Altered platelet alpha 2 adrenoreceptor in acute myocardial infarction and its relation to plasma catecholamine concentrations

Changes in platelet alpha 2 adrenoreceptors and their relation to plasma catecholamine concentrations were studied in 11 patients with acute transmural myocardial infarction. A radiolabelled alpha 2 adrenoreceptor antagonist, [3H]-yohimbine, was used to assay alpha 2 adrenoreceptors on platelet membranes, and plasma catecholamine concentrations were measured by high performance liquid chromatography. The number of platelet alpha 2 adrenoreceptors, the dissociation constant, and plasma noradrenaline and adrenaline concentrations were studied 6.6 (3.3) (mean (SD)) hours after the onset of acute myocardial infarction and one month later. The mean (SD) number of adrenoreceptors increased significantly from 94.5 (50.5) fmol/mg protein immediately after infarction to 157.0 (65.7) fmol/mg protein one month later. The dissociation constant, however, did not change significantly (4.33 (1.40) nmol/l vs 4.37 (1.22) nmol/l). Raised noradrenaline (5.60 (4.37) nmol/l) and adrenaline (0.28 (0.14) nmol/l) concentrations had fallen significantly to normal values (1.21 (0.67) and 0.09 (0.05) nmol/l respectively) a month after infarction. The decrease in the number of alpha 2 adrenoreceptors soon after infarction may be beneficial because such a change will reduce the strength of various reactions to catecholamines, such as vasoconstriction.     

Altered platelet alpha 2 adrenoreceptor in acute myocardial infarction and its relation to plasma catecholamine concentrations.

Changes in platelet alpha 2 adrenoreceptors and their relation to plasma catecholamine concentrations were studied in 11 patients with acute transmural myocardial infarction. A radiolabelled alpha 2 adrenoreceptor antagonist, [3H]-yohimbine, was used to assay alpha 2 adrenoreceptors on platelet membranes, and plasma catecholamine concentrations were measured by high performance liquid chromatography. The number of platelet alpha 2 adrenoreceptors, the dissociation constant, and plasma noradrenaline and adrenaline concentrations were studied 6.6 (3.3) (mean (SD)) hours after the onset of acute myocardial infarction and one month later. The mean (SD) number of adrenoreceptors increased significantly from 94.5 (50.5) fmol/mg protein immediately after infarction to 157.0 (65.7) fmol/mg protein one month later. The dissociation constant, however, did not change significantly (4.33 (1.40) nmol/l vs 4.37 (1.22) nmol/l). Raised noradrenaline (5.60 (4.37) nmol/l) and adrenaline (0.28 (0.14) nmol/l) concentrations had fallen significantly to normal values (1.21 (0.67) and 0.09 (0.05) nmol/l respectively) a month after infarction. The decrease in the number of alpha 2 adrenoreceptors soon after infarction may be beneficial because such a change will reduce the strength of various reactions to catecholamines, such as vasoconstriction.     

The role of leucocytes in the acetyl salicylic acid (aspirin) induced nitric oxide synthesis in the production of interferon-alpha, a potent inhibitor of platelet aggregation and a thrombolytic agent

The role of aspirin-induced NO synthesis in the production of interferon-alpha (IFN-alpha) in leucocytes and the effect of IFN-alpha on platelet aggregation was studied. Treatment of Platelet Rich Plasma (PRP) with the dialyzed supernatant from the leucocyte suspension incubated with 80 microM aspirin resulted in parallel syntheses of NO and IFN-alpha as determined by methemoglobin assay and enzyme linked immunosorbent assay respectively. Incubation of PRP with 10 nM purified IFN-alpha for 40 min resulted in the maximal inhibition of platelet aggregation through the synthesis of NO due to the activation of nitric oxide synthase in platelets by IFN-alpha. The treatment of clotted PRP with IFN-alpha resulted in the lysis of the clot due to the fibrinolysis. Injection of IFN-alpha was found to protect mice from death due to the lysis of ADP-induced coronary thrombus. Interferon-alpha was found to be a potent inhibitor of platelet aggregation and a thromboprotective agent.     

The role of leucocytes in the acetyl salicylic acid (aspirin) induced nitric oxide synthesis in the production of interferon-α, a potent inhibitor of platelet aggregation and a thrombolytic agent

The role of aspirin-induced NO synthesis in the production of interferon-α (IFN-α) in leucocytes and the effect of IFN-α on platelet aggregation was studied. Treatment of Platelet Rich Plasma (PRP) with the dialyzed supernatant from the leucocyte suspension incubated with 80 μM aspirin resulted in parallel syntheses of NO and IFN-α as determined by methemoglobin assay and enzyme linked immunosorbent assay respectively. Incubation of PRP with 10 nM purified IFN-α for 40 min resulted in the maximal inhibition of platelet aggregation through the synthesis of NO due to the activation of nitric oxide synthase in platelets by IFN-α. The treatment of clotted PRP with IFN-α resulted in the lysis of the clot due to the fibrinolysis. Injection of IFN-α was found to protect mice from death due to the lysis of ADP-induced coronary thrombus. Interferon-α was found to be a potent inhibitor of platelet aggregation and a thromboprotective agent. Part of this work was published as an abstract in the proceeding of the Annual Workshop in Biological Sciences, Calcutta, 2005. An erratum to this article can be found at     

Soluble angiopoietin receptor Tie-2 in patients with acute myocardial infarction and its effects on angiogenesis

Tie-2 receptor has been shown to play a role in the neovascularization of tumors, but little is known about the role it may play in acute myocardial infarction (AMI). The aims of this research are (1) To study the variety of soluble Tie-2 (sTie-2) in patients with AMI. (2) To study the effects of recombinant soluble Tie-2/Fc on HUVECs viability and tube formation in vitro. Serum levels of sTie-2 in 27 patients with AMI were measured on admission (day 1), day 2, day 3 and day 7 after onset of chest pain and 28 healthy controls by ELISA. In addition, the viability of HUVECs and tube formation area were measured after stimulated with recombinant Tie-2/Fc chimera. Median level of sTie-2 increased significantly in the AMI patients when compared with the controls and the maximum level appeared at day 2 after onset of AMI. Tie-2/Fc induced EC apoptosis and inhibited HUVEC tube formation in vitro. Results of this study showed that the level of sTie-2 increased in AMI. The effects of Tie-2/Fc on EC viability and tube formation indicated that angiogenesis might be inhibited in the acute phase of AMI.     

High-dose, brief-duration intravenous infusion of streptokinase in acute myocardial infarction: description of effects in the circulation

The effects in the circulating blood of a 1-hour intravenous infusion of 1.5 X 10(6) units of streptokinase (SK) were measured during the subsequent 24-hour period in 7 patients with acute myocardial infarction. At the end of the infusion, the activator activity, expressed in SK units, averaged 65 U/ml, all of the plasminogen had disappeared, only a small amount of free plasmin was still present and functionally active alpha 2 antiplasmin had been reduced to 21% of the preinfusion level. All of the native fibrinogen had been degraded and the thrombin-coagulable protein was composed entirely of fragment X species, but the circulating plasma also contained significant amounts of the more extensively degraded fragments Y, D and E. The biologic half-life of the SK-induced activator activity was 23 minutes and that of the fibrinogen degradation products was 6.3 hours. The lytic effects persisted for 4 hours before any signs of recovery from the hemostatic defect were evident; considerable recovery was present at 25 hours.     

Partial inhibition of platelet thromboxane A2 synthesis by aspirin is associated with myonecrosis in patients with ST-segment elevation myocardial infarction

Heterogeneity in response to aspirin (ASA) treatment, or "aspirin resistance," could be of importance in patients with ST-segment elevation myocardial infarction (STEMI). Decreased effects of ASA in platelets could be due to partial inhibition of cyclo-oxygenase-1 (COX-1) or to COX-1-independent mechanisms. We evaluated the effect of ASA treatment in patients with STEMI for (1) platelet thromboxane A(2) (TXA(2)) synthesis, (2) platelet recruitment elicited by TXA(2)-dependent and -independent mechanisms, and (3) a possible association of these aspects of platelet reactivity with serum markers of myonecrosis. We studied 62 ASA-treated patients within 48 hours of onset of the acute event and 69 ASA-free and 10 ASA-treated controls. TXA(2) synthesis and platelet recruitment (fluid-phase proaggregate activity of cell-free releasate) were assessed after collagen stimulation (1 micro g/ml) of whole blood. Partial inhibition of TXA(2) by ASA was found in 21 patients (34%). This was associated with significant increases in troponin T, creatine kinase-MB mass, creatine kinase, and recruiting activity versus 41 patients with blocked TXA(2) production. This was independent of fibrinolysis, and platelet COX-2 expression was not augmented. TXA(2) blockade was achieved after subsequent daily treatments or platelet incubation with ASA in vitro, suggesting lower sensitivity of COX-1 to ASA. In addition, 28 patients (45%) had an abnormally increased recruiting activity despite TXA(2) blockade, which was also associated with increased myonecrosis. In conclusion, ASA resistance, elicited by TXA(2)-dependent and TXA(2)-independent mechanisms, was prevalent in patients with STEMI. This study describes, for the first time, the association of partial platelet TXA(2) inhibition with myonecrosis.     

Effects of restoration of coronary circulation on the function of the left ventricle in patients with acute myocardial infarction (a follow-up after 1 year)

Values of overall and local left ventricular function were studied in 89 patients in the acute period and 1 year following myocardial infarction. Three patient groups were identified: (1) 26 patients with coronary artery patency recorded by the first coronary angiography; (2) 20 with coronary blood flow recovery made by thrombolytic therapy; and (3) 40 with coronary occlusion. There was a significant improvement of left ventricular function in the patients from Group 1 during their hospital treatment and 1 year after.     

Intense metabolic control by means of insulin in patients with diabetes mellitus and acute myocardial infarction (DIGAMI 2): effects on mortality and morbidity.

AIMS: Patients with diabetes have an unfavourable prognosis after an acute myocardial infarction. In the first DIGAMI study, an insulin-based glucose management improved survival. In DIGAMI 2, three treatment strategies were compared: group 1, acute insulin-glucose infusion followed by insulin-based long-term glucose control; group 2, insulin-glucose infusion followed by standard glucose control; and group 3, routine metabolic management according to local practice. METHODS AND RESULTS: DIGAMI 2 recruited 1253 patients (mean age 68 years; 67% males) with type 2 diabetes and suspected acute myocardial infarction randomly assigned to groups 1 (n=474), 2 (n=473), and 3 (n=306). The primary endpoint was all-cause mortality between groups 1 and 2, and a difference was hypothesized as the primary objective. The secondary objective was to compare total mortality between groups 2 and 3, whereas morbidity differences served as tertiary objectives. The median study duration was 2.1 (interquartile range 1.03-3.00) years. At randomization, HbA1c was 7.2, 7.3, and 7.3% in groups 1, 2, and 3, respectively, whereas blood glucose was 12.8, 12.5, and 12.9 mmol/L, respectively. Blood glucose was significantly reduced after 24 h in all groups, more in groups 1 and 2 (9.1 and 9.1 mmol/L) receiving insulin-glucose infusion than in group 3 (10.0 mmol/L). Long-term glucose-lowering treatment differed between groups with multidose insulin (> or =3 doses/day) given to 15 and 13% of patients in groups 2 and 3, respectively compared with 42% in group 1 at hospital discharge. By the end of follow-up, HbA1c did not differ significantly among groups 1-3 ( approximately 6.8%). The corresponding values for fasting blood glucose were 8.0, 8.3, and 8.6 mmol/L. Hence, the target fasting blood glucose for patients in group 1 of 5-7 mmol/L was never reached. The study mortality (groups 1-3 combined) was 18.4%. Mortality between groups 1 (23.4%) and 2 (22.6%; primary endpoint) did not differ significantly (HR 1.03; 95% CI 0.79-1.34; P=0.831), nor did mortality between groups 2 (22.6%) and 3 (19.3%; secondary endpoint) (HR 1.23; CI 0.89-1.69; P=0.203). There were no significant differences in morbidity expressed as non-fatal reinfarctions and strokes among the three groups. CONCLUSION: DIGAMI 2 did not support the fact that an acutely introduced, long-term insulin treatment improves survival in type 2 diabetic patients following myocardial infarction when compared with a conventional management at similar levels of glucose control or that insulin-based treatment lowers the number of non-fatal myocardial reinfarctions and strokes. However, an epidemiological analysis confirms that the glucose level is a strong, independent predictor of long-term mortality in this patient category, underlining that glucose control seems to be an important part of their management.     

Normalization of impaired response of platelets to prostaglandin E1/I2 and synthesis of prostacyclin by insulin in unstable angina pectoris and in acute myocardial infarction.

The minimal inhibitory concentration of prostaglandin E1 (used as a probe for prostacyclin [PGI2]) needed to inhibit platelet aggregation (36 +/- 16 nM) in normal volunteers (n = 40) increased (64 +/- 30 nM) in patients (n = 46) with acute coronary artery disease. Bolus injection of insulin in 20 patients, 0.1 U/kg body weight 4 times a day (every 6 hours) for 7 days decreased the minimal inhibitory concentration of prostaglandin E1 from 64 +/- 30 to 26 +/- 12 nM (p less than 0.001). Twenty other patients who received only saline solution had no decrease in minimal inhibitory concentration of the prostanoid. The bolus injection of insulin also increased the plasma level of PGI2 (9 +/- 2 pM) two-fold in these patients (28 +/- 10 pM). Administration of aspirin inhibited the insulin-induced increase of plasma prostanoid level. Patients in the placebo group had no increase in plasma PGI2 level. The bolus injection of insulin administered only once to another group of patients (n = 6) demonstrated that the hormonal effects were maximally increased within an hour of insulin administration, and were directly related to the increased insulin level in plasma. These results indicated the feasibility of using physiologic quantities of insulin for controlling of platelet aggregation through resensitization of platelet response to prostaglandin and increased synthesis of PGI2 in vivo in acute coronary artery disease.     

Increased platelet aggregability in response to shear stress in acute myocardial infarction and its inhibition by combined therapy with aspirin and cilostazol after coronary intervention

Although antiplatelet therapy with a specific inhibitor of phosphodiesterase-3 cilostazol improves stent patency compared with use of aspirin (ASA) alone, the specific role of cilostazol on platelet aggregation in patients with acute myocardial infarction (AMI) is less well understood. Thirty-six patients with AMI who were successfully treated with primary angioplasty were randomized to 3 antiplatelet regimens: ASA alone (n = 12), ASA + ticlopidine (n = 12), and ASA + cilostazol (n = 12). We measured shear stress-induced platelet aggregation (SIPA) using a modified cone-plate viscometer on admission and on day 7, and evaluated the inhibitory effects of combination therapy with ASA + cilostazol on SIPA. Compared with cases of stable coronary artery disease, significant increases in SIPA and plasma von Willebrand factor activity were observed in patients with AMI before they received antiplatelet therapy. On day 7 after primary angioplasty, ASA did not inhibit SIPA (65 +/- 15% vs 57 +/- 11%, p = 0.086), whereas both combination therapies of ASA + ticlopidine and ASA + cilostazol significantly inhibited SIPA in patients with AMI (ASA + ticlopidine: 61 +/- 15% vs 45 +/- 13%, p <0. 0001; ASA + cilostazol: 64 +/- 14% vs 43 +/- 9%, p <0.005). There was a significant correlation of SIPA with adenosine diphosphate (ADP)-induced platelet aggregation (r = 0.412, p = 0.003) and with plasma von Willebrand factor activity (r = 0.461, p = 0.0008). These data suggest that patients with AMI have increased platelet aggregability in response to high shear stress. Combined antiplatelet therapy with ASA + cilostazol appears to be as effective as therapy with ASA + ticlopidine for reducing SIPA in patients with AMI who are undergoing primary angioplasty.     

血栓弹力图评价替格瑞洛和氯吡格雷在急性ST段抬高型心肌梗死中抗血小板的疗效

目的:通过血栓弹力图评价替格瑞洛和氯吡格雷在急性ST段抬高型心肌梗死(STEMI)中抗血小板的疗效。方法:60例STEMI患者分为两组,阿司匹林+氯吡格雷组(Ⅰ组,n=30)和阿司匹林+替格瑞洛组(Ⅱ组,n=30),于抗血小板药物负荷剂量给药2 h后和维持治疗3个月后,使用血栓弹力图检测花生四烯酸(AA)途径和二磷酸腺苷(ADP)受体途径诱导的血小板抑制率。结果:抗血小板药物负荷剂量给药2 h后和维持治疗3个月后,Ⅱ组ADP受体途径诱导的血小板抑制率均明显高于Ⅰ组[(54.67±5.83)%对(45.75±16.72)%,P0.05;(59.53±12.18)%对(45.10±16.26)%,P0.05],AA途径诱导的血小板抑制率两组间无明显差异,患者的出血和缺血事件发生率两组间无明显差异。结论:替格瑞洛较氯吡格雷在STEMI治疗中能更快速充分地抑制血小板,血栓弹力图可用于指导STEMI患者抗血小板治疗。     

Serum C-reactive protein and soluble angiopoietin receptor Tie-2 in patients with acute myocardial infarction and its detection by optical proteinchip

Serum C-reactive protein (CRP) and soluble angiopoietin receptor Tie-2 (sTie) were detected in patients with acute myocardial infarction (AMI). The results indicated that mean serum CRP and Tie-2 levels were significantly higher in the patients with AMI than the control group. Increasing CRP was related to an increased infarction area and adverse prognosis. Levels of sTie-2 increased in the AMI patients and the maximum level of sTie-2 appeared at day 2 after onset of AMI. The feasibility of using to detect serum CRP and Tie-2 was also presented in this study. Measurement for CRP by optical proteinchip with imaging ellipsometry (OPC-IE) and immunobidimetric analyzer showed no obvious difference (p<0.01). Also, the measurement for Tie-2 by ELISA and OPC-IE showed no obvious difference (p<0.01).     

Stem cell mobilization by granulocyte-colony-stimulating factor in acute myocardial infarction: lessons from the REVIVAL-2 trial

Experimental studies and early-phase clinical trials suggest that mobilization of bone marrow stem cells by granulocyte-colony-stimulating factor (G-CSF) can be used to improve cardiac regeneration after acute myocardial infarction (AMI). In order to more fully evaluate this intervention in patients with AMI, we conducted the Regenerate Vital Myocardium by Vigorous Activation of Bone Marrow Stem Cells (REVIVAL-2) clinical trial. Following successful reperfusion by percutaneous coronary intervention for AMI, patients were randomly assigned to receive a subcutaneous daily dose of 10 microg/kg G-CSF or placebo for 5 days. Treatment with G-CSF produced a significant mobilization of stem cells. After 4-6 months the reduction in infarct size from baseline, as determined by technetium-99-labeled single-photon-emission CT, did not differ significantly between the G-CSF group and the placebo group. Furthermore, the improvement in left ventricular ejection fraction, as assessed by late-enhancement MRI, did not differ significantly between the two groups. G-CSF treatment did not increase the risk of adverse clinical events and did not promote restenosis. Our trial demonstrates that stem cell mobilization by G-CSF does not improve infarct size, left ventricular function, or coronary restenosis in patients with AMI who have had successful mechanical reperfusion.     

心肌缺血预适应对溶栓治疗的急性心肌梗死患者近期及远期预后的影响

目的 探讨心肌缺血预适应(IPC)对急性心肌梗死(AMI)溶栓治疗患者近期及远期预的影响. 方法 选取152例进行静脉溶栓治疗的首次ST段抬高的急性心肌梗死住院患者,根据AMI发病前24h内是否有IPC分为有IPC组(A组,n=80)和无IPC组(B组,n=72)两组一般临床资料差异无统计学意义(P>0.05),回顾性分析其临床资料、评估心肌梗死面积、左心室功能改变及血管开通率,分析院内(2～3周)及随访(12～36个月)主要心脏不良事件(MACE)及复合终点事件发生率,进而比较IPC对患者近期和远期预后的影响. 结果 ①A组CK峰值、CK-MB峰值、CK到达峰值的时间、QRS积分、白细胞计数、超敏C反应蛋白、室壁运动异常节段数显著低于B组,而血管开通率和左室射血分数(LVEF)显著高于B组,两组差异均有显著性(P<0.05);②近期预后比较住院期间并发症及复合终点事件发生率A组低于B组,差异均具有显著性(P<0.05);③远期预后比较不稳定心绞痛、MACE事件及复合终点事件发生率差异无显著性(P>0.05).结论 心肌缺血预适应对溶栓治疗患者具有明显再灌注保护作用,改善患者的近期预后,但对患者远期预后影响需进一步探讨.     

No evidence that the PLA1/PLA2 polymorphism of platelet glycoprotein IIIa is implicated in angiographically characterized coronary atherosclerosis and premature myocardial infarction.

Platelet membrane glycoprotein IIb/IIIa plays an important role in platelet aggregation. A polymorphism of the gene encoding the IIIa subunit, with the two allele forms PLA1 and PLA2, has been identified. Some, but not all, studies suggest that the PLA2 allele confers an increased risk of suffering a myocardial infarction. Conversely, a recent study suggests that the PLA1 allele may contribute to early atherosclerosis and more rapid progression of stable coronary artery disease. To test whether these associations could be reproduced in a well-characterized sample of survivors of premature myocardial infarction, we examined 369 patients admitted to coronary care units in the Stockholm area who suffered a first myocardial infarction before the age of 60 years. There were no significant differences in extent of coronary artery disease according to PLA genotype group (based on quantitative coronary angiography). In addition, the frequencies of PLA1 and PLA2 alleles did not differ from those of 388 well-matched control subjects without coronary artery disease. These results suggest that the PLA1/PLA2 polymorphism of the platelet glycoprotein IIIa gene does not substantially contribute to the development of coronary atherosclerosis or the genetic susceptibility to premature myocardial infarction.     

不同动脉入路行急诊冠状动脉介入治疗急性心肌梗死的比较

目的探讨急性心肌梗死经不同动脉入路行急诊冠状动脉介入(percutaneous coronary intervention,PCI)治疗的疗效。方法回顾性分析193例行PCI治疗的急性心肌梗死患者的临床资料,其中经桡动脉介入治疗组104例,经股动脉介入治疗组89例,对比观察两组的术中情况、PCI治疗成功率、术后血管情况、局部并发症及住院时间。结果两组穿刺成功率、手术成功率比较,差异无统计学意义(P0.05)。桡动脉组无严重局部出血性并发症,股动脉组有3例(3%,3/89)发生,两组比较差异有统计学意义[0%(0/104)vs.3%(3/89),P0.05]。局部血肿发生率股动脉和桡动脉组分别为12例和1例,两组比较差异有统计学意义[13.5%(12/89)vs.1.0%(1/104),P0.05]。桡动脉组住院时间比股动脉组短,差异有统计学意义[(10±3)d vs.(13±7)d,P0.05]。结论急性心肌梗死患者行PCI治疗时,选择经桡动脉途径安全、有效,是可行的。     

老年心肌梗死患者循环血内皮祖细胞数目和功能的变化及其对心功能的影响

目的 比较不同年龄组心肌梗死患者循环血内皮祖细胞（EPCs）数目及功能的差异,分析蛋白激酶B（Akt）和间质细胞源因子1（SDF-1）表达的差异,探讨老年患者EPCs修复梗死心脏功能的可能机制及临床意义.方法 抽取老年心肌梗死患者（n=26）和中青年心肌梗死患者（n=24）动脉血8 ～10 ml,流式细胞仪检测各组EPCs含量,酶联免疫吸附法检测Akt及SDF-1表达变化情况;利用冠状动脉左前降支结扎术制备大鼠心肌梗死模型后,尾静脉注射老年EPCs、中青年EPCs（1×107/200 ml）或等体积盐水（PBS组）,观察终点时间为28 d,超声心动评价心脏功能,荧光显微镜下观察EPCs在梗死心脏的归巢情况,免疫荧光法计数缺血心肌局部血管数量.结果 老年心肌梗死患者循环血EPCs数量明显少于中青年组（47.23％±14.92％比89.76％ ±7.27％,P＜0.001）;心肌梗死后老年组Akt磷酸化水平和SDF-1表达水平明显低于中青年组（Akt：19.04％±6.41％比43.96％±15.91％;SDF-1：25.81％ ±6.32％比64.04％±16.35％,均为P＜0.001）.将EPCs移植至梗死大鼠后,移植的老年EPCs在梗死心脏的归巢数量明显少于移植的中青年EPCs（3.69±1.97/mm2比12.01 ±5.44/mm2,P ＜0.001）.移植老年EPCs的大鼠梗死心脏的血管密度明显少于移植中青年EPCs的大鼠（42±9/mm2 比96±15/mm2,P ＜0.001）.移植老年EPCs组心功能指标[左心室射血分数（LVEF）和左心室缩短分数（LVFS）]显著低于移植中青年EPCs组（LVEF：58.1％±5.0％比73.8％±7.9％;LVFS：35.4％±3.8％比59.0％±7.6％.均为P＜0.001）.结论 老年心肌梗死患者的循环血EPCs数量及其修复功能均不如中青年患者,可能与Akt-SDF-1信号通路受损有关.