Clinical analysis and risk stratification of ventricular septal rupture following acute myocardial infarction.

BACKGROUND: 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. METHODS: 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 survived >30 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. RESULTS: 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%, P < 0.005. 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%; SPIV <8 indicates a low risk as the 30-day mortality is 28.6%; SPIV between 8 and 9 indicates a moderate risk. CONCLUSIONS: 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.

[Short-term prognosis and risk factors of ventricular septal rupture following acute myocardial infarction].

OBJECTIVE: To analyze the short-term prognosis and risk factors of ventricular septal rupture (VSR) following acute myocardial infarction (AMI). METHODS: 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 survived > 30 days (n = 31) post AMI. A short-term prognosis index of VSR (SPIV) was established based on the logistic regression analysis. RESULTS: 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 P < 0.05). 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). CONCLUSION: 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.

[Real world thirty-day mortality in female patients with acute myocardial infarction from Beijing].

OBJECTIVE: To evaluate the gender differences on the short-term outcomes of patients with acute myocardial infarction in the real world. METHODS: A total of 471 consecutive patients [male 368(78.1%) and female 103(21.9%)] with acute myocardial infarction <72 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. RESULTS: Female patients were older (66.8 ± 10.1 vs. 56.9 ± 12.0, P < 0.001), TIMI score (5.1 ± 2.3 vs. 3.9 ± 2.1, P < 0.001) and GRACE score (162 ± 39 vs. 142 ± 35, P < 0.001) 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 (P < 0.05). 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. CONCLUSIONS: 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.

[Impact of cytochrome P450 2C19 polymorphisms on outcome of cardiovascular events in clopidogrel-treated Chinese patients after percutaneous coronary intervention].

OBJECTIVE: To investigate the impact of cytochrome P450 (CYP) 2C19 681G > A polymorphism on long-term prognosis of clopidogrel-treated Chinese patients after percutaneous coronary intervention (PCI). METHODS: 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. RESULTS: Baseline data were similar between two groups (P > 0.05). 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 P < 0.05). But incidence of angina recurrence, acute myocardial infarction, stent thrombosis and death was similar between two groups (all P > 0.05). 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, P < 0.05). CONCLUSION: CYP2C19 681G > A polymorphism is a determinant of prognosis in coronary heart disease patients receiving chronic clopidogrel treatment after PCI.

Gender difference of clinical characteristics in Chinese patients with spontaneous variant angina.

BACKGROUND: 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. METHODS: 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. RESULTS: 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%, P < 0.001), more likely to have a family history of CAD (33.3% vs. 11.0%, P < 0.01), and to have had a greater incidence of ventricular fibrillation during attack (11.1% vs. 2.2%, P < 0.05). There were no significant differences in other characteristics between the two groups. CONCLUSION: 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.

[Clinical characteristics and outcome comparison between young (< or = 45 years) female and male patients with coronary artery disease undergoing percutaneous coronary intervention].

OBJECTIVE: 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). METHODS: 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. RESULTS: Incidences of dyslipidemia, the history of myocardial infarction and smoking were significantly lower in female patients than in male patients (all P < 0.01). 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 (P < 0.01-0.05). 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, P < 0.05]. 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. CONCLUSIONS: 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.

[The relationship between plasma BNP level and the left ventricular dysfunction parameters in patients with acute myocardial infarction and it's value in diagonosing heart failure.].

OBJECTIVE: To explore the correlation between plasma BNP level and left ventricular dysfunction parameters in patients with acute myocardial infarction (AMI). METHODS: 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. RESULTS: After AMI, lnBNP levels increased significantly in proportion with increasing Killip grades (I-III), and decreasing LVEF (all P < 0.05). lnBNP level was significantly higher in LVEDd > 55 mm group than in the LVEDd < 55 mm group (P < 0.01). lnBNP, LVEDd and LVEF all linearly correlated with Killip grades (P < 0.05) and the best correlation was shown between lnBNP and Killip grades (r = 0.53, P < 0.05). lnBNP also positively correlated with LVEDd (r = 0.17, P < 0.05) and negatively correlated with LVEF (r = -0.41, P < 0.01). Among the parameters, lnBNP level presented the largest AUC in their ROC curves (P < 0.01) 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. CONCLUSION: 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.

[Effect of intracoronary transplantation of autologous bone marrow mononuclear cells on myocardial ischemia reperfusion injury in mini-swine model].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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 (P > 0.05). In the control group, LVEF, intraventricular septa, lateral wall and anterior wall, CO, and + dp/dt(max) significantly decreased 4 weeks after transplantation (P < 0.05). 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. CONCLUSION: 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.

[Autologous bone marrow mononuclear cells and peripheral endothelial progenitor cells differentiation in myocardial ischemia reperfusion injury region in swine].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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, P < 0.05), but was significantly higher than that of control group (P < 0.05). 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. CONCLUSION: BM-MNC and EPC transplanted into myocardial ischemia reperfusion injury region in swine stimulated the formation of blood vessels and inhibited fibrogenesis.

[The predictive value of B-type natriuretic peptide for the mortality from acute myocardial infarction].

OBJECTIVE: To explore the predictive value of B-type natriuretic peptide (BNP) for the mortality of acute myocardial infarction (AMI). METHODS: 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. RESULTS: 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 (P < 0.01) by multiple factors cox regression analysis. The non-cardiac death survival rate in the group of BNP level < or = 864 ng/L was significantly higher than that in the group of BNP > 864 ng/L (97.3% vs 72.3%, P < 0.001), 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, P < 0.01), no matter whether they were suffering from AMI with ST elevation or not, treated with or without primary PCI. CONCLUSION: BNP has the best predictive value for mortality after AMI compared with other traditional indexes.

Post-infarction treatment with simvastatin reduces myocardial no-reflow by opening of the KATP channel.

UNLABELLED: 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+ (K(ATP)) 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<0.01) and decreased the area of no-reflow measured by MCE (78.5+/-4.5% to 43.7+/-4.3%) and pathological evaluation (82.3+/-1.9% to 45.2+/-3.8%) of area at risk (P<0.01). Simvastatin also increased the levels of K(ATP) channel proteins (SUR2 and Kir6.2) (P<0.05), but had no effect on necrosis area. The combination of simvastatin and glibenclamide had no significant effect on the above parameters. CONCLUSIONS: Post-infarction treatment with simvastatin can reduce myocardial no-reflow. This beneficial effect is due to activation of the K(ATP) channel.

[Effects of intracoronary transplantation of autologous bone marrow mononuclear cells or endothelial progenitor cells in mini-swine model of myocardial ischemia-reperfusion].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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 P < 0.05) 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. CONCLUSION: Autologous intracoronary transplantation of BM-MNC or EPC in this model equally improved cardiac systolic function and reduced infarction area.

Inferior-septal myocardial infarction misdiagnosed as anterior-septal myocardial infarction: electrocardiographic, scintigraphic, and angiographic correlations.

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: The diagnostic criteria for basal inferior-septal wall AMI can be formulated as follows: (1) ST segment elevates > or = 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.

[Effects of atenolol and metoprolol on cardiomyocyte apoptosis and related gene expression after acute myocardial infarction in rats].

OBJECTIVE: To compare the beneficial effects of Atenolol and Metoprolol on cardiomyocyte apoptosis and related gene expressions after acute myocardial infarction (AMI) in rats. METHODS: 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. RESULTS: Compared with AMI control group, myocyte apoptosis rate (MAR) significantly decreased only in infarction area (P < 0.01) 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 (P < 0.05, P < 0.01) 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 (P < 0.05). CONCLUSION: 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.

[Serum B-type natriuretic peptide changes in patients with acute myocardial infarction].

OBJECTIVE: To observe the serum B-type natriuretic peptide (BNP) changes post acute myocardial infarction (AMI). METHODS: 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. RESULTS: 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, P < 0.05]. 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 P < 0.001). The BNP level were significantly higher in AMI patients with single or triple coronary arteries stenosis than those without coronary stenosis (P < 0.05), in TIMI blood flow 0 - 1 and 2 groups than in TIMI 3 group (all P < 0.001). 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 P < 0.05 - 0.001). CONCLUSION: Serum BNP was significantly elevated in patients after AMI but decreased after successful primary PCI in patients with AMI.

[Beneficial effects of carvedilol on cardiomyocyte apoptosis and bcl-2/bax expression after acute myocardial infarction an experiment with rats].

OBJECTIVE: To investigate the beneficial effects of carvedilol on cardiomyocyte apoptosis and related gene expression after acute myocardial infarction (AMI). METHODS: 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. RESULTS: 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 P < 0.05). 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 P < 0.05), 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 P < 0.05) 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 (P < 0.05), (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 (P < 0.05 - 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 P > 0.05), and (3) There were no significant difference in the bcl-2 and bax expression between Group A and Group S (all P > 0.05), however, the bcl-2/bax ratios at the 2 time-points of Group C were both significantly higher than those of Group MI. CONCLUSION: 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.

[Effect of adenosine on endothelin-1 in the infarcted reflow and no-reflow myocardium of mini-swine].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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 P < 0.01). In adenosine group, the levels of ET-1 were significantly lower than those in the control group (P < 0.05, P < 0.01). 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 P < 0.01), with the level of ET-1 in no-reflow myocardium significantly higher than that in infarcted reflow myocardium (P < 0.01). In adenosine group, the level of ET-1 in infarcted reflow myocardium was significantly lower than that in the control group (P < 0.01). 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 (P < 0.01), while that of ET-1 in. no-reflow myocardium significantly down-regulated (P < 0.01). In adenosine group, the level of ET-1 in infarcted reflow myocardium was significantly lower than that in the control group (P < 0.01). CONCLUSION: The endothelium injury may be one of the important mechanisms for no-reflow phenomenon. Adenosine cay prevent endothelium from injury to reduce no-reflow.

[Effects of anti-platelet drugs on myocardial no-reflow after acute myocardial infarction and reperfusion: experiment with mini-swine model].

OBJECTIVE: To evaluate the effects of anti-platelet drugs on myocardial no-reflow after acute myocardial infarction (AMI) and reperfusion. METHODS: 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. RESULTS: 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 P < 0.01) with equivalent potency (P > 0.05). The left ventricular function was significantly improved in tirofiban group in comparison with control group (P < 0.05 - 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%, P < 0.01), 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 P < 0.01), and the NA of tirofiban group was 89.2%, significantly smaller than that of Control Group (98.5%, P < 0.05). 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 P > 0.05). CONCLUSION: Tirofiban is markedly effective in attenuating myocardial no-reflow after reperfusion; in contrast, A-C combination is totally ineffective.

[Comparison of doxycycline, losartan, and their combination in the prevention of post-infarction remodeling in rats].

OBJECTIVE: 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. METHODS: 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. RESULTS: Exclusive of the dead rats and the hearts with the myocardial infarction size < 35% or > 50%, 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 (P> 0.05). 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 (P < 0.05, P < 0.01, and P < 0.001, respectively), with LVEDP elevated more significantly in 4 week than in 1 and 2 week subgroups (P < 0.01); 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 (P < 0.001). Compared with AMI controls group, LVEDP was significantly decreased in all 1, 2, and 4 week subgroups of the three treatment groups (P < 0.05, P < 0.01, and P < 0.001, respectively); LVAW and LVRW were significantly decreased in 2 and 4 week subgroups of losartan and combination groups (P < 0.05, P < 0.01, P < 0.001, respectively), and in only 4 week subgroup in doxycycline (P < 0.05, P < 0.01, and P < 0.001, 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 (P < 0.05, P < 0.01, respectively). There is no significant difference in all indices above among the three treatment groups at all three time points (P > 0.05). CONCLUSION: 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.

[Beneficial effects of ischemic preconditioning on myocardial no-reflow in a mini-swine model of acute myocardial infarction and reperfusion].

OBJECTIVE: To evaluate the effects of ischemic preconditioning (IPC) on myocardial no-reflow in a mini-swine model of acute myocardial infarction (AMI) and reperfusion. METHODS: Twenty-four mini-swines were randomized into 3 study groups: 8 in control, 8 in IPC and 8 in sham-operated. Animals in the former two groups were subjected to 3 hours of coronary occlusion followed by 1 hour of reperfusion. Data on hemodynamics and coronary blood flow volume (CBV) were collected, 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. RESULTS: In control group, left ventricular systolic pressure (LVSP), the maximum change rate of left ventricular pressure rise and fall (+/-dp/dtmax) and cardiac output (CO) significantly declined (P < 0.05, P < 0.01), while left ventricular end-diastolic pressure (LVEDP) significantly increased at the end of 3 hours of left anterior descending coronary artery occlusion (both P < 0.01), with +/-dp/dtmax further significantly declined (both P <0.05) at 1 hour of reperfusion. In IPC group, LVSP, +/-dp/dtmax, CO and LVEDP significantly recovered at 1 hour of reperfusion, compared with those in control group. In IPC group, the coronary ligation area was similar on both MCE in vivo and pathological evaluation (P > 0.05), and ANR was both also similarly as high as (16.4 +/- 2.24) % and (17.5 +/- 2.87) %, respectively, with final necrosis area (NA) reaching (78.4 +/- 3.62) %. In IPC group, ANR and final NA were significantly lower than those in control group (P < 0.05, P < 0.01). In the control group, coronary blood flow volumn immediately after release of 3 hours occlusion and at 1 hour of reperfusion were significantly lower than the baseline (both P < 0.01). In IPC group, coronary blood flow volumn were significantly higher than those in the control group (both P < 0.01). CONCLUSION: IPC is effective to prevent myocardial no-reflow, improve left ventricular function and decrease infarct area.