冠心病患者血清VEGF水平的研究

目的 :观测冠心病患者血清血管内皮生长因子 （VEGF）的水平。方法 :行选择性冠脉造影 （SCA）的患者 6 0例 ,分为 4组 ,其中 SCA正常者 10例作为对照组 ,急性心肌梗死 （AMI）组 2 0例 ,陈旧性心肌梗死 （OMI）组 10例 ,心绞痛 （AP）组 2 0例 ,使用 EL ISA方法分别检测其血清 VEGF的水平。结果 :AMI患者血清 VEGF水平显著高于其它各组 （P<0 .0 1） ,且其 VEGF的水平与心肌梗死部位、病变血管及血管病变程度无关 ,AP、OMI组血清 VEGF略高于对照组 ,但无统计学差异 （P>0 .0 5 ）。结论 :AMI患者血清 VEGF水平升高。     

Hepatocyte growth factor and vascular endothelial growth factor in ischaemic heart disease

BACKGROUND: Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are endothelial cell-specific growth factors, but the production of these growth factors in cardiomyocytes has also been demonstrated. However, there have been no reports focusing their attention on the changes in these growth factors after coronary intervention. We investigated the time-course changes of the serum VEGF and HGF levels in angina pectoris (AP) and acute myocardial infarction (AMI). METHODS: The serum HGF and VEGF levels were measured in 60 patients with AP, in 62 patients with AMI (AP, before heparin administration, and at 24 and 48 hours, and one week after intervention; AMI, before heparin, and at 48 and 72 hours, and one, two, three and four weeks) and in 56 patients with neurocirculatory asthenia as controls. We defined the patients with remodelling who showed an increase in left ventricular end-diastolic volume index (LVEDVI) in the sub-acute phase of AMI. RESULTS: Hepatocyte growth factor levels in the AP and AMI were significantly higher than that in the control (p<0.0001). The AMI level was also significantly higher than AP (p<0.001). In the AMI and AP, HGF peaked at 48 hours. Vascular endothelial growth factor level in the AMI was significantly higher than that in the control and AP (p<0.0001). In the AMI, VEGF peaked at two weeks. There was a significant positive correlation between the peak VEGF and LVEDVI in the sub-acute phase of AMI (p=0.0089, r=0.436). Peak VEGF in the remodelling (+) group was significantly higher than that in the remodelling (-) group (p<0.001). In the AP, VEGF was unchanged. CONCLUSION: While both myocardial and vascular damage contribute to an increase in HGF level, vascular damage is not associated with the increase in VEGF. Vascular endothelial growth factor might be related to left ventricular remodelling in the sub-acute phase of myocardial infarction.     

Serial changes in serum VEGF and HGF in patients with acute myocardial infarction

The time course of vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) release in patients with acute myocardial infarction (AMI) is unknown. Blood samples were obtained at the time of admission and 3, 7, 14 and 21 days later in 32 patients with AMI and 30 control patients. Serum VEGF and HGF, as well as C-reactive protein (CRP) and amyloid A protein (SAA), were determined. Both serum VEGF and HGF levels on admission in patients with AMI were higher than control values and peaked on day 7. VEGF levels in patients with preinfarction angina were higher than in patients with no preinfarction angina, whereas the HGF level did not differ. Both CRP and SAA levels peaked on day 3, and the CRP level on day 3 correlate with both VEGF and HGF levels on day 7. We hypothesized that the serum VEGF level is associated with preinfarction ischemia and the increase in VEGF and HGF on day 7 of AMI may represent a response to acute inflammation.     

Serum hepatocyte growth factor predicts ventricular remodeling following myocardial infarction.

Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) stimulate endothelial cell proliferation and induce angiogenesis, but the timing and significance of their release in patients with acute myocardial infarction (AMI) are unknown in relation to future left ventricular remodeling. Venous blood samples were obtained at admission and up to 3 weeks later in 40 patients with AMI and in 40 age- and sex-matched control subjects. Blood samples were also taken from the coronary sinus (CS) in 20 patients on day 7 following AMI. Left ventricular end-diastolic volume in the subacute (1 week) and chronic (3 months) phases was assessed by left ventriculography to identify the remodeling group (n=15), which was defined as an increase in left ventricular end-diastolic volume index > or =5 ml/m(2) relative to the baseline value. Serum HGF and VEGF concentrations were higher in newly admitted patients with AMI than in the controls (HGF, 0.33 +/-0.09 vs 0.24+/-0.08 ng/ml, p<0.01; VEGF, 92.2+/-43.1 vs 67.2+/-29.8 pg/ml, p<0.01), peaking on day 7 (HGF, 0.41+/-0.12; VEGF, 161.7+/-76.9), and gradually decreasing between days 14 and 21. The HGF concentration in the CS did not differ from the concentration in the periphery, but the VEGF concentration was significantly more abundant in the CS than in the peripheral sample on day 7 (p<0.05). The serum HGF concentration on day 7 was higher in the remodeling group than in the nonremodeling group (0.47 +/-0.13 vs 0.36+/-0.09 ng/ml, p<0.01), but there was no difference between the groups on admission, day 14 and day 21. The serum VEGF concentration did not differ between the remodeling and nonremodeling groups at any time. Thus, the serum HGF concentration on day 7 after AMI is mostly from noncardiac sources and predicts left ventricular remodeling.     

Hepatocyte growth factor and cardiovascular thrombosis in patients admitted to the intensive care unit.

BACKGROUND: Hepatocyte growth factor (HGF) has been reported as a marker of atherosclerosis and of thrombi synthesis, but the relationship between HGF and proven coronary thrombi has not been described. The aim of this study was to investigate this relationship in patients with chest pain. METHODS AND RESULTS: The study group comprised 107 patients with chest pain (61 acute myocardial infarction (AMI), 18 unstable angina, 15 stable angina, and 13 others; 65 males, 42 females; 66+/-11 years old). The presence of thrombi was evaluated by angiography, intravascular ultrasonography, angioscopy, and computed tomography. Serum HGF concentrations were measured using a new enzyme-linked immunosorbent assay. Serum HGF was significantly higher in the patients with AMI (335.0 +/-197.5 pg/ml), unstable angina (269.1+/-152.7 pg/ml), acute aortic dissection (320.3+/-116.5 pg/ml), and pulmonary thromboembolism (292.5+/-101.9 pg/ml), than in those with stable angina (171.2+/-56.1 pg/ml). Serum HGF concentration was also higher in those patients with proven thrombi than in those patients without (326.7+/-189.7 pg/ml vs 226.9+/-110.8 pg/ml). CONCLUSION: Increased serum HGF concentrations correlate with the presence of thrombi in patients with acute coronary syndrome, acute aortic dissection, and pulmonary thromboembolism.     

Production of hepatocyte growth factor during acute myocardial infarction

OBJECTIVE—To investigate the clinical significance of circulating hepatocyte growth factor (HGF) and the role of peripheral blood mononuclear cells (monocytes), which are a possible source of HGF, in patients with acute myocardial infarction.
DESIGN AND PATIENTS—37 patients with acute myocardial infarction and 13 normal control subjects were recruited. Peripheral venous blood samples were drawn from the infarct patients 1, 7, 14, and 21 days after onset. Monocytes were isolated from peripheral blood at those times. HGF concentrations in serum and in a culture medium of monocytes after incubation for 24 hours (monocyte HGF levels) were measured by enzyme linked immunosorbent assay.
RESULTS—Serum HGF and monocyte HGF values within seven days after onset of myocardial infarction were significantly higher than those of control subjects and decreased by day 14. There were significant positive correlations between serum HGF and monocyte HGF levels on day 7; between maximum plasma creatine phosphokinase levels and serum HGF levels on day 1; between maximum plasma C reactive protein and serum HGF levels; and between maximum C reactive protein and monocyte HGF levels. Monocyte HGF levels were raised in the patients with progression of ventricular enlargement in the course of acute myocardial infarction.
CONCLUSIONS—Early serum HGF concentrations reflect the extent of myocardial damage in acute myocardial infarction patients. Inflammation after acute myocardial infarction is supposed to be involved in enhanced HGF production. Monocytes may play an important role in ventricular remodelling after acute myocardial infarction by releasing the cardiovascular protective mitogen HGF.


Keywords: C reactive protein; cytokines; ischaemic heart disease; remodelling; hepatocyte growth factor     

Increased blood vascular endothelial growth factor levels in patients with acute myocardial infarction

Vascular endothelial growth factor (VEGF) is a growth factor for vascular endothelial cells in vitro. The present study was designed to determine whether serum VEGF levels increase in patients with acute myocardial infarction (AMI) compared with patients with stable exertional angina and control subjects, and to examine the serial changes of serum VEGF levels in patients with AMI. We examined serum VEGF levels by using antibody prepared from serum immunized with human VEGF(121). The serum VEGF level (pg/ml) was higher (p < 0. 0001) on admission in the patients with AMI (177 +/- 19) than in those with stable exertional angina (61 +/- 7) and control subjects (62 +/- 6). The serum VEGF level (pg/ml) of the patients with AMI was 177 +/- 19 on admission, 125 +/- 9 on day 3, 137 +/- 11 on day 5, 242 +/- 18 at 1 week, and 258 +/- 22 at 2 weeks after admission. The value was higher on admission than on day 3 after admission (p = 0.014), the values were higher at 1 week and 2 weeks than on admission, on day 3, and 5 (p < 0.01). Furthermore, there were correlations between peak VEGF levels at 1 week or 2 weeks after admission and peak creatine kinase levels. The increase of VEGF on admission in the patients with AMI may be due to the hypoxia of acute myocardial ischemia. The elevation at 1 week and 2 weeks from the onset may cause the development of collateral circulation in relation to the healing of the infarction site.     

Serum levels of the angiogenic cytokines basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) in multiple myeloma

Angiogenesis is a crucial process in growth and progression of cancer and there is growing evidence that neovascularisation is important in hematological malignancies. Since an increased angiogenic potential has been identified in multiple myeloma, we simultaneously measured circulating serum levels of the cytokines bFGF, VEGF, HGF and IL-6 by ELISA in 67 patients with multiple myeloma or monoclonal gammopathies of undetermined significance (MGUS) and in 20 controls. Median values of bFGF were 4.7 pg/ml in healthy volunteers, 6.2 in MGUS, 6.3 in myeloma stage I, 13.4 in stage II and 21.7 in stage III. Myeloma patients had significantly higher bFGF serum levels than controls (p<0.001). Pretreatment bFGF levels differed significantly in the Salmon and Durie stages I-III (p=0.02) and were significantly elevated in stage II-III compared to stage I myeloma (p=0.02). In patients responding to chemotherapy according to the CLMTF criteria, a significant decrease in serum bFGF, VEGF and HGF levels occurred (median pretreatment values for bFGF 23.9 pg/ml, post-treatment 6.5 pg/ml; p<0.001, for VEGF 223 pg/ml versus 105 pg/ml; p=0.02 and for HGF 1429 pg/ml versus 1077 pg/ml; p=0.02, respectively). In 11 patients who did not achieve a remission, there was no significant decrease in bFGF, VEGF and HGF levels. These data show that myeloma in stages II and III is associated with an increase in serum bFGF concentrations and give the first report that effective chemo-therapy is accompanied by a significant decrease in the angiogenic factors bFGF, VEGF and HGF, while no decrease of these factors could be found in nonresponders.     

Clinical significance of vascular endothelial growth factor and hepatocyte growth factor in multiple myeloma

Angiogenesis is a crucial process in the progression of multiple myeloma (MM). Vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) are multifunctional cytokines that potently stimulate angiogenesis including tumour neovascularization. Serum levels of VEGF and HGF were measured in 52 patients with MM by enzyme-linked immunosorbent assay (ELISA). Serum levels of VEGF and HGF were elevated in MM patients compared with healthy controls (VEGF: mean 0.31 ng/ml and 0.08 ng/ml respectively, P < 0.01; HGF: mean 2.17 ng/ml and 0.45 ng/ml, respectively, P < 0.001). In serial samples taken after chemotherapy, serum VEGF and HGF levels were correlated with M-protein levels. Serum levels of VEGF were higher in patients with extramedullary plasmacytomas than in patients without them (P < 0.05). They were also significantly higher in a group of patients who showed poor response to chemotherapy (P < 0.01). Serum levels of HGF were higher in patients with complications such as anaemia, hypercalcaemia and amyloidosis than in patients without these complications (P < 0.01, P < 0.05, P < 0.05 respectively). Both serum VEGF and HGF levels were significant predictors of mortality (P = 0.01, P = 0.02, respectively, log-rank test). The present study demonstrated that serum levels of VEGF and HGF are significantly elevated and dependent on the severity of MM, suggesting that measurement of VEGF and HGF may be useful for assessing disease progression and for predicting the response to chemotherapy in MM patients.     

Elevated concentration of soluble vascular endothelial cadherin is associated with coronary atherosclerosis.

BACKGROUND: Vascular endothelial (VE)-cadherin, a Ca(2+)-dependent cell adhesion molecule, is expressed in atherosclerotic lesions by endothelial cells and is associated with neovascularization, although the relationship between circulating VE-cadherin and coronary artery disease has not been studied. METHODS AND RESULTS: The plasma concentration of VE-cadherin was measured in peripheral blood (femoral artery) and the coronary sinus of 24 patients with acute myocardial infarction (AMI), 26 with stable angina pectoris (AP), 18 with old myocardial infarction (OMI), and 30 control subjects (Control) who had no coronary artery stenosis on angiography. For the patients with AMI, blood samples were obtained in the acute (day 1) and chronic (day 21) phases. The plasma concentration of VE-cadherin was measured by enzyme-linked immunosorbent assay. The correlation between the plasma VE-cadherin concentration and the Gensini score was also determined as an index of the severity of coronary atherosclerosis. The plasma concentrations of VE-cadherin (ng/ml) in both the peripheral and coronary sinus blood were higher in patients with AMI, AP, and OMI than in the control subjects, and were similar in the 3 groups with coronary artery disease (femoral artery: AMI 5.1+/-2.5, AP 4.7+/-2.4, OMI 4.5+/-3.3, Control 2.6+/-2.3; coronary sinus: AMI 5.6+/-2.6, AP 5.0+/-2.3, OMI 5.0+/-2.9, Control 2.4+/-2.1, respectively). Plasma VE-cadherin concentrations were higher in the coronary sinus than peripheral blood samples in patients with AMI (p<0.01), AP (p<0.01), and OMI (p<0.05). The plasma VE-cadherin concentration was the same in the acute and chronic phases in patients with AMI. In the 3 groups of patients with coronary disease, both the peripheral plasma VE-cadherin concentration and the coronary sinus concentration correlated with the Gensini score (r=0.32, p<0.01 and r=0.42, p<0.001, respectively). Multiple regression analysis revealed that the plasma VE-cadherin concentration predicted the Gensini score independently of sex, age, hypertension, diabetes mellitus, smoking, and the lipid profiles. CONCLUSION: Increased secretion of VE-cadherin from the epicardial arteries is associated with the degree of coronary atherosclerosis, indicating the presence of atherosclerosis rather than disease activity.     

Changes of serum hepatocyte growth factor in coronary artery disease

Hepatocyte growth factor (HGF) is an endothelial cell specific growth factor involved in the repair of endothelial cells and collateral formation, however, the role for coronary artery disease is still unknown. We measured serum HGF level in various coronary artery diseases to examine the clinical significance. Serum HGF level was measured using the enzyme-linked immunosorbent assay method in patients with stable effort angina pectoris (n = 26), old myocardial infarction (n = 18), unstable angina pectoris (UAP; n = 10) and acute myocardial infarction (AMI; n = 21). As a control group, we selected 11 patients with neurocirculatory asthenia. Blood samples from peripheral veins were collected at cardiac catheterization before heparin administration. In the AMI group, blood samples were also collected at 48, 72 hr, 1, 2, 3 and 4 weeks from the peripheral veins and 48 and 72 hr after reperfusion from the coronary sinus. Serum HGF level was significantly higher in the UAP (0.41 +/- 0.12 ng/ml, p < 0.001) and AMI groups (0.38 +/- 0.26 ng/ml, p < 0.05) compared to the control group (0.19 +/- 0.09 ng/ml). Serum HGF level peaked 48 hr after reperfusion in both the peripheral veins (0.42 +/- 0.16 ng/ml) and coronary sinus (0.58 +/- 0.23 ng/ml) in the AMI group, with a significantly higher level in the coronary sinus than the peripheral veins (p < 0.05). No significant correlation between peak HGF level in the peripheral veins and peak creatine kinase (CK), CK-MB, ejection fraction and cardiac index was observed. Serum HGF was elevated in acute coronary syndrome, indicating advanced endothelial cell damage. HGF is produced, at least partially, in the heart in patients with AMI. Serum HGF level may be useful to detect endothelial cell damage rather than myocardial cell damage.     

Effect of preinfarction angina pectoris on ST-segment resolution after primary coronary angioplasty for acute myocardial infarction

The presence of preinfarction angina has been shown to exert a favorable effect on left ventricular function after acute myocardial infarction (AMI). Whether or not preinfarction angina is beneficial for myocardial tissue reperfusion, however, remains to be determined. We sought to evaluate the influence of preinfarction angina on resolution of ST-segment elevation, which could be affected by microcirculatory damage after recanalization therapy. We studied 96 patients with a first AMI in whom Thrombolysis In Myocardial Infarction (TIMI)-3 flow in the infarct-related artery was established by primary angioplasty. Percent reduction in the sum of ST elevation from baseline to 1 hour after angioplasty (percent delta summation operator ST) was examined. Poor ST resolution, defined as percent delta summation operator ST <50%, was observed in 25 patients, who had a worse clinical outcome, larger infarct size, and poorer left ventricular function. On multivariate analysis, the absence of preinfarction angina, as well as anterior wall infarction, were major independent predictors of poor ST resolution, whereas age, sex, coronary risk factors, ischemic time, Killip class on admission, multivessel disease, initial TIMI flow grade, and extent of collaterals were not significant. Patients with preinfarction angina had a greater degree of ST-segment resolution than those without angina (71 +/- 21% vs 49 +/- 43%, p = 0.02). Additional ST elevation after reperfusion was noted exclusively in patients without preinfarction angina (p = 0.02). Preinfarction angina is associated with a greater degree of ST-segment resolution in patients with TIMI-3 flow after primary angioplasty, suggesting a protective effect of preinfarction angina against microcirculatory damage after reperfusion.     

冠心病患者血浆神经肽Y水平变化及其临床意义

目的 ,研究不同类型冠心病患者发病不同阶段血浆神经肽 Y（NPY）水平的变化 ,探讨其与冠心病心肌缺血的关系。方法 ,选急性心肌梗死、不稳定型心绞痛、稳定劳力型心绞痛、陈旧性心肌梗死患者各 30余例发病不同阶段血浆 NPY浓度 ,并选 32例健康者作为对照组。结果 ,急性心肌梗死急性期 （2 4h） ,不稳定型心绞痛患者疼痛发作期血浆 NPY水平均明显高于对照组 ,差异非常显著。稳定劳力型心绞痛患者 ,陈旧性心肌梗死患者血浆 NPY水平与对照组比较差异无显著性意义。不稳定型心绞痛患者疼痛发作期血浆 NPY水平高于治疗后 2周病情稳定期 ,差异非常显著 （P<0 .0 1）。急性心肌梗死患者血浆 NPY水平在心梗后 8h左右开始升高 ,2 4h达高峰 （34 6 .2± 5 9.6 pg/ ml） ,7d左右恢复至正常水平 （2 2 8.1± 38.6 pg/ m l）。结论 ,冠心病患者出现心肌急性缺血时 ,血浆 NPY水平升高 ,提示 NPY参与了冠心病患者急性心肌缺血时的病理生理过程 ,NPY可作为观察冠心病患者病情变化的一项指标。     

肝细胞生长因子对急性心肌梗死后左室重构的预测作用

目的: 探讨血清肝细胞生成因子(HGF)对急性心肌梗死(AMI)后早期左室重构的预测价值。方法: 36例AMI患者入院时及发病7 d测定血清HGF水平;AMI其中的26例分别于发病后7~10 d及发病后3个月行超声心动图检查,3个月时左室舒张末期容积指数（LVEDVI）与7~10 d时比增加≥5 ml/m2定义为左室重构组(n=11),对两组血清HGF值进行比较。结果: AMI患者入院时血清HGF浓度较对照组明显升高［(809±288)ng/L vs.(620±162)ng/L,P<0.01］,7 d时升高更显著［(1 607±1 355)ng/L,P<0.01］。发病7 d时血清HGF浓度在左室重构组较非左室重构组升高［(2 216±1 522)ng/L vs.(1 176±593)ng/L,P<0.05］,而入院时两组浓度则无显著差异。结论: AMI时血清HGF浓度升高,AMI后7 d时增高的血清HGF可能预示心室重构。     

Differences in inflammatory activity at the onset of acute myocardial infarction according to the clinical presentation of preinfarction angina

It is unknown whether the pathogenetic mechanisms underlying acute myocardial infarction (AMI) differ according to the clinical presentation of preinfarction angina, so the present study measured plasma levels of C-reactive protein (CRP) in 280 patients with AMI in whom serum creatine kinase levels were normal on admission and increased subsequently. Patients were classified into 3 groups according to the type of preinfarction angina: no angina (n=95), stable angina (n=48), and unstable angina (n= 137). Patients with unstable angina were subdivided according to the Braunwald classification: class IB (n=39), class IIB (n=22), and class RIB (n=76). There were no differences among the 5 groups in baseline characteristics. CRP on admission was significantly higher and the level of physical activity at symptom onset was significantly lower in the Braunwald class RIB group than in the other groups, but no differences were observed among the other groups. Patients with preinfarction Braunwald class IIB unstable angina had higher CRP levels on admission and symptom onset at a lower level of physical activity. In such patients, the pathogenetic mechanisms may differ from those in other subsets of patients with AMI and active inflammation may play a more important role in AMI onset.     

Effect of preinfarction angina pectoris on microcirculation in patients with reperfused acute myocardial infarction

Preinfarction angina pectoris has been suggested in some studies to have a beneficial effect on left ventricular function after acute myocardial infarction (AMI). The precise mechanisms of this protection have not been fully elucidated. The effect of preinfarction angina on myocardial tissue perfusion also needs to be clarified. In this study, we investigated the influence of preinfarction angina on microvasculatory damage by using ST-segment resolution and pressure-derived collateral flow index (CFIp) as a marker of microcirculatory perfusion. METHODS: We studied 41 patients with a first AMI in whom thrombolysis in myocardial infarction (TIMI) grade 3 flow in the infarct-related artery was established by thrombolytic therapy. The percent resolution of ST-segment deviation (deltasigma ST) after thrombolysis was determined. All of the patients had TIMI grade 3 flow in IRA at the coronary angiography, which was done a mean of 4 days after AMI. Intracoronary pressure measurements and stent implantation to the IRA were performed. After angiography, CFIp was calculated as the ratio of simultaneously measured coronary wedge pressure-central venous pressure (Pv) to mean aortic pressure-Pv. RESULTS: Patients with preinfarction angina pectoris had greater percent deltasigma ST than those without PA (67 +/- 18% vs. 44 +/- 24%, p = 0.03).The mean of the coronary wedge pressure (16.4 +/- 7.4 compared with 23.2 +/- 9.4, P < 0.03) and the pressure-derived collateral flow index (0.15 +/- 0.10 compared with 0.22 +/- 0.08, P < 0.03) were significantly lower in patients with preinfarction angina compared to those without. CONCLUSION: Preinfarction angina is associated with a greater degree of ST-segment resolution and lower CFI-p in patients with TIMI-3 reflow after thrombolysis. These findings suggest that a protective effect of preinfarction angina against reperfusion injury may result in greater ST resolution and lower CFIp after AMI.     

血清肝细胞生长因子与高血压患者合并急性冠脉综合征的相关性

目的 探讨肝细胞生长因子（HGF）在原发性高血压及急性冠脉综合征（ACS）患者血清中的表达水平及其临床意义.方法 采用双抗体夹心酶联免疫荧光吸附法（ELISE）测定25例单纯高血压患者、20例高血压合并不稳定型心绞痛（UA）患者、25例高血压合并急性心肌梗死（AMI）患者、25名健康者的HGF血清浓度.结果 单纯高血压组、高血压合并UA组和高血压合并AMI组血清HGF浓度较正常对照组明显高,差异有统计学意义（P＜0.01）;高血压合并UA组、高血压合并AMI组血清HGF浓度较单纯高血压组明显高,差异有统计学意义（P＜0.05）;高血压合并AMI组血清HGF浓度较高血压合并UA组明显高,差异有统计学意义（P＜0.05）.结论 高浓度的HGF与血管内皮损伤和修复以及不稳定的粥样斑块破裂有关.测定HGF浓度将成为早期诊断高血压及其分级的重要指标和早期筛查不稳定冠状动脉粥样硬化斑块的新手段.     

Effect of preinfarction angina pectoris on outcome in patients with acute myocardial infarction treated with primary angioplasty (results from the Myocardial Infarction Registry

Preinfarction angina is associated with better clinical outcome in patients with acute myocardial infarction (AMI) who receive intravenous thrombolysis. This has not been proved in patients with AMI treated with primary angioplasty. We analyzed the data of the prospective multicenter Myocardial Infarction Registry (MIR). Of 14,440 patients with AMI, 774 with a prehospital delay of < or =12 hours were treated with primary angioplasty. Five hundred thirty-two patients (68.7%) had preinfarction angina. Patients with preinfarction angina were slightly older than patients without (63 vs 62 years, p = 0.042), prehospital delay was 1 hour longer (180 vs 120 minutes, p = 0.001), and arterial hypertension was more prevalent (47.6% vs 32.2%, odds ratio [OR] 1.91, 95% confidence intervals [CI] 1.39 to 2.62). There was no significant difference in hospital mortality (5.6% vs 3.3%, OR 1.75, 95% CI 0.79 to 3.87), reinfarction, stroke, or the combined end point of death, reinfarction, or stroke between the 2 groups. Logistic regression analysis showed no association of preinfarction angina with the occurrence of either death (OR 2.21, 95% CI 0.91 to 6.08) or the combined end points (OR 1.10, 95% CI 0.55 to 2.31). There was also no significant difference in mortality (6% vs 5.1%, OR 1.19, 95% CI 0.56 to 2.52), reinfarction, stroke, postinfarction angina, or the combined end points between patients with preinfarction angina within 48 hours compared with patients with preinfarction angina between 49 hours and 4 weeks before the AMI. Thus, the MIR data showed no protective effects of preinfarction angina in patients with AMI treated with primary angioplasty.     

梗死前心绞痛对急性心肌梗死患者经皮冠状动脉介入治疗术后无再流现象的影响

目的探讨梗死前心绞痛(PIA)对急性心肌梗死(AMI)患者经皮冠状动脉介入治疗(PCI)后无再流现象的影响。方法100例首次AMI患者均在发病12h内行PCI术。所有患者按照有无无再流现象分为2组:无再流组(15例)和再流组(85例)。监测心肌酶谱和C反应蛋白(CRP)变化;放射性核素测定心功能;观察室壁瘤、心力衰竭发生率和住院病死率。结果无再流组PIA发生率显著低于再流组(P<0.01);而前壁梗死的发生率高于再流组(P<0.05);肌酸激酶同工酶峰值和CRP水平均显著高于再流组(P<0.01)。无再流组放射性缺损面积显著大于再流组(P<0.01);左室射血分数显著低于再流组(P<0.01);心力衰竭、室壁瘤发生率和死亡率均高于再流组(P<0.05)。多元Logistic回归分析结果显示,缺乏PIA是发生无再流现象的独立预测因素(OR=6.12,P=0.01)。结论缺乏PIA是发生无再流现象的独立预测因素,而无再流现象与心力衰竭和死亡率增高密切相关。     

Elevated circulating levels of basic fibroblast growth factor and vascular endothelial growth factor in patients with acute myocardial infarction

Basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) have both shown strong angiogenetic effects in ischemic animal models and it has been reported that these growth factors were increased after acute myocardial ischemia. However, there have been few reports on the serum levels of bFGF and VEGF after acute myocardial infarction (AMI), in particular there has not been a comparative study of bFGF and VEGF in human subjects. The time course of circulating levels of bFGF and VEGF was examined in 36 patients with AMI who were within 24h of the onset of the AMI. The serum bFGF and VEGF levels of 50 age- and sex-matched healthy volunteers served as the baseline value. All the patients had undergone coronary angiography on the day of admission (Day 0), but prior to that the serum bFGF and VEGF levels were examined by enzyme-linked immunoassay. The serum bFGF and VEGF levels were also evaluated on Days 7, 14 and 28. Creatine kinase, myosin light chain I and troponin-T were measured subsequently and radionuclide examinations were performed during the early phase of AMI to determine the infarct size. The serum bFGF levels were significantly increased at Day 0 and were maintained until Days 7 and 14. Although serum VEGF levels at Day 0 were similar to the baseline values, they showed a remarkable increase by Days 7 and 14. A high serum level of bFGF was detected in the acute phase of AMI, and a later increase in VEGF was determined in the sub-acute phase, which suggest that these 2 growth factors play an important role at different time points of the reconstructing process of infarcted myocardial tissue.