent predictors for thirty-day mortality while systolic blood pressure (OR = 1.027, 95%CI:1.002-1.052, P = 0.036) and left ventricular ejection fraction (OR = 1.108, 95%CI:1.032-1.190, P = 0.005) were independent predictors for MACCE.Female gender itself is not an independent predictor for thirty-day mortality and MACCE despite poorer clinical characteristics, higher incidence of complications, and worse prognosis in female patients.

Ventricular septal rupture (VSR) remains an infrequent but devastating complication of acute myocardial infarction (AMI). The best time to undergo surgical repair is controversial and there is currently no risk stratification for patients with VSR to guide treatment. The purpose of this study was to review the clinical outcomes of 70 patients with VSR, to analyze the short-term prognosis factors of VSR following AMI, and to make a risk stratification for patients with VSR.A total of 70 consecutive VSR patients following AMI treated in our hospital from January 2002 to October 2010 were enrolled in this study retrospectively. The difference of clinical characteristics were observed between patients with VSR who survived ≤30 days and survived30 days. We analyzed the short-term prognosis factors of VSR and established the short-term prognosis index of VSR (SPIV) based on the Logistic regression analysis to stratify patients with VSR.Among 12 354 patients with acute ST-segment elevation myocardial infarction, 70 (0.57%) patients (33 males and 37 females) were found to have VSR. The average age was (68.1±8.5) years. Fifty-four (77.1%) patients were diagnosed with an acute anterior infarction. Patients with VSR selected for surgical repair had better outcomes than patients treated conservatively; 1-year mortality 9.5% versus 87.8%, P0.005. Logistic regression analysis revealed that female (P = 0.013), anterior AMI (P = 0.023), non-ventricular aneurysm (P = 0.023), non-diabetes (P = 0.009), Killip class 3 or 4 (P = 0.022) and time from AMI to VSR less than 4 days (P = 0.027) were independent risk determinants for shortterm mortality. SPIV ≥9 indicates a high risk as the 30-day mortality is 77.4%; SPIV8 indicates a low risk as the 30-day mortality is 28.6%; SPIV between 8 and 9 indicates a moderate risk.VSR remains a rare but devastating complication of AMI. The independent risk determinants for short-term mortality of VSR were female gender, anterior AMI, non-ventricular aneurysm, non-diabetes, Killip class 3 or 4, and the time from AMI to VSR less than 4 days. It is reasonable to take more active treatments for the patients at high risk to save more lives.

To analyze the short-term prognosis and risk factors of ventricular septal rupture (VSR) following acute myocardial infarction (AMI).A total of 70 consecutive VSR patients following AMI hospitalized in our hospital from January 2002 to October 2010 were enrolled in this study. We compared the clinical characteristics of patients with VSR who survived ≤ 30 days (n = 39) and survived30 days (n = 31) post AMI. A short-term prognosis index of VSR (SPIV) was established based on the logistic regression analysis.The single factor analysis showed that the risk factors of death within 30 days of VSR patients were female, anterior AMI, Killip class 3 or 4, apical VSR and non-aneurysm (all P0.05). Logistic regression analysis revealed that female (P = 0.013), anterior AMI (P = 0.023), non-aneurysm (P = 0.023), non-diabetes (P = 0.009), Killip class 3 or 4 (P = 0.022) and time from AMI to VSR less than 4 days (P = 0.027) were independent risk determinants for death within 30 days post VSR. Patients with SPIV ≥ 9 were associated with high risk [77.4% (24/31)] of dying within 30 days post AMI. SPIV ≤ 8 were associated with low risk as the 30 days mortality is 28.6% (8/28).Female gender, anterior AMI, non-aneurysm, non-diabetes, Killip class 3 or 4 and time from AMI to VSR less than 4 days are independent risk factors of short-term mortality of VSR.

To investigate the impact of cytochrome P450 (CYP) 2C19 681GA polymorphism on long-term prognosis of clopidogrel-treated Chinese patients after percutaneous coronary intervention (PCI).Between January 1, 2009 and August 31,2009, 267 patients with coronary heart disease who received PCI and treated with clopidogrel for 12 months were enrolled. CYP2C19 * 2 was detected by MALDI-TOF MS and patients were grouped into CYP2C19 * 1/ * 1 (n = 130) and CYP2C19 * 2 carriers group (n = 137). Follow-up was 12 months. The primary endpoint was angina recurrence, urgent coronary revascularization, acute myocardial infarction, stent thrombosis, death and the combined end points.Baseline data were similar between two groups (P0.05). Urgent coronary revascularization and the combined end points occurred more frequently in CYP2C19 * 2 carriers than in CYP2C19 * 1/* 1 patients (7.3% vs. 1.5% and 8.0% vs. 2.3% respectively, all P0.05). But incidence of angina recurrence, acute myocardial infarction, stent thrombosis and death was similar between two groups (all P0.05). Hazard risk of 1 year cumulative survival of CYP2C19 * 2 carriers group was significantly higher than CYP2C19 * 1/ * 1 group after PCI ( HR = 3.59, 95% CI: 1.02 - 12.87, P0.05).CYP2C19 681GA polymorphism is a determinant of prognosis in coronary heart disease patients receiving chronic clopidogrel treatment after PCI.

Spontaneous attack of variant angina (VA) is a unique component of coronary artery disease (CAD), and associated with severe cardiac events. However, no data are available regarding sex differences in Chinese patients with spontaneous attacks of VA. Accordingly, the present retrospective study was initiated to evaluate the Clinical characteristics of Chinese female patients with spontaneous attacks of VA.From January 2003 to January 2008, a total of 209 patients were diagnosed to have had a spontaneous attack of VA at Fu Wai Hospital. Of them, 27 were female, and their clinical findings were collected and compared with male patients for aspects of risk factors, clinical features and angiographical findings.Spontaneous attacks of VA was relatively uncommon in female (12.9%) compared with male patients. The female patients were less likely to have a history of smoking (14.8% vs. 79.7%, P0.001), more likely to have a family history of CAD (33.3% vs. 11.0%, P0.01), and to have had a greater incidence of ventricular fibrillation during attack (11.1% vs. 2.2%, P0.05). There were no significant differences in other characteristics between the two groups.Chinese female patients who experienced a spontaneous attack of VA had the characteristics of less smoking history, more family history of CAD and higher occurrence of ventricular fibrillation than male patients.

To compare the clinical characteristics and clinical outcomes in young (/ = 45 years) female and male coronary artery disease (CAD) patients undergoing percutaneous coronary intervention (PCI).Angiographic and clinical data from 124 premenopausal female patients who underwent elective PCI from April 2004 to February 2008 were compared to age-matched 430 male patients who underwent elective PCI between 2006 and 2007 in our department. All patients were treated according to guidelines and coronary angiography was repeated after 6 months. One year clinical follow-up were performed in all patients.Incidences of dyslipidemia, the history of myocardial infarction and smoking were significantly lower in female patients than in male patients (all P0.01). Left main, left anterior descending and bifurcation lesions were more common while type C lesion and right coronary lesion were less common in young female CAD group compared to young male CAD group (P0.01-0.05). The average lesion length in female patients was significantly longer than that in male patients [(20.36 +/- 13.37) mm vs. (23.04 +/- 13.86) mm, P0.05]. The in-hospital and follow-up incidences of major adverse cardiac events, stent thrombosis and in-stent restenosis were similar between young female and male CAD patients.CAD risk factors were less and vessel lesions were more likely to be found at left main, left anterior descending and bifurcation in young female CAD patients compared to young male CAD patients. The clinical outcomes were similar between young female and male CAD patients.

To explore the correlation between plasma BNP level and left ventricular dysfunction parameters in patients with acute myocardial infarction (AMI).Plasma BNP level was determined in 230 consecutive inpatients with AMI and 111 normal controls. Patients were grouped according Killip grades, LVEF and LVEDd, respectively. BNP was transformed into lnBNP for the normal distribution. The receiver operator characteristic curve (ROC curve) was drawn to determine the best threshold and criteria for diagnosing heart failure.After AMI, lnBNP levels increased significantly in proportion with increasing Killip grades (I-III), and decreasing LVEF (all P0.05). lnBNP level was significantly higher in LVEDd55 mm group than in the LVEDd55 mm group (P0.01). lnBNP, LVEDd and LVEF all linearly correlated with Killip grades (P0.05) and the best correlation was shown between lnBNP and Killip grades (r = 0.53, P0.05). lnBNP also positively correlated with LVEDd (r = 0.17, P0.05) and negatively correlated with LVEF (r = -0.41, P0.01). Among the parameters, lnBNP level presented the largest AUC in their ROC curves (P0.01) for diagnosing decompensated heart failure and cardiogenic shock. The sensitivity, specifiticity and accuracy rates for diagnosing decompensated heart failure were 84.9%, 45.0% and 70.0% respectively by lnBNP at the cut point of 140 ng/L. The sensitivity, negative predicting value and accuracy rate for diagnosing cardiac shock were 82.8%, 66.7% and 67.4% respectively by BNP at the cut point of 400 ng/L.lnBNP level in hospitalized patients with AMI was positively correlated with Killip grades and LVEDd, negatively correlated with LVEF and could serve as a parameter for diagnosing the decompensated heart failure and excluding the cardiac shock.

To investigate the therapeutic effectiveness of intracoronary transplantation of autologous bone marrow mononuclear cells (BM-MNC) on myocardial ischemia reperfusion injury in mini-swine model.Myocardial ischemia reperfusion injury model was established by ligating in 16 mini-swines, which were further randomized into two groups: (3.54 +/- 0.90) x 10(8) BM-MNC was intracoronarily transplanted in BM-MNC group (n = 9), and phosphate buffer saline was intracoronarily applied in the control group (n = 7). Ultrasonic cardiograhpy, hemodynamics, neovascular density, and myocardium infarction size were evaluated before and 4 weeks after transplantation.In BM-MNC group, left ventricular ejection fraction (LVEF), intra-ventricular septa, lateral wall and anterior wall, cardiac output (CO) and + dp/dt(max) had no significant differences before and 4 weeks after transplantation (P0.05). In the control group, LVEF, intraventricular septa, lateral wall and anterior wall, CO, and + dp/dt(max) significantly decreased 4 weeks after transplantation (P0.05). Left ventricular end-diastolic pressure and- dp/dt(max) had no significant differences before and after cell transplantation. Capillary density was significantly larger in the BM-MNC group than in the control group [(13.39 +/- 6.96) /HP vs. (3.50 +/- 1.90) /HP]. The percentage and size of myocardial infarction was significantly lower in the BM-MNC group than in the control group.Transplantation of BM-MNC into the myocardial ischemic reperfusion-injury area can increase capillary density and decrease infarction area, and thus remarkably improve cardiac systolic function.

To explore the infarct sites in patients with inferior wall acute myocardial infarction (AMI) concomitant with ST segment elevation in leads V1-V3 and leads V3R-V5R.Five patients diagnosed as inferior, right ventricular, and anteroseptal walls AMI at admission were enrolled. Electrocardiographic data and results of isotope 99mTc-methoxyisobutylisonitrile (MIBI) myocardial perfusion imaging and coronary angiography (CAG) were analyzed.Electrocardiogram showed that ST segment significantly elevated in standard leads II, III, aVF, and leads V1-V3, V3R-V5R in all five patients. The magnitude of ST segment elevation was maximal in lead V1 and decreased gradually from lead V1 to V3 and from lead V1 to V3R-V5R. There was isotope 99mTc-MIBI myocardial perfusion imaging defect in inferior and basal inferior-septal walls. CAG showed that right coronary artery was infarct-related artery.The diagnostic criteria for basal inferior-septal wall AMI can be formulated as follows: (1) ST segment elevatesor = 2 mm in lead V1 in the clinical setting of inferior wall AMI; (2) the magnitude of ST segment elevation is the tallest in lead V1 and decreases gradually from lead V1 to V3 and from lead V1 to V3R-V5R. With two conditions above, the basal inferior-septal wall AMI should be diagnosed.

To compare the effects of intracoronary transplantation of autologous bone marrow mononuclear cells (BM-MNC) or peripheral endothelial progenitor cells (EPC) in mini-swine model of myocardial ischemia-reperfusion.The Mini-swine acute myocardial infarction and reperfusion model was created with 90 min occlusion of the left anterior descending coronary artery followed by reperfusion and the animals were then divided into BM-MNC group (3.54 x 10(8) +/- 0.90 x 10(8), n = 9), EPC group (1.16 x 10(7) +/- 1.07 x 10(7), n = 7) and control group (saline, n = 7). Echocardiography, hemodynamic measurements and myocardium infarction size were evaluated before and 4 weeks after intracoronary cell transplantations.The net decrease from baseline to 4 weeks after transplantation of left ventricular ejection fraction (LVEF), left ventricular end systolic pressure, cardiac output and +dp/dt(max) were significantly attenuated post BM-MNC and EPC therapy compared to control group (all P0.05) and were similar between BM-MNC and EPC groups. Transplantation of BM-MNC and EPC also significantly decreased myocardial infarction size compared to control group.Autologous intracoronary transplantation of BM-MNC or EPC in this model equally improved cardiac systolic function and reduced infarction area.

To investigate the differentiation status of autologous bone marrow mononuclear cells (BM-MNC) and peripheral endothelial progenitor cells (EPC) transplanted into myocardial ischemia reperfusion injury region in swine.BM-MNC marked with PKH26 (n = 9), EPC marked with CM-DiI (n = 7), phosphate buffer saline (control, n = 7) were transplanted into myocardial ischemia reperfusion injury region of swine by intracoronary artery injection. Specimens were harvested 4 weeks after injection for histological analysis (HE, immunochemical stain for vWF, alpha-sarcomeric-actin and fibronectin antibody). Cell differentiation was observed under transmission electronmicroscope.The number of small blood vessels was similar between BM-MNC group and EPC group (13.39 +/- 6.96/HP vs.12.39 +/- 4.72/HP, P0.05), but was significantly higher than that of control group (P0.05). Responsive intensity of immunochemical stain for fibronectin antibody was significantly lower in BM-MNC and EPC groups than that in control group. Responsive intensity of immunochemical stain for alpha-sarcomeric-actin antibody was similar among the three groups. Cluster cells were observed in one swine from BM-MNC group which might relate to the proliferation of stem cells in situ. Immature endothelial cells and myocytes were also detected by transmission electronmicroscope in BM-MNC and EPC group.BM-MNC and EPC transplanted into myocardial ischemia reperfusion injury region in swine stimulated the formation of blood vessels and inhibited fibrogenesis.

To explore the predictive value of B-type natriuretic peptide (BNP) for the mortality of acute myocardial infarction (AMI).Follow-up was made in 264 consecutive patients with AMI, with an average period of (14.7 +/- 5.3) months and follow-up rate of 87.1% (230 cases). Cardiac death was recorded in the 1st, 6th and 12th month after AMI. Among one to seven days after AMI, the MB isoenzyme of creatine kinase (CK-MB), troponin T (TnT), echocardiographically measured left ventricular end-diastolic internal diameter (LVEDd), left ventricular ejection fraction (LVEF) and BNP were determined. The Receiver Operating Characteristic (ROC) were drawn to determine the predictive value for the cardiac death after AMI comparing BNP with the classical risk factors mentioned above. Analysis was made to define the relative independent risk factors of cardiac death and non-cardiac death survival rate after AMI.The ROC curves comparing CK-MB, TnT, LVEDd and LVEF with BNP and lnBNP showed that BNP was the only index for predicting cardiac death after AMI, the cut off point value of BNP determined according to ROC curve was 864 ng/L and the sensitivity, specificity, accuracy, positive and negative predictive values for predicting the cardiac death was 76.2% - 92.9%, 84.3% - 85.6%, 82.2% - 86.1%, 21.3% - 36.2% and 97.3% - 98.9% at the 1st 16th, 12th month after AMI respectively. Furthermore, BNP showed the only independent risk factor for predicting the cardiac death in the short and long term period after AMI (P0.01) by multiple factors cox regression analysis. The non-cardiac death survival rate in the group of BNP levelor = 864 ng/L was significantly higher than that in the group of BNP864 ng/L (97.3% vs 72.3%, P0.001), and the median survival time of the dead in the former group was also significantly longer than in the latter group (16.0 vs 10.7, P0.01), no matter whether they were suffering from AMI with ST elevation or not, treated with or without primary PCI.BNP has the best predictive value for mortality after AMI compared with other traditional indexes.

To compare the beneficial effects of Atenolol and Metoprolol on cardiomyocyte apoptosis and related gene expressions after acute myocardial infarction (AMI) in rats.AMI model was established with the ligation of anterior descending coronary artery in 251 randomly selected female SD rats. Twenty-four hours after operation, the 124 survivors were randomly assigned to AMI control group (MI group, n = 43), Atenolol group (group A, 10 mg x kg(-1) d(-1), n = 39), and Metoprolol group (group B, 20 mg x kg(-1) x d(-1), n = 42). Sham operation group (group S, n = 27) was also established. Two subgroup (48 h subgroup and 4 weeks subgroup) was randomly divided in each group according to the time points. Drugs were given to each treatment group by gastric gavage 24 h after ligation. Cardiomyocyte apoptosis was detected with terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) and DNA ladder. Bcl-2, bax and caspase-3 genes were detected with immunohistochemistry and Western blot analysis.Compared with AMI control group, myocyte apoptosis rate (MAR) significantly decreased only in infarction area (P0.01) in group B. Bcl-2 expression was found to increase in myocytes of infarction, border and non-infarcted areas except for non-infarcted area of group A. Changes of the expressions of bax and caspase-3 was not significant. Four weeks after AMI, MAR was found to decrease significantly in scar, border and non-infarcted areas (P0.05, P0.01) in both group A and group B. No significant changes of bcl-2, bax and caspase-3 expressions was found except for a significant decrease of bax expression in non-infarcted area of group A. As indicated by Western blot, no significant change of the expressions of caspase-3, bcl-2 and bax were found in myocytes of group A and group B compared with AMI control group; however, bcl-2/bax ratio significantly increased to the same level of sham-operated group (P0.05).Both Atenolol and Metoprolol treatment can reduce cardiomyocyte apoptosis in infarction/scar, border and non-infarcted areas after AMI, mainly through the increase of bcl-2 expression and bcl-2/bax ratio.

To observe the serum B-type natriuretic peptide (BNP) changes post acute myocardial infarction (AMI).The serum BNP level was determined in 230 consecutive patients with AMI admitted to CCU and in 111 normal cases from October 2002 to October 2003 in Fuwai Hospital. The 230 AMI patients were further divided into various subgroups according to first or recurrent AMI, ST elevations myocardial infarction (STEMI) or non-ST elevations myocardial infarction (NSTEMI) group, infarction location, coronary arteries involved, infarction related arteries (IRA), TIMI blood flow of IRA and primary PCI or not. Serum BNP, CK-MB, TnT and heart function were analyzed.The serum BNP level was significantly increased in patients with AMI (553.7 +/- 735.1) ng/L than that in normal subjects [(26.4 +/- 27.4) ng/L, P0.05]. LVEF was significantly lower, and LVEDd, BNP and LnBNP were all significantly higher in the first time AMI group compared to recurrent AMI group (all P0.001). The BNP level were significantly higher in AMI patients with single or triple coronary arteries stenosis than those without coronary stenosis (P0.05), in TIMI blood flow 0 - 1 and 2 groups than in TIMI 3 group (all P0.001). The CK-MB and TnT were significantly increased while BNP significantly decreased in the patients underwent primary PCI group compared with patients did not receive PCI therapy (all P0.05 - 0.001).Serum BNP was significantly elevated in patients after AMI but decreased after successful primary PCI in patients with AMI.

To investigate the beneficial effects of carvedilol on cardiomyocyte apoptosis and related gene expression after acute myocardial infarction (AMI).Eighty-three female SD rats underwent ligation of left anterior descending coronary artery, and were randomly assigned to 2 groups 24 hours later: carvedilol (n = 40, 10 mg.kg(-1).d(-1)was administered via direct gastric gavage 24 hs after the ligation, Group C) and AMI control group (n = 43, normal saline of the same volume was given by gastric gavage, Group MI). Another 27 rats were used as sham operation group (Group S, administered with normal saline too). The rats of each group were killed and their hearts were taken out 48 hours and 4 weeks after observation respectively (MI-48 h, MI-4 week, C-48 h, C-4 week, S-48 h, and S-4 week subgroups). TUNEL and DNA gel electrophoresis were used to detect the cardiomyocyte apoptosis. Immunohistochemistry and Western blotting were used to detect the expression of bcl-2 and bax.The apoptotic indices of the infracted/scar, border and non-infarcted areas at any time-point of Group MI were all significantly higher than those of Group S (all P0.05). Only the apoptotic indices of the infracted/scar and border areas of the C-4 week subgroup were significantly lower than those of the MI-4 week subgroup (both P0.05), and were close to those of the non-infarcted area. DNA gel electrophoresis showed that the positive rate of Group S at any time-point were both 0, the positive rate of MI-48 h subgroup and C-48 h subgroup were both significantly higher than that of Group S (both P0.05) without significant difference between these 2 groups, and the positive rates of the MI-4 week subgroup and C-4 week subgroup were both 0. Immunohistochemistry showed that the bax gene expression was slightly to significantly increased in the infarcted/scar, border, and non-infarcted areas of the MI-48 h and MI-4 week subgroups. The bcl-2 expression was significantly increased only in the infracted area of the MI-48 h subgroup. The bcl-2 expression was slightly increased in the infracted and border areas of the C-48 h subgroup and the bax expression was significantly decreased in the infracted/scar area of the C-4 week subgroup. Western blotting showed that (1) the bcl-2 expression of the S-4 week subgroup was significantly higher than that of the S-48 h subgroup (P0.05), (2) the bcl-2 expression and bax expression of the MI-48 h subgroup were significantly higher than that of the S-48 h subgroup (P0.05 - 0.01), the bcl-2/bax ratio of the MI-48 h subgroup was significantly lower that that of the S-48 h subgroup, however, there were no significant differences in the bcl-2 and bax expression and bcl-2/bax ratio between the MI-4 week subgroup and S-48 h subgroup (all P0.05), and (3) There were no significant difference in the bcl-2 and bax expression between Group A and Group S (all P0.05), however, the bcl-2/bax ratios at the 2 time-points of Group C were both significantly higher than those of Group MI.Cardiomyocyte apoptosis occurs in the infarction/scar, border and non-infarcted areas after AMI. Prolonged treatment with carvedilol reduces cardiomyocyte apoptosis in the scar and border areas and increases the expression ratio of bcl-2/bax.

To evaluate the effect of adenosine on endothelin-1 (ET-1) after acute myocardial infarction (AMI) and reperfusion and explore the possible mechanism of no-reflow.Twenty-four mini-swine were randomized into three study groups: control group (n=8), adenosine treated group (n=8), and sham-operated group (n=8). The mini-swine in the groups were subjected to 3 hours of coronary occlusion, followed by 60 minutes of reperfusion except those in the sham-operated group. The levels of ET-1 in blood sample, normal, infracted reflow and no-reflow myocardium were evaluated by radioimmuno-assay (RIA). The gene expressions of ET-1 in normal, infracted reflow and no-reflow myocardium were quantified by reverse transcription-polymerase chain reaction.In both control group and adenosine group, compared with that at the baseline, ET-1 in blood sample significantly increased at 5 minutes and 180 minutes of left anterior descending coronary artery occlusion, as well as 5 and 60 minutes of reperfusion (all P0.01). In adenosine group, the levels of ET-1 were significantly lower than those in the control group (P0.05, P0.01). In both control group and adenosine group, compared with that in normal myocardium, ET-1 levels in both infarcted reflow and no-reflow myocardium significantly increased (both P0.01), with the level of ET-1 in no-reflow myocardium significantly higher than that in infarcted reflow myocardium (P0.01). In adenosine group, the level of ET-1 in infarcted reflow myocardium was significantly lower than that in the control group (P0.01). In both control and adenosine groups, compared with that in normal myocardium, the gene expression of ET-1 in infarcted reflow myocardium was significantly up-regulated (P0.01), while that of ET-1 in. no-reflow myocardium significantly down-regulated (P0.01). In adenosine group, the level of ET-1 in infarcted reflow myocardium was significantly lower than that in the control group (P0.01).The endothelium injury may be one of the important mechanisms for no-reflow phenomenon. Adenosine cay prevent endothelium from injury to reduce no-reflow.

To study the growth and differentiation of adult canine autologous skeletal myoblasts after being transplanted into acute myocardial infarction (AMI) region by intramyocardium injection (IMI) and intracoronary infusion (ICI).Autologous skeletal myoblasts were procured by a modified method. AMI model of adult canine was obtained through left anterior descending branch ligation and was divided into 4 groups (n = 5 for each group). Autologous skeletal myoblasts (1.0 - 1.4 x 10(8) cells) were injected locally into AMI region or infused into infarction-related coronary artery. Specimens were harvested 4 weeks after cellular transplantation for histological study including HE, PTH, immunochemical stain and transmission electronmicroscope.In both two transplantation groups, newborn muscle-derived cells, striated muscle tissue and mature skeletal myofibril were demonstrated existing in MI region by electronmicroscope, PTH stain or anti-skeletal myosin heavy chain (slow) immunochemical stain, respectively. Newborn striated muscle tissues arranged in order of consistency with host myocardial fibers in two treatment groups. Newborn striated muscle tissue was more inclined to gather in MI region in the local injection group but distracted from each other in the intracoronary infusion group.Autologous skeletal myoblasts appears to live and differentiate into mature striated muscle tissue after transplanting into AMI region by IMI or ICI routes.

Simvastatin can prevent cardiac remodelling after myocardial infarction, though the exact mechanisms are uncertain. Myocardial no-reflow is associated with progressive cardiac remodelling. However, it remains unknown whether post-infarction treatment with simvastatin can also reduce myocardial no-reflow for which suppression of adenosine triphosphate-sensitive K+ (KATP) channel opening is an important mechanism. Methods: Area at risk and the area of no-reflow were determined by myocardial contrast echocardiography (MCE) and by pathology in 45 mini-swine randomised into 5 groups: 10 control, 9 simvastatin, 9 glibenclamide, 9 simvastatin plus glibenclamide and 8 sham-operated. A myocardial infarction and reperfusion model was created by 3-h occlusion of the coronary artery followed by 4 weeks of reperfusion. Results: Compared with the control group, simvastatin significantly increased coronary blood volume (P

To evaluate the effects of anti-platelet drugs on myocardial no-reflow after acute myocardial infarction (AMI) and reperfusion.Thirty-two mini-swine were randomized into 4 equal groups: Control Group, without any intervention; Group A approximately C, pretreated with aspirin-clopidogrel (A-C) combination (300 mg loading dose followed by 75 mg per day of clopidogrel and 10 mg x kg(-1) x d(-1) of aspirin for 3 days), Group Tirofiban, given an intravenous infusion of tirofiban (15 microg/kg in intravenous bolus followed by 0.5 microg x kg(-1) x min(-1) in continuous intravenous infusion from 30 min before occlusion to the end of protocol; and Sham Operation Group, undergoing sham operation. The former 3 groups underwent three-hour occlusion of the left anterior descending (LAD) coronary artery followed by one-hour reperfusion Before the adminisfration of drngs and hefore lipation of LAD flood sanpks were collocfed to detoif the platelet aggregation rate (PAR). Hemodynamic examination and myocardial contrast echocardiography (MCE) were performed before AMI, 3 h after AMI, and 1 h after reperfusion. The coronary ligation area (LA) and area of no-reflow (ANR) were determined with both MCE in vivo and pathological examination after the swine were killed.The platelet aggregation rates (MAR) after AMI were 46.8% and 45.7% respectively in tirofiban group and A-C Combination group, and significantly decreased to 12.9% and 14.3% respectively after the administration of drugs (both P0.01) with equivalent potency (P0.05). The left ventricular function was significantly improved in tirofiban group in comparison with control group (P0.05 - 0.01), the coronary blood flow volume (CBV) 1 h after reperfusion was 73.2% in tirofiban group, significantly higher than that of control group (45.8%, P0.01), and the ANR of tirofiban group was 22.8% and 23.2% judged by MCE and pathological examination respectively, both significantly smaller than those of control group (78.5% and 82.3%, both P0.01), and the NA of tirofiban group was 89.2%, significantly smaller than that of Control Group (98.5%, P0.05). However, there were not significant differences in left ventricular function, central blood volume, ANR and NA between A-C combination group and control group (all P0.05).Tirofiban is markedly effective in attenuating myocardial no-reflow after reperfusion; in contrast, A-C combination is totally ineffective.

To compare the effects of doxycycline, losartan, and their combination in the prevention of left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in rats.Twenty-four hours after the induction of AMI, the 254 survival rats were randomly assigned to the following groups and received drug treatment: (1) AMI controls (n=64), (2) doxycycline (30 mg x kg(-1) x d(-1), n = 63), (3) losartan (10 mg x kg(-1) x d(-1), n = 62), and (4) combination doxycycline and losartan (30 and 10 mg x kg(-1) x d(-1) respectively, n = 65) treatment groups. Also, sham operated rats (n = 30) were selected randomly. Each group was further divided into three subgroups of 1, 2, and 4 weeks of treatment. After the completion of treatment, hemodynamic studies were performed. Then, the heart of rat was fixed and analyzed pathologically.Exclusive of the dead rats and the hearts with the myocardial infarction size35% or50%, complete experimental data were obtained in 157 rats. Besides sham operated rats, there was no significant difference in myocardial infarction sizes among the 12 subgroups of AMI control and drug treatment groups (P0.05). Compared with sham operated rats, left ventricular end diastolic pressure (LVEDP) and left ventricular absolute weight and relative weight (LVAW and LVRW) were significantly increased in 1, 2, and 4 week subgroups of AMI controls (P0.05, P0.01, and P0.001, respectively), with LVEDP elevated more significantly in 4 week than in 1 and 2 week subgroups (P0.01); whereas the maximum rising and dropping rate of left ventricular pressure (+/-dp/dt) and its corrected value by left ventricular systolic pressure (+/-dp/dt/LVSP) were all significantly decreased only at 4 week subgroup of AMI controls (P0.001). Compared with AMI controls group, LVEDP was significantly decreased in all 1, 2, and 4 week subgroups of the three treatment groups (P0.05, P0.01, and P0.001, respectively); LVAW and LVRW were significantly decreased in 2 and 4 week subgroups of losartan and combination groups (P0.05, P0.01, P0.001, respectively), and in only 4 week subgroup in doxycycline (P0.05, P0.01, and P0.001, respectively); whereas the maximum dropping rate of left ventricular pressure and the corrected value of left ventricular pressure rising and dropping rate were significantly increased only in 4 week subgroups of all three treatment groups (P0.05, P0.01, respectively). There is no significant difference in all indices above among the three treatment groups at all three time points (P0.05).It is indicated that doxycycline can prevent left ventricular remodeling and improve its systolic and diastolic function after AMI in rats, with the equivalent effect to that of losartan. There seems no additive effect when the two drugs are used in combination.

To evaluate the effects of fosinopril on myocardial no-reflow in a mini-swine model of acute myocardial infarction and reperfusion.Twenty-four mini-swines were randomized into 3 study groups: 8 in control group, 8 in fosinopril-treated group (1 mg.kg(-1).d(-1)) and 8 in sham-operated group. Animals in the former two groups were subjected to 3 hours of coronary occlusion followed by 60 minutes of reperfusion. Data on haemodynamics and coronary blood flow volume (CBV) were collected, and the area of no-reflow was evaluated with both myocardial contrast echocardiography (MCE) in vivo and pathological means. Necrosis area was measured with triphenyltetrazolium chloride (TTC) staining.(1) In the control group, systolic and diastolic blood pressure (SBP and DBP), left ventricular systolic pressure (LVSP), maximal rate of increase and decrease in left ventricular pressure (+/- dp/dt(max)) and cardiac output (CO) significantly declined (P0.05-0.01), while left ventricular end-diastolic pressure (LVEDP) and pulmonary capillary wedge pressure (PCWP) significantly increased at the end of 3 hours occlusion of left anterior descending artery (both P0.01). Compared with those at the end of 3 hours of occlusion, +/- dp/dt(max) further significantly declined (P0.05) at 60 minutes of reperfusion. In the fosinopril group, the changes of SBP and DBP, LVSP, +/- dp/dt(max), CO, LVEDP and PCWP were similar as those in the control group after 3 hours of acute myocardial infarction. In contrast, LVSP, +/- dp/dt(max), CO, LVEDP and PCWP recovered significantly at 60 minutes of reperfusion. (2) In the control group, the coronary ligation area was similar on both MCE in vivo and pathological evaluation, and the area of no-reflow was similarly as high as 78.5% and 82.3%, respectively, with final necrosis area reaching 99% of ligation area. In the fosinopril group, there was no significant difference in ligation area on both MCE and pathological evaluations between the fosinopril and control groups, although the area of no-reflow on both methods was significantly decreased to 24.5% and 25.2%, respectively, (P0.01) with final necrosis area of pathological evaluation being also significantly decreased to 88.9% of LA (P0.05). (3) In the control group, CBV was significantly declined to 45.8% and 50.6% from at baseline, immediately after release of occlusion (3 hours) and at 60 minutes of reperfusion (P0.01). In the fosinopril group, CBV was also significantly declined immediately after release of occlusion (3 hours), and at 60 minutes of reperfusion (P0.05), but significantly increased to 69.1% and 72.1% from at baseline, that were significantly greater than those in the control group (both P0.01).Fosinopril is effective in preventing myocardial no-reflow, improving left ventricular function, and reducing infarct area during acute myocardial infarction and reperfusion in mini-swine.

To assess the efficacy of Mytrolimus (CCI-779), a derivative of rapamycin, eluting stents in preventing restenosis in the porcine model.The bare stents (n = 10), stents coated with polyolefin (n = 10) or stents coated with Mytrolimus (160 microg/18 mm) in polyolefin (n = 8) were implanted in left anterior descending coronary arteries or right coronary artery of mini-swine. Coronary angiography was performed after 4 weeks then the animals were sacrificed. The cross sections of the stented coronary arteries were analyzed, the injury score, luminal area, neointimal thickness above the struts and between the struts of stents, neointimal area and percentage of restenosis were measured.The mean injury scores and luminal area were similar in three groups. There was no difference in above-stated items between the polyolefin coating stent and bare mental stent. To compare Mytrolimus-eluting stent with bare-stent, neointimal thickness above the struts [(0.18 +/- 0.08) mm vs (0.33 +/- 0.25) mm, P0.05] and between the struts [(0.14 +/- 0.05) mm vs (0.28 +/- 0.23) mm, P0.05] and neointimal area [(1.09 +/- 0.24) mm(2) vs (2.44 +/- 1.59) mm(2), P0.05] were significantly decreased in the Mytrolimus-eluting stent group than in bare mental stent group. Compared with bare-stent, the Mytrolimus eluting stent was associated with a 55.33% reduction in neointimal area. No restenosis developed in the Mytrolimus group.The Mytrolimus-eluting stents can effectively inhibit the neointimal hyperplasia in stented areas of coronary arteries 4 weeks after stent implantation in porcine model.

To evaluate the beneficial effects of Tong-xin-luo on myocardial no-reflow after acute myocardial infarction (AMI) and reperfusion.Forty mini-swine were randomized into 5 equal groups: control group, low-dose group (pretreated with Tong-xin-luo 0.05 g.kg(-1).d(-1) for 3 days), medium-dose group (pretreated with Tong-xin-luo 0.2 g .kg(-1).d(-1) for 3 days), high-dose group (pretreated with Tong-xin-luo 0.5 g.kg(-1).d(-1) for 3 days), and sham-operation group. The swine in the former four groups were subjected to 3 hours of coronary occlusion followed by 60 minutes of reperfusion. Left ventricle systolic pressure (LVSP), left ventricle end diastolic pressure (LVEDP), rate of maximum pressure change in left ventricle (+/- dp/dt(max)), cardiac output (CO), and heart rate (HR) were measured 5 min before AMI in all groups and 180 min after AMI and 60 min after reperfusion in the groups 1-4. Coronary blood volume (CBV) was recorded 5 min before AMI in all groups and immediately and 60 min after reperfusion in the group 1-4. Myocardial contrast echography (MCE) was used before AMI, 3 h after AMI, and 60 min after reperfusion in the group 1-4 so as to calculate the left ventricle wall area (LVWA), ligation area (LS), and %LA. Sixty minutes after reperfusion thioflavin-S was injected into the left ventricle to dye the reperfusion area, then the descending anterior branch was re-ligated at the original site and Evan's blue was injected into the left ventricle to dye the area outside the reperfusion area blue. The heart was taken out immediately to undergo pathological examination and calculation of LVWA, LS, area of no-reflow (SNR), LA, ANR. necrosis area (NS), and NA.(1) In the control group, systolic and diastolic blood pressures (SBP and DBP), LVSP, +/- dp/dt(max), and CO significantly decreased (P0.05 or P0.01), while LVEDP significantly increased (P0.01) 3 hour after AMI, and then LVSP was significantly recovered while +/- dp/dt(max) further significantly decreased (both P0.05) 60 minutes after reperfusion. In the 3 Tongxinluo groups, the changes of LVSP, +/- dp/dt(max), CO and LVEDP were the same as those in the control group 3 hours after AMI, and 60 minutes after reperfusion, +/- dp/dt(max), CO and LVEDP were recovered significantly in the high-dose group to degrees better than those in the control group (all P0.05). (2) In the control group, the LS values measured by MCE in vivo and by pathological evaluation were similar (P0.05), and the SNR was 78.5% by MCE in vivo and was 82.3% by pathological evaluation with the final NS reaching 98.5% of LS. There was no significant difference in LS by both MCE and pathological evaluation between the Tongxinluo groups and control group, though the values of SNR by both methods in the medium and high-dose groups were 41.1% and 42.4% and 24.1% and 25.0% respectively, all significantly lower than those in the control group and low-dose group (P0.05 or P0.01) with the values in the high-dose group being significantly lower than those in the median-dose group (P0.05 and P0.01). The final NS of pathological evaluation was also significantly decreased to 90.2%and 81.2% of LS (P0.05). In the control group, CBV was significantly decreased to 45.8% and 50.6% of the baseline value immediately at the beginning of reperfusion and 60 minutes after reperfusion (both P0.01). In the high-dose group, CBV was also significantly decreased to 76% and 73.5% of the baseline value immediately at the beginning of reperfusion and 60 minutes after reperfusion (both P0.05), however, both significantly higher than those in the control group (both P0.01).Tongxinluo is effective in preventing myocardial no-reflow, improving left ventricular function and reducing infarct area during AMI and reperfusion.

To evaluate the effects of nicorandil on myocardial no-reflow state in a mini-swine model of acute myocardial infarction (AMI) and reperfusion.Twenty-four mini-swine were randomly divided into three study groups: 8 in control group, 8 in nicorandil-treatment group, and 8 in sham-operated group. Animals in the former two groups were subjected to 3 hours of coronary occlusion followed by 1 hour of reperfusion. Hemodynamics and coronary blood flow volume (CBV) were monitored, and the area of no-reflow (ANR) was evaluated with both myocardial contrast echocardiography (MCE) in vivo and pathological means. Necrosis area (NA) was measured with triphenyltetrazolium chloride (TTC) staining.(1)In control group, left ventricular systolic pressure (LVSP), the maximum change rate of left ventricular pressure rise and fall (+/-dp/dt max) and cardiac output (CO) significantly declined, while left ventricular end-diastolic pressure (LVEDP) significantly increased at the end of 3 hours of LAD occlusion compared to that prior to AMI (P0.05 or P0.01), and +/-dp/dt max further significantly declined, while LVSP significantly rose (all P0.05) at 1 hour of reperfusion. In the nicorandil-treatment group, the changes of LVSP, +/-dp/dt max, CO and LVEDP were the same as those in the control group after 3 hours of AMI. In contrast, LVSP, +/-dp/dt max, CO and LVEDP significantly elevated at 1 hour of reperfusion, and the changes were more significant compared to those of the control group (all P0.05). (2)In control group, the vascular area after coronary ligation (LA) as determined by MCE in vivo was consistent with that of pathological evaluation(P0.05), and the range of ANR (ANR%) was also similar [(78.50+/-4.35)% and (82.30+/-1.90)% respectively], with final range of NA (NA%) reaching (98.50+/-1.35% of LA. In the nicorandil-treatment group, there was no significant difference in the range of LA (LA%) for both MCE and pathological evaluation (P0.05), which were also not significantly different from those in control group, while ANR% and NA% significantly decreased (P0.05 or P0.01). (3)In the control group, CBV was significantly declined to 50.6% and 45.8% of the baseline immediately after release of 3 hours occlusion and at 1 hour of reperfusion (both P0.01). In the nicorandil-treatment group, CBV was also significantly declined immediately after release of 3-hour occlusion, and at 1 hour of reperfusion (both P0.05), though it was significantly increased to 69.4% and 67.9% of the baseline, and they were both significantly higher than those in the control group (both P0.01).Nicorandil is effective in preventing myocardial no-reflow, improving left ventricular function and reducing infarct area after coronary artery occlusion and reperfusion in mini-swine.

To evaluate the beneficial effects of adenosine on myocardial no-reflow in a mini-swine model of acute myocardial infarction (AMI) and reperfusion.Twenty-four animals were randomly assigned to 3 groups: 8 in controls, 8 in adenosine-treated and 8 in sham-operated. The groups were subjected to 3 hours of coronary occlusion followed by 60 minutes of reperfusion except the sham-operated group. Data on hemodynamics and coronary blood flow volume (CBV) were collected. The area of no-reflow was evaluated by both myocardial contrast echocardiography (MCE) in vivo and histopathological means and necrosis area was measured with triphenyltetrazolium chloride staining.(1) In control group, systolic and diastolic blood pressure (SBP and DBP), left ventricular systolic pressure, maximal rate of increase and decline in left ventricular pressure (+/- dp/dtmax) and cardiac output significantly declined (P0.05-0.01), while left ventricular end-diastolic pressure (LVEDP) and pulmonary capillary wedge pressure (PCWP) significantly increased at the end of 3 hours of LAD occlusion (both P0.01), with +/- dp/dtmax further significantly declined (both P0.05) at 60 minutes of reperfusion. In adenosine treated group, the changes of SBP and DBP, left ventricular systolic pressure, +/- dp/dtmax, cardiac output, LVEDP and PCWP were the same as those in the control group after AMI and reperfusion, while left ventricular systolic pressure, +/- dp/dtmax, cardiac output, LVEDP and PCWP recovered significantly at 60 minutes of reperfusion compared with those at 6 hours AMI. (2) In control group, the coronary ligation areas (LA) were similar (P0.05) detected by MCE in vivo and histopathological evaluation, and the areas of no-reflow were both as high as 67.5% and 69.3%, respectively. The final necrosis area reached 99% of LA. Compared with those in the control group, there was no significant difference in LA on both MCE and histopathological evaluation in the adenosine-treated group, though the areas of no-reflow on both methods were significantly decreased to 21% and 22% (both P0.01) and final necrosis area was also significantly decreased to 75% of LA (P0.05). (3) In the control group, CBV were significantly declined to 45.8% and 50.6% of the baseline at immediately after release of 3 hours occlusion and at 60 minutes of reperfusion, respectively (both P0.01). In the adenosine-treated group, CBV were also significantly declined at immediately after release of 3 hours occlusion, and at 60 minutes of reperfusion (both P0.05), though significantly increased to 79.5% and 79.9% of the baseline which were both significantly higher than those in the control group.Adenosine has an effective role in preventing myocardial no-reflow, improving left ventricular function and reducing infarct area during AMI and reperfusion in mini-swine.

This study was sought to compare the sensitivity, specificity and accuracy of (1) dual isotope simultaneous acquisition single-photon emission computed tomography (DISA SPECT) myocardial image with (99m)Tc-sestamibi/(18)F-fluorodeoxyglucose ((99m)Tc-MIBI/(18)FDG); (2) low dose dobutamine alone and combined with Isosorbide Dinitrate (ISDN: Isoket) stress two dimensional echocardiography (2DE) to predict regional movement recovery after revascularization (CRV) in patients with old myocardial infarction (OMI) and severe left ventricular dysfunction.Twenty-six patients (mean age 51 +/- 8 years, male 25, female 1) with OMI and severe left ventricular dysfunction (mean left ventricular ejection fraction, LVEF (38.6% +/- 4.9%) underwent low dose dobutamine 10 microg x kg(-1) x min(-1) (Dob10 microg) and ISDN (286 +/- 31 microg/min) combined with Dob5 microg (ISDN-Dob 5 microg) 2DE and DISA SPECT within one week. In echocardiogram and DISA SPECT images: the left ventricle (LV) was divided into 16 segments. The semi-quantitative scoring system was used for both images. Myocardial viability was defined as an improvement of at leastor= 1 grade in at least two contiguous segments at rest 2DE after CRV. The viable segments detecting rate with stress 2DE and DISA SPECT were compared. Compared with the results of post-CRV, the sensitivity, specificity and accuracy of detecting viable segments of two methods were calculated.Among 272 abnormal segments in 26 patients, 156 (57.4%) segments showed contractile improvement after CRV. The viable segments detecting rate with DISA SPECT was 72.4% (134/254), which was significantly higher than the contractile improved rate after CRV (P0.001). During Dob10 microg 2DE and ISDN-Dob5 microg 2DE, the detecting rates were 65.5% (163/249) and 65.7% (176/268), respectively, which were both comparable to the improved rate after CRV (both P0.05). With DISA SPECT, the sensitivity, specificity and accuracy were 93.7%, 55% and 76.8%, respectively. Compared with DISA SPECT, Dob10 microg 2DE showed similar sensitivity (88.6%), specificity (64.2%) and the accuracy (77.9%). When ISDN combined with Dob5 microg, the sensitivity (91.4%), specificity (68.1%) and accuracy (81.4%)were comparable to those of Dob10 microg 2DE and DISA SPECT (all P0.05), while the specificity was even higher than DISA SPECT (P0.05).In identifying myocardial viability in patients with OMI and severe left ventricular dysfunction, DISA SPECT has higher sensitivity, lower specificity and better accuracy. Dob10 microg and ISDN-Dob5 microg 2DE are both equivalent to DISA SPECT in sensitivities, specificities and accuracies, and even higher in specificity in ISDN-Dob5 microg 2DE.

To evaluate the beneficial effects of diltiazem on myocardial no-reflow.Twenty-four mini-swine were randomized into 3 equal groups: diltiazem-treated group subjected to 3 hours of coronary occlusion to cause acute myocardial infarction (AMI), followed by 60 minutes of reperfusion and injected with diltiazem into the coronary artery 1 minute before reperfusion, control group undergoing coronary occlusion followed by 60 minutes of reperfusion and injected with normal saline, and sham operation group. 5 minutes before AMI in all groups and 180 minutes after AMI and 60 minutes after re-perfusion in the diltiazem and control groups, hemodynamic data, such as heart rate (HR), left ventricular systolic pressure (LVSP). Left ventricular end diastolic pressure (LVEDP), +/- dp/dt(max), cardiac output (CO), and coronary blood volume (CBV) were measured. Myocardial contrast echography (MCE) was used to measure the left ventricle wall area (LVWA) and ligation area (LA) so as to calculate LA and to measure the area of no-reflow (ANR) so as to calculate ANR. 60 minutes after reperfusion thioflavin-S was injected into left ventricle so as to color the reperfused area and then the descending anterior branch was re-ligated and Evan's blue was injected into the left ventricle to color the area outside the ligation area. The heart was taken out to undergo histological examination.(1) In comparison with the values before AMI the LVSP, +/- dp/dt(max), and CO of the control group significantly declined (P0.05, 0.01), while the LVEDP significantly increased (P0.01) by the end of 3 hours after LAD occlusion; and the LVSP significantly increased and the +/- dp/dt(max) further significantly declined (both P0.05) 60 minutes after reperfusion. In the diltiazem group, the changes of LVSP, +/- dp/dt(max), CO, and LVEDP were the same as those in the control group after 3 hours of AMI, while the +/- dp/dt(max), CO, and LVEDP recovered significantly, more significantly than those in the control group, 60 minutes after reperfusion (all P0.05). (2) In the control group, the sizes of coronary ligation area (LA) measured by both MCE in vivo and histopathological evaluation were similar (P0.05), and the values of area of no-reflow (ANR) measured by MCE in vivo and histopathological evaluation were 78.5% and 82.3% respectively with the final necrosis area (NA) reaching 99% of the LA. There was no significant difference in LA measured by both MCE and histopathological evaluation between the control and diltiazem groups, while the values of ANR measured by both methods was significantly decreased to 19.9% and 20.6% that before AMI respectively in the diltiazem group (both P0.01). There was no significant difference in NA between the control and diltiazem groups (P0.05). The CBV of the control group was significantly declined to 45.8% and 50.6% of the baseline value respectively immediately and 60 minutes after reperfusion (both P0.01), while the CBV of the diltiazem group became 80.4% and 79.3% of the baseline value respectively immediately and 60 minutes after reperfusion (both P0.05), both significantly higher than those of the control group (both P0.01).Diltiazem is effective both in preventing myocardial no-reflow and improving left ventricular function, but not in reducing MI size during AMI and reperfusion.

To compare the effects of matrix metalloproteinase (MMP) inhibitor doxycycline, losartan, and their combination on the expression of MMP-8, 13, tissue inhibitor of MMP-1, 2 (TIMP-1, 2), and collagen remodeling in the noninfarcted myocardium after acute myocardial infarction (AMI) in rats.Two hundred and fifty-four AMI rats, induced by left coronary ligation, were randomly assigned to the following groups: (1) AMI controls group (n = 64); (2) doxycycline group (30 mg x kg(-1) x d(-1), n = 63); (3) losartan group (10 mg x kg(-1) x d(-1), n = 62); (4) concomitant doxycycline and losartan group (30 and 10 mg x kg(-1) x d(-1) respectively, n = 65); and (5) Sham-operated rats (n = 30), which were randomly selected to serve as noninfarction controls. Each group was further divided into three subgroups of 1, 2, and 4 weeks that received treatment. After the completion of treatment, the rats were killed. The mRNA and protein expression of MMPs and TIMPs in the noninfarcted myocardium were quantified by RT-PCR and Western blot, respectively. The type I and type III collagen volume fraction (CVF) of the noninfarced myocardium were assessed immunohistochemically.No significant difference existed in myocardial infarction sizes among the 12 subgroups of AMI controls and the three treatment groups (42%-48%, all P0.05). Compared with sham operated rats, the mRNA and protein expression of MMP-8 and 13 significantly increased by 39%-183% in all three subgroups of AMI controls (all P0.05), except both of their mRNA expressions in 2-week subgroups; the mRNA and protein levels of TIMP-1 increased only in 1-week subgroup of AMI controls by 104% and 67%, respectively (both P0.05); the mRNA of TIMP-2 increased in all 1, 2, and 4-week subgroups by 144%-232% (all P0.05), but its protein expression lagged and only enhanced in 2 and 4-week subgroups of AMI controls by 231% and 332%, respectively (both P0.05). Meanwhile, both type I and type III CVF of noninfarcted myocardium significantly increased in all three subgroups of AMI controls (type I CVF: 3.01%-5.64% vs 1.53%-1.67%, P0.01-0.001; type III CVF: 2.19%-4.42% vs 1.46%-1.59%, P0.05-0.001), with type I CVF being higher in 4-week than in 1 and 2-week subgroups (5.64% vs 3.01% and 3.02% respectively, all P0.05). Compared with AMI controls, all three kinds of treatment significantly reduced the increased mRNA and protein expressions of MMP-8, 13 and TIMP-1, 2 after AMI by 14%-60% (all P0.05), as well as type I/III CVF in their 2 and 4-week subgroups (type I CVF: 1.56%-2.38% vs 3.02%-5.64%, P0.05-0.001; type III CVF: 1.92%-2.65% vs 4.19%-4.42%, P0.05-0.01), except for doxycycline's effect on type III CVF in any of its three subgroups (all P0.05). Among the three treatment groups, significant differences existed in the above mentioned indicators only at some subgroup levels (all P0.05).Like losartan, doxycycline can also suppress the enhanced mRNA and protein expression of MMP-8, 13 and TIMP-1, 2, and reduce type I collagen deposition in the noninfarcted myocardium after AMI in rats. However, it has no effect on type III collagen deposition.

To assess the effects of doxycycline, a matrix metalloproteinase (MMP) inhibitor, on the expression of MMP-8 and -13, and tissue inhibitor of MMP-1 and -2 (TIMP-1 and -2), and on collagen remodeling in the noninfarcted myocardium after acute myocardial infarction (AMI).212 female SD rats underwent ligation of left coronary artery so as to cause AMI. Twenty-four hours after the 127 surviving rats were randomly divided into 2 groups: AMI control group (n = 64) and AMI doxycycline treatment (30 mg.kg(-1).d(-1)) group (n = 63). Then the rats in these 2 groups were re-divided into 3 sub-groups of 18 approximately 24 rats according to the course of treatment: 1-week, 2-week, and 4-week subgroups. Thirty female SD rats underwent sham operation and then were re-divided into 3 groups of 10 rats: 1-week, 2-week, and 4-week subgroups. By the end of each course the rats were killed and their hearts were taken out. A piece of myocardium from the left ventricle was taken and stained with hematoxyline and eosin to examine the area of infarction. The mRNA expressions of MMP and TIMP in the non-infarcted myocardium were detected by RT-PCR. The protein expressions of MMP and TIMP in the non-infarcted myocardium were detected by Western blotting. The type I and type III collagen volume fraction (CVF) in the noninfarcted myocardium was examined by immunohistochemistry.There was no significant difference in the MI size among the 6 subgroups of AMI control and doxycycline groups (42% approximately 48%, all P0.05). Compared with sham operated rats, the mRNA expressions of MMP-8 and 13 were significantly increased by 54% approximately 183% in all three subgroups of AMI controls (all P0.05), and the mRNA expressions of MMP-8 and 13 in the 1-week and 4-week were significantly increased by 39% approximately 160% in these 3 subgroups (all P0.05). The mRNA and protein expressions of TIMP-1 were enhanced only in the 1-week subgroup of AMI controls by 104% and 67% respectively (both P0.05). The mRNA expression of TIMP-2 was significantly increased in all 1-, 2-, and 4-week subgroups by 144% approximately 232% (all P0.05), however, the protein expression of TIMP-2 was increased only in the 2- and 4-week subgroups of AMI control group by 231% and 332% respectively (both P0.05). Compared with the sham operation group, both the type I CVF and type III CVF of the noninfarcted myocardium were significantly increased in all three subgroups of the AMI control group (type I CVF: 3.01% approximately 5.64% vs 1.53% approximately 1.67%, P0.01 approximately 0.001; type III CVF: 2.19% approximately 4.42% vs 1.46% approximately 1.59%, P0.05 approximately 0.001), with type I CVF being higher in the 4-week subgroup than in the 1 and 2-week subgroups (5.64% vs 3.01% and 3.02% respectively, all P0.05). In comparison with the 3 subgroups of the AMI control group, the mRNA and protein expressions of MMP-8 and 13 and TIMP-1 and 2 after AMI in the doxycycline group were significantly lower by 14% approximately 51% (all P0.05). In comparison with that in the AMI control group, the type I collagen deposition in the doxycycline group was significantly lower 2 and 4 weeks after AMI (1.94% vs 3.02% and 1.97% vs 5.64% respectively, P0.01 approximately 0.001), however, there was no significant difference in type III CVF among the different subgroups (all P0.05).Doxycycline suppresses the enhanced mRNA and protein expressions of MMP-8 and 13 and TIMP-1 and 2, and type I collagen deposition in the noninfarcted myocardium after AMI, but it has no effect on type III collagen deposition.

To investigate the characteristics of coronary lesions in patients after first myocardial infarction (MI).From May 1998 to December 2000, coronary angiography was performed on 878 consecutive cases who had had first MI within 6 months and without history of previous coronary revascularization, 481 with anterior-lateral MI, 368 with inferior-posterior MI, 19 with posterio-lateral MI, and 10 with location-undetermined MI, and 394 receiving thrombolytic therapy 176 (44.7%) of which were treated successfully, and 525 (59.8%) with history of pre-infarction angina pectoris and 428 (48.7%) with history of post-infarction angina pectoris.(1) Normal coronary vessels or lesions less than 50% stenosis were seen only in 5.9% (52) of the patients. One-, two- and three-vessel diseases were present in 32.8% (288), 26.4% (232) and 34.9% (306) patients respectively. 3.2% (28) had concomitant left main stem (LMS) disease. Three-vessel coronary disease was significantly more common in the patients with a history of pre-infarction angina in comparison with those without such history (39.2% vs 28.3%, P0.01), and was significantly more common in the patients who did not undergo thrombolytic therapy in comparison with those who had received thrombolytic therapy (38.4% vs 30.5%, P0.05). (2) Only in 5.1% (41) cases the infarct-related artery (IRA) was normal or with lesions less than 50% stenosis. Total occlusion (100% stenosis), subtotal occlusion (95% to 99% stenosis), severe stenosis (70% to 94% stenosis) and borderline stenosis (50% to 69% stenosis) of IRA were seen in 29.6% (240), 22.6% (183), 37.9% (307) and 4.9% (40) of the cases respectively. Total occlusion of IRA occurred significantly less often in the thrombolytic group than in the non-thrombolytic group (24.6% vs 33.7%, P0.01). IRA could not be determined in 67 cases. (3) 90.5% (795), 79.4% (697), 57.2% (502) and 35.6% (313) of the patients hador = 70% stenosis,or = 90% stenosis,or = 95% stenosis and total occlusion coronary lesions in at least one major coronary artery respectively, and coronary revascularization including PCI and CABG was needed on 84% (736/878) of the patients.Patients with a first MI usually have multi-vessel disease and severe coronary stenosis, with IRA having severe stenotic lesions. Revascularization treatment is needed in the majority of the patients. It is true too for the MI patients without history of pre- or post-infarction angina pectoris and those with successful thrombolytic therapy. Coronary angiography should routinely be performed on the patients who need further coronary revascularization.

This report provides analysis of the complication rates, the risk factors, prevention and treatments of the complications of selective coronary interventions.The types, the incidence, and the annual distribution characteristics of the complications in 2 868 cases of coronary interventions performed from October 1987 to December 2000 were reviewed, and the risk factors, prevention and treatments of the complications were analyzed.During the study period, 2 868 procedures of percutaneous coronary interventions (PCI) were performed. The total complication rate of PCI was 8.30% (6.33% - 20.00%). The procedure-related mortality rates were 0.07%. The complications included non-fatal Q wave myocardial infarctions (0.17%), coronary artery dissecting (2.58%), acute coronary artery occlusion (1.99%), coronary artery thrombosis (0.38%), coronary artery spasm (1.32%), coronary artery perforation (0.31%), severe arrhythmia (0.63%), severe contrast allergic reaction (0.07%), peripheral vascular complication (0.90%), and heart failure (0.10%). Emergent coronary artery bypass surgery (CABG) was required in 0.10% of the patients with PCI. The independent risk factors of the complications of PCI included unstable angina, coronary multivessel disease, and heart failure.The complication rates of PCI decreased with the accumulation of experiences. The complication rates in this group of patients are lower than the reported ones. This result is probably due to strictly selecting the indication, actively preventing and treating the complications.

To study the incidence rates, risk factors, prevention and treatments of complications of selective coronary arteriography.A retrospective survey was conducted on the data of the incidence and annual distribution characteristics of complications among 9 196 cases that underwent selective coronary arteriography performed October 1987 to December 2000, and analyze the risk factors and prevention and treatment of these complications.The total complication rate was 1.33%. The procedure-related mortality rates were 0.02%. The incidence rate of non-fatal Q wave myocardial infarction, coronary artery spasm, severe arrhythmia, severe contrast allergic reaction, peripheral vascular complication, and heart failure in coronary arteriography was 0.01%, 0.13%, 0.29%, 0.04%, 0.35%, and 0.08%, respectively. No emergent coronary artery bypass surgery was required in patients with coronary arteriography. The independent risk factors of the complications of coronary arteriography included unstable angina, coronary multivessel disease, left main coronary artery disease and heart failure.The complication rate of coronary arteriography decrease with the accumulation of experience. The complication rate in this group is lower than in other reports probably due to strictly selecting of indication and active prevention and treatment of complications.

It has been verified that losartan has beneficial effects on ventricular remodeling (VRM) after acute myocardial infarction (AMI), but the effects of carvedilol alone or in combination with losartan on this condition have not been defined. The present study used rats to compare the effects of carvedilol and losartan alone and in combination for preventing VRM after AMI. After ligation of the left coronary artery, 100 surviving female Sprague-Dawley rats were randomly assigned to 1 of 4 groups: (1) AMI control (n=25), (2) carvedilol (Car, 1 mg x kg(-1) x day(-1)) (n=25), (3) losartan (Los, 3 mg x kg(-1) x day (-1)) (n=25), and (4) Car (1 mg x kg (-1). day(-1)) + Los (3 mg x kg(-1) x day (-1)) (n=25). A sham-operated group (n=17) was also randomly selected. Drugs were administered by gastric gavage for 4 weeks. After hemodynamic studies, the hearts were fixed and analyzed pathologically. Exclusive of the rats that had died or had an infarct size 55%, complete data were obtained for 65 rats, comprising AMI control (n=13), Car (n=12), Los (n=13), combination (n=14), and sham (n=13) groups. There were no significant differences in the size of infarct among the 4 AMI groups (45.8 approximately 46.7%, all p>0.05). Compared with the sham group, left ventricular (LV) end-diastolic pressure (LVEDP), volume (LVV), weight (LVW) and septal thickness (STh) were all significantly increased (all p

Objectives To compare the effects of cilazapril, carvedilol and their combination in preventing left ventricular remodelling (LVRM) after acute myocardial infarction (AMI) in rats. Methods Twenty-four hours after left coronary artery ligation, 100 surviving AMI female Sprague-Dawley rats were randomly assigned to: (1) AMI control (n=25); (2) cilazapril (Cila, 1 mg/kg/day) (n=25); (3) carvedilol (Car, 1 mg/kg/day) (n=25), and (4) cilazapril (1 mg/kg/day)+ carvedilol (1 mg/kg/day) (combination) (n=25) groups. A sham-operated group (n=17) was selected randomly as a non-infarction control. After four weeks of therapy with the drugs given by gastric gavage, haemodynamic studies were performed, following which the rat hearts were fixed and pathologically analysed. Rats with MI size 55% were excluded. Complete data were obtained in 64 rats, comprising AMI control (n=13), Cila (n=12), Car (n=12), Combination (n=14), and sham-operated (n=13) groups. Results There were no significant differences in MI size between the four AMI groups (45.2—46.7%, p>0.05). Compared with the sham-operated group, left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), weight (LVW), septal thickness (STh) and right ventricular weight (RVW) were all significantly increased (all p Conclusions Cilazapril, carvedilol and their combination are all effective in preventing LVRM after AMI in rats, and in improving haemodynamics and LV function, with the combination therapy being superior to monotherapy in all respects.