急性心肌梗死与心绞痛患者血清胆红素水平的比较

目的 探讨心绞痛和急性心肌梗死患者血清胆红素的差异。方法 收集符合1979年WHO诊断标准的心绞痛(AP)患者71例,急性心肌梗死(AMI)患者61例,其中单纯前壁AMI 11例,下壁AMI 14例。采清晨空腹静脉血测定血清总胆红素(Tbil)、直接胆红素(Dbil)、间接胆红素(Ibil)浓度并进行比较。结果 AMI组各型血清胆红素(Tbil 14.56±6.46μmol/L,Dbil 6.20±2.71μmol/L,Ibil 8.31±4.66μmol/L)均高于AP组(Tbil 11.25±4.79μmol/L,Dbil 4.94±1.82μmol/L,Ibil 6.25±3.99μmol/L),P<0.01。前壁AMI患者血清胆红素水平(Tbil 15.99±8.79μmol/L,Dbil 6.88±4.99μmol/L,Ibil 9.11±5.12μmol/L)较下壁AMI患者血清胆红素水平(Tbil 12.34±2.86μmol/L,Dbil 5.15±0.81μmol/L,Ibil 7.18±2.32μmol/L)高,但无统计学差异(P>0.05)。结论 AMI患者与AP患者血清胆红索水平存在显著性差异,但前壁AMI患者与下壁AMI患者血清胆红素水平的差异无统计学意义。     

Comparison of plasma serotonin levels in patients with variant angina pectoris versus healed myocardial infarction

Patients with variant angina pectoris showed greater serotonin plasma levels than did control subjects and patients with healed myocardial infarction. The levels also tended to be greater in those with >1 episode/month than in those with fewer episodes. Moreover, patients with variant angina pectoris also had greater levels of nitrite and nitrate plasma levels than did control subjects or patients with healed myocardial infarction, partly, perhaps, as a compensatory mechanism.     

Comparison of C-reactive protein and terminal complement complex in patients with unstable angina pectoris versus stable angina pectoris

Elevated C-reactive protein (CRP) can identify patients with coronary artery disease who are prone to future acute events. We investigated whether elevated CRP is related to the activation of the terminal complement cascade in 66 patients with unstable angina pectoris (UAP), in 45 patients with stable angina pectoris, and in 42 controls. CRP, additional acute phase reactants, the terminal complement complex (sC5b-9), leukocytes, and troponin T were measured. In 47 patients with UAP the CRP values were regarded as elevated (>0.3 mg/dl). In patients with UAP and elevated CRP, the plasma levels of sC5b-9 were markedly higher than in patients with UAP and lower CRP (245 +/- 14 vs 188 +/- 19 ng/ml, p <0.02) and in patients with stable angina pectoris with slightly (0.4 +/- 0.1 mg/dl) increased CRP (sC5b-9 173 +/- 21 vs 130 +/- 7 ng/ml [controls; p <0.05]). A further acute phase reaction was present only in patients with UAP and elevated CRP already on admission (p <0.01). sC5b-9 was not related to troponin release. Thus, elevated CRP levels are associated with activation of the plaque destabilizating terminal complement system in patients with UAP during the acute phase reaction. This may explain the prognostic value of CRP in acute coronary syndromes (ACS).     

Comparison of hemorheological variables in ST-elevation myocardial infarction versus those in non-ST-elevation myocardial infarction or unstable angina pectoris

The aim of this study was to evaluate hemorheologic variables in patients with acute coronary syndromes in relation to the occurrence of ST-segment elevation myocardial infarction (STEMI). In 370 consecutive patients with acute coronary syndromes, 215 with STEMIs and 155 with non-ST-segment elevation myocardial infarctions or unstable angina pectoris, who underwent percutaneous coronary intervention, hemorheologic studies were performed by assessing whole-blood viscosity (at shear rates of 0.512 and 94.5 s(-1)), plasma viscosity, and erythrocyte deformability index. A significant difference in hematocrit and in whole-blood viscosity at 0.512 s(-1) was found between the 2 groups of patients. Hematocrit at admission in the highest tertile compared with the lowest tertile remained independently associated with the occurrence of STEMI on multivariate analysis adjusted for traditional cardiovascular risk factors, previous coronary artery disease, multivessel disease, bleeding complications, and leukocyte count. In conclusion, erythrocyte concentration seems to play a role per se in the occurrence of STEMI and complete coronary artery occlusion and might be considered in stratifying high-risk cardiovascular patients and as a possible therapeutic target in patients presenting with acute coronary syndromes.     

舒血宁对不稳定型心绞痛患者CRP和MMP-9的影响

目的观察经舒血宁治疗后,不稳定型心绞痛（unstable angina pectoris,UAP）患者体内高敏C-反应蛋白（highsensitivity C．reactive protein,hs-CRP）和基质金属蛋白酶-9（matrix metalloproteinase-9,MMP-9）水平的变化。方法：100例UAP患者随机分为试药组和对照组,各50例。对照组给于常规治疗,试药组在此基础上加用舒血宁30mm溶于250 ml 50 s／L葡萄糖注射液中静脉滴注,1次／d,连续治疗两周。在人院时、入院后12 h、24 h、48 h、7 d及14d抽取外周血,检测各组患者hs-CRP和MMP-9表达水平变化。结果：两组UAP患者外周血hs-CRP水平在入院后均开始升高,于24 h达高峰,24 h后逐渐下降;两组MMP-9水平入院后12 h达高峰,后逐渐下降;与对照组相比,试药组hs-CRP和MMP-9水平在入院后12 h、24 h、48 h、7 d及14 d均显著降低。结论：舒血宁可显著降低UAP患者体内hs-CRP和MMP-9表达水平。     

急性心肌梗塞患者行PCI前后激活素A与血清基质金属蛋白酶水平的变化

目的:探讨激活素A(ACT-A)及血清基质金属蛋白酶-9(MMP-9)在急性心肌梗塞(AMI)患者急诊介入治疗前后的变化及临床意义。方法:采用酶联免疫吸附法(ELISA)检测60例行急诊经皮冠状动脉介入(PCI)术治疗患者及30例冠状动脉造影正常者术前及术后第1 d及第3 d血清ACT-A及MMP-9的含量。结果:AMI患者术前,术后第1 d及第3 d的血浆ACT-A及MMP-9水平均明显高于冠脉造影正常者(P均0.05),AMI患者PCI术后1d、3d血清ACT-A水平均较术前明显降低[(421±224)pg/ml:(451±190)pg/ml:(551±289)pg/ml,P均0.05],血清MMP-9水平均较术前明显升高[(769±198)μg/L:(849±208)μg/L:(710±178)μg/L,P均0.05]。且MMP-9与ACT-A呈负相关(r=-0.36,P0.05)。结论:激活素A与基质金属蛋白酶-9参与了心肌梗塞的病理生理过程,二者可用作评价急性心肌梗塞患者介入术后预后的指标。     

中期因子对大鼠急性心肌梗死后心室重构和基质金属蛋白酶9水平的影响

目的探讨中期因子(MK)对大鼠急性心肌梗死(AMI)后心室重构及血清基质金属蛋白酶9(MMP-9)水平的影响。方法雄性Wistar大鼠60只采用随机数字抽样法分为4组,每组15只:空白组(Control组),伪手术组(Sham组),AMI组,MK治疗组(MK组)。结扎大鼠左冠状动脉前降支制作AMI模型,模型建立成功后,MK组立即给予MK心肌注射。4周后,取各组剩余大鼠称重,测血流动力学指标;ELISA法测定血清MMP-9水平;心脏称重,计算心体比;取心尖部分切片,一部分MASSON染色,测定左心室游离壁梗死区厚度、长度和梗死面积,心肌梗死区及非梗死区胶原容积分数(CVF),另一部分HE染色,观察毛细血管生成情况。结果 A MI组较Control组和Sham组心室重构和心功能受损明显(P<0.05),血清MMP-9水平明显升高[(6.93±0.09)ng/ml比(4.66±0.06)ng/ml和(4.71±0.06)ng/ml,均为P<0.05];MK组较AMI组心室重构程度轻、心功能改善明显(P<0.05),血清MMP-9水平明显降低[(5.33±0.06)ng/ml比(6.93±0.09)ng/ml,P<0.05 ]。结论 AMI后立即给予MK能够有效抑制心室重构,改善心功能;降低血清MMP-9水平是MK发挥心肌保护作用的途径之一。     

心肌标志物在不稳定型心绞痛和急性心肌梗死的临界值

目的 探讨不稳定型心绞痛和急性心肌梗死心肌标志物的临界值。方法 测定不稳定型心绞痛34例和急性心肌梗死病人64例在发病后5日内多时间点的血清心肌标志物浓度,包括心肌肌钙蛋白、肌酸激酶同工酶MB质量和活性、肌红蛋白、肌酸激酶、天冬氨酸转氨酶和乳酸脱氢酶活性,并通过时量曲线分析心肌标志物诊断急性心肌梗死的临界值。结果 34例不稳定型心绞痛病人中仅有7例心肌标志物不同程度升高;而在急性心肌梗死病人,心肌肌钙蛋白、肌酸激酶同工酶MB和肌红蛋白的峰值分别为24,16,8小时。其诊断急性心肌梗死临界峰值分别为0.25,16.6,75.6 μg/L,结论 诊断区分急性心肌梗死和不稳定型心绞痛的心肌标志物的临界值为心肌肌钙蛋白0.25 μg/L,肌酸激酶同工酶MB为16.6 μg/L,肌红蛋白为75.6 μg/L。     

Comparison of enoxaparin versus unfractionated heparin in patients with unstable angina pectoris/non-ST-segment elevation acute myocardial infarction having subsequent percutaneous coronary intervention

Patients with unstable angina or non-ST-segment elevation myocardial infarction (MI) may undergo invasive revascularization procedures shortly after admission to hospital or after a brief period of stabilization. In the Thrombolysis In Myocardial Infarction (TIMI) 11B trial and Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-Wave Coronary Events (ESSENCE) trial 1,326 patients underwent percutaneous coronary intervention (PCI). A total of 924 patients underwent PCI during the initial hospitalization period, and of these, 445 patients did so while receiving treatment with unfractionated heparin (UFH) or the low-molecular-weight heparin, enoxaparin. This analysis compared efficacy and clinical events in the enoxaparin and UFH groups in patients who: (1) underwent PCI while on treatment versus those who did not, and (2) underwent PCI in hospital. We also compared those who did not undergo PCI. Treatment with enoxaparin (1 mg/kg given as twice daily subcutaneous injections) was beneficial and well tolerated in patients with unstable angina and non-ST-segment elevation MI who underwent PCI. Compared with UFH, enoxaparin significantly reduced the likelihood of clinical events (death and nonfatal MI after PCI) in patients who underwent PCI after 1 year (p = 0.003 for in-hospital PCI; p = 0.005 for on-treatment PCI), with a trend toward a reduced event rate at 43 days. In addition, patients treated with enoxaparin who did not undergo PCI also showed a reduction in the risk of death, nonfatal MI, and urgent revascularization when compared with those treated with UFH (significant at 43 days, with a trend persisting at 1 year). Study limitations were that PCI was nonrandomized, the analysis was post hoc, and the sample size was relatively small. Nevertheless, in the absence of large clinical trials, this study suggests that treatment with enoxaparin was well tolerated, and exhibited a similar risk of major hemorrhage to UFH in patients who underwent PCI.     

Increased serum leptin concentrations in patients with chronic stable angina pectoris and ST-elevated myocardial infarction

Leptin is an adipocytokine that is produced mainly by adipose tissue; it is also identified in atherosclerotic lesions in human coronary atherosclerosis. However, the relation of serum leptin concentrations to ischemic heart disease (IHD) is still obscure. The aims of the present study were to investigate serum leptin concentrations in patients with ST-elevated myocardial infarction (STEMI) and with chronic stable angina pectoris (CSAP) and to evaluate the possible correlations of leptin to other atherosclerotic risk factors; including serum high sensitive C-reactive protein (Hs-CRP), serum homocysteine, and fibrinogen concentrations. For this purpose, 35 patients with CSAP, 40 with acute STEMI, and 30 control subjects with normal findings from coronary angiography were taken into the study prospectively. Serum leptin concentrations were significantly higher in patients with CSAP and STEMI compared to the control group (7.74 +/-1.34 vs 6.37 +/-1.85 ng/mL, p=0.021 and 8.22 +/-3.13 vs 6.37 +/-1.85 ng/mL, p=0.023, respectively). In addition, serum homocysteine concentrations were significantly increased in patients with CSAP (15.23 +/-5.96 vs 11.40 +/-2.11 micromol/L, p=0.025) and patients with STEMI (15.90 +/-5.02 vs 11.40 +/-2.11 micromol/L, p=0.012) compared to the control group. Serum fibrinogen concentrations were significantly increased only in the CSAP group as compared to controls (4.15 +/-1.39 vs 3.45 +/-1.19 g/L, p=0.025). No significant correlation was found between leptin levels and selected risk factors. In conclusion, serum leptin concentrations were significantly higher in both the CSAP and STEMI groups. However, owing to the lack of correlation between the leptin levels and selected classical coronary risk factors, it may be considered that leptin can be evaluated as one of the independent risk factors for IHD. Further randomized and controlled studies will be required to determine the pathophysiological meaning of the increased leptin levels and the central role between adipocyte function and atherosclerosis.     

Cardiolipin antibodies in patients with myocardial infarction and unstable angina pectoris]

The clinical value of IgG and IgM cardiolipin antibodies (CLa) was examined in 22 patients with myocardial infarction and 9 patients with unstable angina (UA). Higher IgG levels were observed in 41% of MI patients and 55% of UA patients. There was a significant correlation between the detection of IgG CLa in patients with a history of myocardial infarction and the presence of left ventricular intracavitary thrombosis. The levels of IgG CLa were increased in 78% of patients with history of MI and in 32% without MI history. In addition, those of IgG CLa was higher in 80% of IM patients with signs of intracavitary thrombosis and in 38% with cavitary thrombosis. The findings suggest that antibodies to cardiolipin (of IgG in particular) make contribution to the development of thrombotic events in patients with coronary atherosclerosis in the absence of autoimmune pathology.     

Usefulness of high-sensitivity C-reactive protein in predicting long-term risk of death or acute myocardial infarction in patients with unstable or stable angina pectoris or acute myocardial infarction.

High-sensitivity C-reactive protein (CRP), proposed as a new coronary risk marker, may reflect either an acute phase reaction or the level of chronic inflammation. Thus, CRP may be less predictive of long-term outcomes when measured after acute myocardial infarction (AMI) than after unstable angina pectoris (UAP) or stable angina pectoris (SAP). A total of 1,360 patients with severe coronary artery disease (>/=1 stenosis >/=70%) had CRP levels obtained at angiography. Presenting diagnoses were SAP (n = 599), UAP (n = 442), or AMI (n = 319). During follow-up (mean 2.8 years), death or nonfatal AMI (D/AMI) occurred in 19.5%, 16.1%, and 17.2% (p = NS) with SAP, UAP, and AMI, respectively. Corresponding median CRP levels were 1.31, 1.27, and 2.50 mg/dl (p <0.001). For the overall cohort, increasing age, low ejection fraction, revascularization, and elevated CRP were the strongest of 6 independent predictors for D/AMI. Among those presenting with SAP, CRP levels above the first tertile were associated with an adjusted hazard ratio of 1.8 (95% confidence interval [CI] 1.2 to 2.8, p <0.009) for D/AMI. After UAP, the hazard ratio was 2.7 (95% CI 1.4 to 5.0, p <0.002). However, when measured during hospitalization for AMI, CRP was not predictive of long-term outcome (hazard ratio 1.0 [95 % CI 0.5 to 1.7] p = 0.86). In conclusion, predischarge CRP levels are higher after AMI than after UAP or SAP. However, whereas CRP is strongly predictive of long-term D/AMI for patients presenting with SAP or UAP, it is not predictive shortly after AMI, suggesting that measurements should be delayed until the acute phase reaction is over and levels have returned to baseline.     

Increased plasma levels of the soluble form of Fas ligand in patients with acute myocardial infarction and unstable angina pectoris

OBJECTIVES: To examine whether the Fas/Fas ligand system is involved in the pathogenesis of acute myocardial infarction (AMI), we measured the levels of the soluble form of the Fas ligand (sFasL) in the plasma of patients with AMI and stable or unstable angina pectoris (AP). BACKGROUND: The Fas ligand (FasL) is rapidly cleaved off by a metalloproteinase from the cell membrane to become a soluble form as a cytokine. Fas is expressed in most cells, including cardiomyocytes, whereas FasL is mainly expressed in inflammatory cells such as macrophages, which are greatly accumulated in unstable plaque. METHODS: Thirty patients with AMI, 10 patients with unstable AP, 10 patients with stable AP and 30 control subjects were enrolled in the present study. RESULTS: Plasma sFasL levels were significantly elevated on hospital admission in patients with AMI and unstable AP, compared with control subjects. Time-course studies revealed that plasma sFasL levels rapidly decreased within 3 h and then increased again after percutaneous transluminal coronary angioplasty in patients with AMI, but not in patients with stable AP. Importantly, the sFasL levels were higher in the coronary sinus than in the circulation. In addition, in vitro studies showed that the expression of FasL messenger ribonucleic acid was upregulated in mononuclear cells isolated from patients with AMI and that hypoxia stimulated the release of sFasL from isolated mononuclear cells. CONCLUSIONS: This demonstration of elevated levels of sFasL in patients with AMI and unstable AP suggests that activation of the Fas/FasL system may play a pathogenic role in AMI and acute coronary syndromes.     

Measurement of plasma lipids in patients admitted with acute myocardial infarction or unstable angina pectoris.

We assessed the reliability of early (first day) plasma lipid measurements in patients admitted with acute myocardial infarction or unstable angina pectoris. In 55 such patients, plasma levels of cholesterol and triglycerides measured within the first 24 hours after admission were significantly lower than the corresponding values at 6 weeks, which means that even very early in-hospital lipid measurements could lead to potentially serious underestimation of the lipid risk in these patients ad defined by the current criteria.     

Adhesive activity of blood platelets in patients with stable or unstable angina pectoris and acute myocardial infarct

Platelet adhesive activity was assayed in patients with stable angina (SA) or unstable angina (UA) and acute myocardial infarction (AMI). With scanning electron microscopy, platelet adhesions to Type IV collagen (C-IV) and plastic material, which had been stimulated by low-dose ADP, epinephrine and U-46 619, a stable thromboxane A2 analogue (agonist-induced adhesion) were determined. As compared with the control group, patients with SA or UA, showed significantly higher adhesion of platelets to the collagen substrate, whereas UA patients alone displayed a significantly increased agonist-induced adhesion when epinephrine was employed as an agonist. A sharp enhancement of platelet adhesion was characteristic of patients with AMI on days 1-3 of the onset. On days 4-5, the adhesive activity slightly dropped, and on day 7-10, it returned to the control level of healthy volunteers. The time course of adhesive activity decrease correlated with lower blood levels of creatine phosphokinase in patients with AMI. A high correlation was established between the alterations found in all the types of platelet adhesion during the course of AMI, which suggests there is an unspecific nature of increase and subsequent decrease platelet responses to all the inductors used. A comparison of patients taking and not taking aspirin (250 mg/day) revealed no differences both in the magnitude of an increase in platelet adhesion in the first 3 days and in that of its decrease on days 7-10 of AMI.     

Serum levels of interleukin-18 in patients with stable and unstable angina pectoris

Recent evidence suggests that atherosclerosis is an inflammatory disorder in which cytokines appear to play an important role. Special attention centered over the possible contribution of cytokines to the destabilization of the plaque. IL-18 is a proinflammatory cytokine of the IL-1 family, recognized for its ability to promote IFN-gamma secretion. It has recently been detected in human plaques and its administration was associated with increased atherosclerosis in apolipoprotein E (apoE) mice concomitant with an increase in plaque infiltrating inflammatory cells. In our study, we investigated whether patients with established atherosclerosis, with either stable or unstable angina, possessed high levels of IL-18. Patients with stable angina (n=48) were from the outpatient clinic whereas patients with unstable angina (n=73) were recruited upon admission and prior to performance of coronary angiography. Control patients (n=19) were healthy subjects with no evidence of coronary artery disease. Serum levels of IL-18 were assayed by ELISA. Patients with stable and unstable angina exhibited higher serum levels of IL-18 (77.1+/-7.2 and 61.5+/-5.1 pg/ml, respectively) in comparison to control subjects (p=0.002 and p=0.02, respectively). However, levels of IL-18 did not differ significantly between patients with stable and unstable angina. No differences were evident in the serum concentrations of IL-18 in patients with unstable angina (n=17) upon admission and 1-3 months later when the angina was already controlled. Although IL-18 serum levels appear elevated in the presence of coronary atherosclerosis, there is no evidence to associate this progression towards plaque instability.     

Cardiovascular risk factors for stable angina pectoris versus unheralded myocardial infarction

Background

Ischemic heart disease can vary substantially in its clinical presentation. Some patients have acute myocardial infarction (MI) without any previous signs of myocardial ischemia, whereas other patients may have stable angina pectoris for years without periods of acute unstability. This study compared baseline risk factors between subjects in whom stable angina pectoris developed and subjects in whom unheralded fatal or nonfatal MI developed during the follow-up period.

Methods

In 1970 to 1973, all 50-year-old men in Uppsala, Sweden, were invited to participate in a health survey aimed at identifying risk factors for cardiovascular disease. The present study is a nested case-control study of subjects who were free of coronary heart disease (CHD) at baseline and who then underwent revascularization (percutaneous transluminal coronary angioplasty or coronary artery bypass grafting) because of angina pectoris without preceding MI (n = 70) or in whom fatal or nonfatal MI developed without prior known CHD (n = 372) during the period until 1998.

Results

In multivariate Cox proportional hazard models, low-density lipoprotein and high-density lipoprotein levels (protective) were significant independent risk factors for stable angina pectoris demanding revascularization, whereas smoking, diastolic blood pressure, serum proinsulin levels, and serum lipid levels were significant independent predictors of subsequent unheralded MI. When comparing hazard ratios (HR), significantly higher HR for diastolic blood pressure (1.40 vs 1.00, for 1 SD increase) and serum proinsulin (1.82 vs1.20, for 1 SD increase) were found in the group in which unheralded MI developed than in the group with stable angina pectoris.

Conclusions

Serum lipid levels were important risk factors for the development of both stable and acute coronary heart disease. In addition, proinsulin levels and blood pressure were independent predictors of unheralded MI only, which suggests that these factors are involved in thrombosis, plaque rupture, or both.     

Comparison of results of percutaneous coronary intervention for non-ST-elevation acute myocardial infarction or unstable angina pectoris in men versus women

Previous randomized trials have addressed the impact of gender on outcomes, showing worse results in women assigned to invasive strategies compared with men with non-ST-elevation (NSTE) acute coronary syndrome (ACS). However, there is still a significant amount of controversy on strategies of treatment on the basis of gender. This study evaluated the impact of gender on treatment strategies and outcomes in patients with NSTE ACS in a high-volume, single-site tertiary center. We identified 1,197 consecutive patients with NSTE ACS (381 women, 816 men) who underwent percutaneous coronary intervention during their index hospitalizations. Patients were stratified by gender and baseline clinical and angiographic characteristics, and in-hospital and 9-month clinical outcomes were compared between the 2 groups. There were clear differences in baseline characteristics between men and women with ACS at presentation. Women were, on average, slightly older than men, with more hypertension and morbid obesity, but there were no differences in racial backgrounds or the prevalence of diabetes or dyslipidemia, nor were there treatment disparities in pharmacologic interventions. Women and men with ACS had similar rates of percutaneous coronary intervention on index admission. Women had a greater incidence of bleeding complications requiring blood transfusions. Overall, in-hospital and 9-month event-free survival were equivalent for the 2 genders. In conclusion, in this single-site observational study, patients with NSTE ACS who underwent angiography followed by percutaneous coronary intervention demonstrated no significant gender differences in treatment or in-hospital or 9-month event-free survival. From these results, interventional strategies should not be based on gender.     

急性心肌梗死患者MMP-9水平与心室重构的相关性及其缬沙坦的干预效果

目的: 探讨急性心肌梗死（AMI）患者基质金属蛋白酶-9(MMP-9)的变化及与心室重构的相关性，并观察缬沙坦对其干预的效果。方法: 选AMI患者90例，随机分为常规治疗组和缬沙坦组，正常体检者45例为正常对照组，AMI患者于入选时检测MMP-9，测定超声心动图指标［左室收缩末期容积(LVESV)、舒张末期容积(LVEDV)和左室射血分数(LVEF)］，服药１周、4周、12周后再测定MMP-9、超声心动图指标，正常对照组病例入选后测定MMP-9。比较各组病例MMP-9值；比较两治疗组患者用药1周及4周后MMP-9值、用药4周及12周后超声心动图指标及其变化。结果: AMI患者与正常对照组MMP-9值、超声心动图指标比较，差异有统计学意义（P<0.05）；用药1周时B组较A组MMP-9值减小（P<0.05）；用药4周时A、B两组MMP-9值均减小，而超声心动图指标差异无统计学意义，12周后A、B两组超声心动图指标发生变化（P<0.05）；用药1周后、4周后两组MMP-9值均较用药前减小（P<0.05）。结论: 缬沙坦能降低AMI患者MMP-9的表达，降低心室重构发生率。