恶性血液肿瘤中ADAMTS13活性与TSP1水平改变

目的:观察血管性血友病因子裂解蛋白酶(von Willebrand factor cleaving protease,ADAMTS13)活性、血管性血友病因子(von Willebrand factor,v WF)及凝血酶敏感蛋白1(thrombospondin 1,TSP1)水平在恶性血液肿瘤患者治疗前后的变化,并探讨其相关的临床意义。方法:收集82例恶性血液肿瘤(包括20例急性白血病,48例恶性淋巴瘤,14例多发性骨髓瘤)患者和45例与之匹配的健康对照者的血浆标本,用酶联免疫吸附试验(ELISA)检测2组血浆中的v WF抗原和TSP1水平,用残余胶原结合试验(R-CBA)检测2组血浆中的ADAMTS13活性水平。结果:初发恶性血液肿瘤患者血浆中ADAMTS13活性(71.48±19.62)%明显低于正常对照组(92.31±21.82)%(P0.05);v WF抗原水平和TSP1水平高于正常对照组(P0.05)。初发组血浆中ADAMTS13活性(71.48±19.62)%低于治疗后缓解组(89.84±20.70)%(P0.05);初发组v WF抗原水平高于治疗后缓解组(P0.05)。在82例初发恶性血液肿瘤中有25例合并感染,治疗前合并感染者的ADAMTS13活性(49.80±18.44)%明显低于无感染组(73.82±21.41)%(P0.05);感染组v WF抗原水平与TSP1水平明显高于无感染组(P0.05)。治疗过程中有8例发生了血栓事件,发生血栓事件的患者血浆中ADAMTS13活性较无血栓组明显降低(P0.05);8例急性早幼粒细胞白血病中有1例合并弥散性血管内凝血。结论:恶性血液肿瘤患者中ADAMTS13活性降低和TSP1水平升高,而发生感染及血栓事件的恶性血液肿瘤患者中ADAMTS13活性进一步降低。检测恶性血液肿瘤患者血浆中的ADAMTS13活性和TSP1水平有可能更好地预防感染及血栓事件的发生。     

血栓性血小板减少性紫癜患者vWF裂解蛋白酶抗原和活性的检测及意义

目的研究血管性血友病因子裂解蛋白酶(ADAMTS13)抗原含量和活性在血栓性血小板减少性紫癜(TTP)患者及遗传性 TTP 家族突变携带者中变化的情况。方法用残余胶原结合实验(RCBA)检测13例 TTP 患者共28份血浆标本[含血浆置换(PE)前后]及10例携带者的 ADAMTS13活性;用新近建立的三抗体夹心酶联免疫反应法检测标本的 ADAMTS13抗原含量。结果正常对照组 ADAMTS13含量为(600.93±145.36)mU/ml(设白种人混合血浆的 ADAMTS13抗原含量为1000mU/ml),活性为(74.79±11.81)%。遗传性 TTP 患者 ADAMTS13抗原含量和活性治疗前和发病间期均明显减低,PE 后恢复;其家族中携带者 ADAMTS13抗原含量为(331.40±109.85)mU/ml,活性为(66.79±12.82)%(与对照组比较,P 值分别<0.01和>0.05);原发性 TTP 患者 PE 前 ADAMTS13抗原含量为(98.7±82.08)mU/ml,活性为(22.23±19.07)%(与对照组比较,P 值均<0.01);PE 后ADAMTS13 抗原含量为(449.4±232.33)mU/ml,活性为(60.92±22.33)%(与对照组比较,P 值分别<0.01和>0.05);1例继发性 TTP 患者 PE 后 ADAMTS13抗原含量远高于正常,活性仅为6.00%结论治疗前的 TTP 患者 ADAMTS13抗原含量和活性均明显减低。大多数患者两指标变化趋势一致,也有个别患者两指标变化趋势相反,前者可能因为遗传因素或体内免疫系统的廓清作用,后者可能因为抗 ADAMTS13抗体仅抑制了 ADAMTS13的活性而未影响其抗原的含量或其他未知原因所致。     

急性髓系白血病中ADAMTS13活性和vWF的水平变化及其意义

本研究观察血管性血友病因子裂解蛋白酶（ADAMTS13）活性和血管性血友病因子（vWF）抗原在急性髓系白血病（AML）患者治疗前后的变化情况,探讨相关的临床意义。收集73例初治AML患者缓解前后的血浆标本,荧光标记v WF73底物荧光共振能量转移试验（FRETS-vWF73）检测患者血浆中的ADAMTS13活性,以ELISA试剂盒检测v WF抗原量。结果表明,初治AML患者治疗缓解前的ADAMTS13活性明显低于正常对照组：（63.3±25.5）%vs（105.1±37.7）%,（P〈0.01）;vWF抗原则高于正常对照组（226.6±127.0）%vs（111.4±39.7）%,（P〈0.01）。经标准诱导化疗后缓解期患者的ADAMTS13活性明显高于治疗前组（P〈0.01）,与正常对照组比较无显著差异;vWF抗原则明显低于治疗前组（P〈0.01）,但仍高于正常对照组（P〈0.05）。初治AML患者治疗前合并感染者的ADAMTS13活性明显低于无感染组：（52.2±20.6）%vs（73.9±24.7）%,（P〈0.01）;感染组vWF抗原明显高于无感染组：（262.2±135.7）%vs（193.8±110.2）%,（P〈0.05）。伴弥散性血管内凝血（DIC）者的ADAMTS13活性明显低于无DIC组：（42.0±14.5）%vs（73.4±22.7）%,（P〈0.01）;DIC患者的vWF抗原明显高于无DIC组：（274.2±140.0）%vs（204.7±115.5）%,（P〈0.05）。结论：初治AML患者治疗前伴有ADAMTS13活性的降低和v WF的升高,以合并感染和DIC的患者表现最显著。ADAMTS13和v WF在肿瘤的发生发展,炎症和DIC的形成过程中起一定作用。     

血栓性血小板减少性紫癜患者血浆置换前后ADAMTS 13抗原变化及临床意义

血栓性血小板减少性紫癜(TTP)是一种罕见的微血管血栓——出血综合征.该病进展迅速,临床表现多样,病死率高.TTP典型临床表现为Moschcowitz's五联征:血小板减少、溶血性贫血、发热、中枢神经系统和肾脏受累表现[1].现已证实血管性血友病因子裂解蛋白酶(ADAMTS 13)缺陷,导致超大分子量vWF多聚体(ULvWF)不能被裂解而引起血小板聚集、微血管血栓形成是TTP的重要发病机制[2-3].血浆置换(PE)是治疗该病的一种安全有效的方法,使患者的病死率由90％以上降至25％[3-4].我们对6例TTP患者进行了PE治疗,同时对患者PE前后ADAMTS13抗原含量和vWF多聚体结构进行分析,报道如下.     

ADAMTS13和TSP-1在糖尿病视网膜病变的意义

目的研究血管性血友病因子裂解蛋白酶(ADAMTS13)及凝血酶敏感蛋白-1(TSP-1)与糖尿病眼底视网膜病变(DR)的关系。方法选取114例糖尿病患者分为单纯糖尿病(DM)组38例和糖尿病视网膜病变(DR)组76例,同时选取30例健康体检者作为对照组。用残余胶原结合试验法检测ADAMTS13活性;同时用酶联免疫吸附试验法检测血浆中TSP-1及血管性血友病因子(vWF)抗原水平。结果 DM组患者血浆中ADAMTS13活性低于对照组,差异有统计学意义(P0.01),vWF抗原和TSP-1水平均高于对照组,差异有统计学意义(P0.01);DR组ADAMTS13活性明显低于DM组,差异有统计学意义(P0.05),vWF抗原和TSP-1水平均高于DM组,差异有统计学意义(P0.05)。结论 ADAMTS13活性降低及TSP-1水平升高可能导致糖尿病眼底视网膜病变的发生和发展。     

血管性假血友病因子与ADAMTS13在动脉瘤性蛛网膜下腔出血患者中的动态变化及意义

目的 了解血管性假血友病因子(vWF)与ADAMTS13在动脉瘤性蛛网膜下腔出血患者(aneurysmal subarachnoid hemorrhage,aSAH)中的动态变化及意义.方法 采用回顾性分析方法,将苏州大学附属第一医院神经外科2010年4月至2011年4月收治的动脉瘤性蛛网膜下腔出血患者29例,分成迟发性脑缺血组(DCI组)和非迟发性脑缺血组(无DCI组)、脑血管痉挛组(CVS组)和无痉挛组(无CVS组)、预后良好组和预后不良组,并引入正常健康体检者20例作为对照组.所有入选患者均行CT、DSA和(或)CTA确诊为颅内动脉瘤破裂致蛛网膜下腔出血.排除标准:(1)入院时发病已超过72 h或即将死亡患者;(2)在外院已接受手术、介入或内科保守治疗患者;(3)正在使用抗血小板药物如阿司匹林、氯吡格雷,或其他抗凝药物如华法林等;(4)有血液系统疾病、肝肾功能不全、近期有感染性疾病、孕期患者.分别在SAH后第1天、第4天、第10天收集静脉血,使用ELISA方法检测vWF抗原和ADAMTS13活性,观察其动态变化,TCD检测大脑中动脉的血流速度(VMCA),出院时行GOS预后评分.使用SPSS 13.0统计软件进行统计学处理,计量资料以均数±标准差((x)±s)表示,并行t检验,多组比较采用方差分析.以P ＜0.05为差异有统计学意义.结果 血浆vWF水平在DCI组、CVS组及预后不良组第1天、第4天、第10天3个时间点均高于健康对照组,DCI组与无DCI组相比在第1天、第4天时间点组间比较差异具有统计学意义(P＜0.05),在第4天、第10天,CVS组与无CVS组,预后良好组与预后不良组组间比较差异具有统计学意义(P＜0.01).DCI组与预后不良组在T1时间点血浆ADAMTS13活性显著下降;而在是否发生CVS患者之间血浆ADAMTS13活性差异无统计学意义.结论 早期血浆vWF水平升高、ADAMTS13活性下降与DCI发生有关,并日早期ADAMTS13活件下降与预后相关.     

ADAMTS13在血栓前疾病状态中的水平及其相关因素分析

目的:检测血栓前状态病例血浆中血管性血友病因子裂解蛋白酶(ADAMTS13)的活性水平并探讨其临床意义,同时分析ADAMTS13与血管性血友病因子(v WF)、凝血酶敏感蛋白1(TSP1)、C-反应蛋白(CRP)、肌酐等生化指标和血压等因素是否存在一定的相关性。方法:用残余胶原结合试验(R-CBA)检测病例组(急性早幼粒细胞白血病、恶性肿瘤、败血症等患者共260例)及50例正常对照组血浆中ADAMTS13的活性,ELISA试剂盒检测两组血浆中TSP1和v WF蛋白水平,同时对病例组血浆CRP、肌酐等生化指标和血压水平等与ADAMTS13活性关系进行相关性分析。结果:病例组血浆中ADAMTS13活性均显著低于正常对照组(P0.05),TSP1及v WF蛋白水平均高于对照组(P0.05);相关性分析发现,ADAMTS13活性与TSP1、肌酐、血糖、血压、D-二聚体及CRP呈负相关(r=-0.25至r=-0.54,P0.05),与血脂、血型、血小板数目、血红蛋白无明显相关性(P0.05)。结论:血栓前状态病例血浆中ADMATS13活性降低,提示ADAMTS13的减少与血栓前状态疾病的发病相关。检测血浆中ADAMTS13的活性有助于对血栓前疾病的诊断。     

ADAMTS13依赖性血管性血友病因子水解相关影响因素的研究进展

血浆中血管性血友病因子(vWF)多聚体的相对分子质量的大小主要是由血浆中的血管性血友病因子裂解酶(ADAMTS13)通过剪切vWF A2功能域内的Tyr1605-Met1606之间的肽键而实现的.ADAMTS13对vWF的水解是受多种因素调控或影响的,此种ADAMTS13依赖性vWF水解过程的改变具有重要的生理或病理意义.     

影响获得性血栓性血小板减少性紫癜首次缓解期内复发的相关指标研究

目的 探讨血管性血友病因子裂解蛋白酶(ADAMTS) 13活性和抗ADAMTS13抗体表达水平,与获得性血栓性血小板减少性紫癜(TTP)于首次缓解期内复发的关系.方法 选择2008年3月至2014年6月于陕西延安大学附属医院和陕西省渭南市富平县医院诊治的37例获得性TTP患者为研究对象,按照其在首次缓解随访期内是否复发,分为研究组(n=15)和对照组(n=22).分别采用残余胶原结合试验、ELISA、免疫印迹等方法,检测两组患者的ADAMTS13活性,ADAMTS13抗原水平,抗ADAMTS13抗体,ADAMTS13抑制物,血管性血友病因子(vWF)抗原和超大分子量vWF(ULVWF)多聚体等指标,并且进行统计学分析;采用多因素非条件logistic回归分析法,评估获得性TTP患者于首次缓解期内复发的独立影响因素.本研究遵循的程序符合病例收集医院人体试验委员会所制定的伦理学标准,得到该伦理会批准,分组征得受试对象本人的知情同意,并与之签订临床研究知情同意书.结果 ①研究组患者的中位ADAMTS13活性为11％(7％～124％),低于对照组的53％(7％～151％),差异有统计学意义(u=4.018,P＜0.05).研究组与对照组患者的ADAMTS13活性显著降低率分别为53.3％(8/15)和22.7％(5/22),二者比较,差异有统计学意义(P=0.049).②37例获得性TTP患者的血浆ADAMTS13活性和ADAMTS13抗原水平呈正相关关系(rs=0.810,P=0.001).研究组患者的中位ADAMTS13抗原水平为33％(3％～99％),低于对照组的59％(3％～128％),差异有统计学意义(u=4.121,P＜0.05).研究组与对照组ADAMTS13抗原水平显著降低率分别为13.3％(2/15)和9.1％(2/22),二者比较,差异有统计学意义(P=0.008).③研究组患者的抗ADAMTS13抗体检出率为66.7％(10/15),高于对照组的36.4％(8/22),差异有统计学意义(P=0.007).④研究组患者中抗ADAMTS13抑制物检出率为46.7％ (7/15),高于对照组患者的18.2％ (4/22),差异有统计学意义(P=0.011).⑤研究组与对照组患者ULVWF多聚体检出率分别为20.0％(3/15)和13.6％(3/22),二者比较,差异有统计学意义(P=0.042).⑥多因素非条件logistic回归分析结果显示,获得性TTP患者于首次缓解期内复发的独立危险因素包括ADAMTS13活性显著降低(OR=2.95,95％ CI:1.13～6.96,P＜0.05),检出抗ADAMTS13抗体(OR=3.31,95％CI:1.08～8.19,P＜0.05),检出抗ADAMTS13抑制物(OR=3.24,95 ％CI:1.24～9.03,P＜0.05).结论 获得性TTP患者在首次缓解期内,ADAMTS13活性水平显著降低,存在抗ADAMTS13抗体及抗ADAMTS13抑制物,会显著增加疾病复发风险,可以考虑将其作为预测获得性TTP患者于首次缓解期内复发的重要指标.     

ADAMTS-13活性水平检测在ITP与TTP鉴别中的意义

目的　探讨VWF裂解蛋白酶(ADAMTS -13,vWP cp)活性水平的检测在特发性血小板减少性紫癜(ITP)与血栓性血小板减少性紫癜(TTP)鉴别中的意义。方法　采用残余胶原结合实验(Residual CollagenBindingAssay)分别对35例ITP、6例TTP及32例健康人血浆ADAMTS 13活性水平进行检测。结果　ITP及TTP患者血浆ADAMTS 13活性水平[(47.6 2±2 4 . 2 2 ) %、(12 .5 4±11.6 9) % ]显著低于正常人[(78 .6 0±10 .0 3) % ](P <0 . 0 1) ,ITP患者血浆ADAMTS 13活性水平明显高于TTP患者(P<0. 0 1) ,ITP患者血浆ADAMTS 13活性水平阳性率[6 8 5 7% (2 4 /35 ) ]明显低于TTP患者[10 0 % (6 /6 ) ](P <0 . 0 1)。结论　ADAMTS 13活性水平检测在ITP与TTP鉴别诊断中具有一定的意义。     

蛋白质Z检测在心脑血管疾病中的临床意义

目的研究蛋白质Z(Protein Z,PZ)在心脑血管疾病中的变化,并探讨其临床意义及与血液凝固因子X(FX)的关系.方法PZ及FXAg用ELISA法检测,血浆FXC采用一期法测定.对170例急性缺血性脑卒中(AIS)、40例急性心肌梗死(AMI)、60名健康者的PZ、FXC、FXAg进行测定及相关性比较,同时对初发与再发、不同年龄、不同性别患者PZ、FXC、FXAg水平进行比较.结果AIS组和AMI组的PZ水平分别为(940.02±229.82)μg/L与(1071.44±180.52)μg/L,与对照组[(2257.97±479.76)μg/L]相比明显下降(P值均＜0.001).AIS组的FXC、FXAg水平分别为(136.73±34.93)%、(135.54±54.39)%,AMI组分别为(139.53±29.18)%、(129.75±21.91)%,与对照组[分别为(94.33±20.00)%和(77.22±13.19)%]相比显著升高(P值均＜0.001).AIS、AMI组及对照组中的PZ水平与FXC、FXAg水平之间均存在明显负相关(P值均＜0.001),同时再发AIS、AMI组PZ、FXC、FXAg分别与初发组比较,有显著性差异(P值均＜0.05),显示PZ水平的下降程度反映了疾病的病理过程.PZ水平随年龄增加而下降(P＜0.05),而FXC、FXAg水平与年龄因素无关(P＞0.05),PZ、FXC、FXAg水平与性别之间未发现相关性(P＞0.05).结论PZ水平在AIS、AMI患者中明显减低,PZ与FXC、FXAg存在明显负相关,FX水平升高的机制可能部分与PZ水平下降有关.PZ水平与疾病初发与再发有关,并随年龄增加而呈下降的趋势.提示PZ缺乏可能是心脑动脉血栓性疾病存在的一个危险因素.     

ADAMTS‐13 activity and autoantibodies classes and subclasses as prognostic predictors in acquired thrombotic thrombocytopenic purpura

Summary. Background: Thrombotic thrombocytopenic purpura (TTP) is a rare life‐threatening disease. Of surviving patients, 45% develops an exacerbation or a late recurrence. Severe ADAMTS‐13 deficiency, both during the acute episode and remission, is a well‐established predictor of recurrence. The predictive value of anti‐ADAMTS‐13 antibodies, their inhibitory activity and Ig class subtype for disease recurrence is still to be established. Objectives: To analyze ADAMTS‐13‐related biomarkers (ADAMTS‐13 and anti‐ADAMTS‐13 immunoglobulins, classes and subclasses) and their potential relationship with prognosis. Patients/Methods: In 115 patients with TTP, we assessed the association between levels of these biomarkers and the severity of acute episodes; we analysed also the hazard ratio (HR) and 95% confidence interval (CI) of recurrence in association with biomarkers levels retrieved at the previous acute episode or during remission, using Cox regression models. Results: During the acute phase, higher IgA, IgG1 and IgG3 titers showed the strongest association with acute episode severity. In the survival analyzes, the only biomarker significantly associated with a high hazard of recurrence after an acute episode was the presence of IgG. Conversly, low ADAMTS‐13 activity or antigen levels (< 10%), the presence of ADAMTS‐13 inhibitor or IgG during remission were all significantly associated with a higher hazard of recurrence. Conclusions: Both the Ig class and subclass are of predictive value for acute episode severity in patients with TTP. Although markers that could predict the risk of recurrence in the acute phase are limited, a thorough assessment of ADAMTS‐13‐related parameters during remission is warranted.     

Circulating pregnancy-associated plasma protein A is not an early marker of acute myocardial infarction

OBJECTIVE: The purpose of this study was to assess whether serum levels of pregnancy-associated plasma protein A (PAPP-A) are elevated early in patients with acute myocardial infarction (AMI). DESIGN AND METHODS: We measured serum levels of PAPP-A in 80 patients with AMI and in 80 age-matched healthy control subjects. The mean (+/-SEM) time from onset of symptoms to blood sampling was 6.3 +/- 2.8 h in the group with AMI. RESULTS: The PAPP-A levels did not differ between the control group and the AMI group (1.24 +/- 0.07 vs. 1.29 +/- 0.02 mIU/l; P = 0.54). CONCLUSIONS: Measurement of serum PAPP-A does not seem to be a useful early marker for AMI.     

Serum levels of osteoprotegerin and RANKL in patients with ST elevation acute myocardial infarction

OPG (osteoprotegerin) has been suggested to have an important role in atherogenesis and vascular calcification. In the present study, we have investigated serum OPG and RANKL (receptor activator of nuclear factor kappaB ligand) concentrations in patients with ST elevation AMI (acute myocardial infarction) and established CAD (coronary artery disease). OPG and RANKL were measured in 58 male patients hospitalized in the coronary care unit with ST elevation AMI, in 52 asymptomatic male patients with an established diagnosis of CAD and in 52 healthy male controls. These last two groups were matched with the AMI patients for age and body mass index. OPG was significantly (P<0.05) higher in patients with AMI at 1 h after AMI (8.04+/-4.86 pmol/l) than in both patients with established CAD (4.92+/-1.65 pmol/l) and healthy subjects (3.15+/-1.01 pmol/l). Subjects with established CAD had significantly (P<0.05) increased OPG levels compared with controls. RANKL levels in patients with established CAD (0.02+/-0.05 pmol/l) and with AMI (0.11+/-0.4 pmol/l) were significantly (P<0.05) lower compared with controls (0.32+/-0.35 pmol/l). In the AMI group, OPG decreased significantly (P<0.05) at 1 and 4 weeks after infarction (8.04+/-4.86 compared with 6.38+/-3.87 and 6.55+/-2.6 pmol/l respectively), but OPG levels, either at 1 h or 1-4 weeks after AMI, remained significantly (P<0.05) higher compared with established CAD (4.92+/-1.65 pmol/l) and controls (3.15+/-1.01 pmol/l). Our data show for the first time that OPG levels are increased in ST elevation AMI within 1 h of infarction. Whether the increase in OPG is a consequence or a causal factor of plaque destabilization deserves further investigation.     

白细胞介素-18含量变化与急性心肌梗死的炎症关系

目的:探讨IL-18在急性心肌梗死(AMI)中改变的意义.方法:用酶联免疫吸附双抗体夹心法动态检测44例AMI患者和20例健康对照者的血清IL-18含量,分析IL-18与梗死部分、面积积分、临床积分、血清肌酸激酶同工酶(CK-MB)之间的相关性.结果:AMI患者血清IL-18含量明显升高,第2 d达高峰,以后开始下降,第14 d接近正常对照组;且IL-18含量变化与血清CK-MB含量变化、临床积分、梗死面积均呈明显的正相关性(P均<0.05);死亡组IL-18含量明显高于存活组(P<0.05).结论:IL-18含量与AMI患者的病情变化相一致,其可能参与了AMI的病理生理过程,可作为AMI患者病情监测和预后的参考指标之一.     

血栓疾病患者血浆肝素辅因子Ⅱ活性和抗原水平检测及意义

目的　了解肝素辅因子Ⅱ (HCⅡ )活性及抗原水平在动、静脉血栓性疾病中的变化及其与动、静脉血栓性疾病之间的关系。方法　用发色底物法测定 5 0名正常人 ,75例脑梗死、5 0例心肌梗死及 36例深静脉血栓患者血浆HCⅡ活性 ;发色底物法检测深静脉血栓患者中HCⅡ缺乏者血浆抗凝血酶 (AT)活性 ;Westernblot检测部分样品 (每组 36例 )血浆HCⅡ抗原含量。结果　血浆HCⅡ活性与其抗原呈平行变化 ;正常对照组血浆HCⅡ活性及抗原水平分别为 (96 .80± 2 0 .11) % ,0 .93± 0 .19与脑梗死组 [(99.97± 2 1.14 ) % ,0 .96± 0 .2 4 ]、心肌梗死组 [(98.18± 2 9.35 ) % ,0 .95± 0 .2 0 ]及深静脉血栓形成组 [(89.5 7± 17.12 ) % ,0 .87± 0 .18]比较 ,差异无显著性 ,但深静脉血栓形成组HCⅡ活性和抗原均呈降低趋势 ;HCⅡ明显减低者在正常人及患者之间的分布频度无显著差异 ;深静脉血栓中HCⅡ缺乏者血浆抗凝血酶活性及纤维蛋白原浓度正常。结论　血浆HCⅡ变化可能不是中国湖南汉族人心、脑血栓病的危险因子 ;是否与静脉血栓形成相关有待进一步证实。     

急性心肌梗死并发心源性休克的临床特征与救治

目的　评价急性心肌梗死 (AMI)并心源性休克的临床特征 ,总结救治经验。方法　 10 8例 AMI患者 ,分为休克组 (11例 )与非休克组 (97例 ) ,对比分析两组患者的临床特征、处理与近期预后的异同。结果　两组患者年龄、性别、糖尿病、冠心病、高脂血症、陈旧性心肌梗死病史及梗死部位无显著性差异 (P均 >0 .0 5 )。与非休克组比较 ,休克组肌酸磷酸激酶和心肌肌钙蛋白 I升高〔(31979.7± 2 2 2 71.1) nm ol· s- 1· L- 1比 (17795 .2± 14 979.7) nmol· s- 1· L- 1和 (90 .7± 6 1.1) μg/ L 比 (39.9± 5 2 .1) μg/ L,P均 <0 .0 5〕,左室射血分数降低 (0 .4 6± 0 .12比 0 .5 5± 0 .12 ,P<0 .0 5 ) ,急性肺水肿、心律失常和肺炎合并症增多 (6 4 %比 14 % ,P<0 .0 0 1;5 5 %比 2 1% ,P<0 .0 5 ;4 6 %比 12 % ,P<0 .0 1) ,采用溶栓治疗、冠状动脉造影、主动脉内气囊反搏者多 (46 %比 18% ,73%比 2 6 %和 36 %比 4 % ,P均 <0 .0 5 )。两组住院期病死率无显著性差异 (0比 4 % ,P>0 .0 5 )。结论　 AMI并休克者心肌梗死面积大 ,急性肺水肿、心律失常和肺炎合并症多 ,需主动脉内气囊反搏者多。正确判断、严密监测、及时有效处理 ,可明显改善患者的早期预后。     

Sympathetic neural hyperactivity and its normalization following unstable angina and acute myocardial infarction

Impaired autonomic function occurs after AMI (acute myocardial infarction) and UA (unstable angina), which may be important prognostically. However, the pattern of sympathetic nerve hyperactivity has been investigated only after AMI. We aimed to quantify central sympathetic output to the periphery in patients with UA, investigate its progress over time relative to that after uncomplicated AMI and to explore the mechanisms involved. Muscle sympathetic nerve activity (MSNA) assessed from multiunit discharges and from single units (s-MSNA) was obtained in matched patients with UA ( n =9), AMI ( n =14) and stable CAD (coronary artery disease, n =11), patients with chest pain in which AMI was excluded (NMI, n =9) and normal controls (NCs, n =14). Measurements were obtained 2-4 days after UA or AMI, and repeated at 3 monthly intervals until they returned to normal levels. The respective MSNA and s-MSNA early after UA (72+/-4.0 bursts/100 beats and 78+/-4.2 impulses/100 beats respectively) were less than those after AMI (83+/-4.4 bursts/100 beats and 93+/-5.5 impulses/100 beats respectively). Relative to the control groups of NCs (51+/-2.7 bursts/100 beats and 58+/-3.4 impulses/100 beats respectively) and patients with CAD (54+/-3.7 bursts/100 beats and 58+/-3.9 impulses/100 beats respectively) and NMI (52+/-4.5 bursts/100 beats and 59+/-4.9 impulses/100 beats respectively), values returned to normal after 6 months in UA (55+/-5.0 bursts/100 beats and 62+/-5.5 impulses/100 beats respectively) and 9 months after AMI (60+/-3.8 bursts/100 beats and 66+/-4.2 impulses/100 beats respectively). In conclusion, both UA and AMI result in sympathetic hyper-activity, although this is of smaller magnitude in UA and is less protracted than in AMI. It is suggested that this hyperactivity is related to the degree of left ventricular dysfunction and reflexes.     

Plasma cardiotrophin-1 following acute myocardial infarction: relationship with left ventricular systolic dysfunction.

The glycoprotein 130 (gp 130) signalling pathway is important in the development of heart failure. Cardiotrophin-1 (CT-1), a cytokine acting via the gp 130 pathway, is involved in the process of ventricular remodelling following acute myocardial infarction (AMI) in animals. The aims of the present study were to examine the profile of plasma CT-1 following AMI in humans, and its relationship with echocardiographic parameters of left ventricular (LV) systolic function. Serial measurements of plasma CT-1 levels were made in 60 patients at 14-48 h, 49-72 h, 73-120 h and 121-192 h following AMI and at a later clinic visit. LV function was assessed using a LV wall motion index (WMI) score on admission (WMI-1) and at the clinic visit (WMI-2). Compared with values in control subjects (29.5+/-3.6 fmol/ml), the plasma CT-1 concentration was elevated in AMI patients at 14-48 h (108.1+/-15.1 fmol/ml), 49-72 h (105.2+/-19.7 fmol/ml), 73-120 h (91.2+/-14.9 fmol/ml) and 121-192 h (118.8+/-22.6 fmol/ml), and at the clinic visit (174.9+/-30.9 fmol/ml) (P<0.0001). Levels were higher following anterior compared with inferior AMI. For patients with anterior AMI, CT-1 levels were higher at the clinic visit than at earlier times. WMI-1 correlated with CT-1 at all times prior to hospital discharge (P<0.05). On best subsets analysis, the strongest correlate with WMI-1 was CT-1 level at 49-72 h (R(2)=20%, P<0.05). In conclusion, plasma levels of CT-1 are elevated soon after AMI in humans and rise further in the subsequent weeks in patients after anterior infarction. CT-1 measured soon after AMI is indicative of LV dysfunction, and this cytokine may have a role in the development of ventricular remodelling and heart failure after AMI.