肌氨肽苷治疗老年冠心病心衰的临床观察

选择老年冠心病心衰患者79例,随机分成观察组(36例)和对照组(43例).两组均予以血管紧张素转换酶抑制剂(ACEI)、β受体阻滞剂、利尿剂、洋地黄制剂及抗感染等常规治疗,观察组和对照组分别在此基础上加用肌氨肽苷和硝酸甘油静点治疗,疗程10 d,观察两组治疗前后心功能指标变化、血压、心率及治疗期间头痛的发生情况,并进行统计学分析.结果治疗后两组临床疗效满意,且治疗前后比较血流动力学指标均明显改善(P<0.01),但两组比较差异无统计学意义.观察组头痛发生率为3%,而对照组为19%,两组头痛发生率差异有统计学意义(P<0.05)).认为肌氨肽苷治疗老年冠心病心衰的疗效和硝酸甘油相当,但头痛发生率明显降低.     

老年冠心病患者血管内皮功能与动脉粥样硬化的关系

目的 观察老年冠心病(CAD)患者血管内皮舒张功能、动脉硬化的状况及与冠状动脉病变的相关性.方法 选择经冠状动脉造影确诊为CAD的患者90例(CAD组),冠状动脉造影证实无冠状动脉狭窄并无其他疾病史的患者30例为对照组,采用二维超声检测肱动脉内皮依赖性和非依赖性舒张功能及动脉内膜的变化,应用二维彩色多普勒超声检查颈动脉、股动脉,观察管腔、管径、内膜及有无斑块、血流变化、血流频谱形态及性质.动脉粥样硬化斑块积分采用Crouse法.对血管内皮细胞功能、动脉硬化与冠状动脉病变程度进行分析.结果 反应性充血引起的肱动脉内径变化在单支组及多支组明显减弱[(9.08±2.28)%、(6.14±2.21)%],与对照组[(15.58±2.20)%]比较,差异有统计学意义(P<0.01).CAD组颈动脉内膜中层厚度(IMT)高于对照组(P<0.05).结论 内皮细胞功能障碍和动脉粥样硬化与冠状动脉粥样硬化的病变密切相关.     

肌氨肽苷治疗冠心病不稳定型心绞痛52例

目前认为猝死和急性心肌梗死与不稳定型心绞痛有密切关系 ,有效控制不稳定型心绞痛可预防猝死和急性心肌梗死。现治疗不稳定型心绞痛的药物一般应用硝酸酯类、β受体阻滞剂、钙离子拮抗剂及抗凝剂 ,但亦有部分病人控制不理想 ,在条件好的医院可行经皮冠状动脉造影 ,以了解冠状动脉病变 ,但对基层医院使用药物治疗还是常用的手段。笔者应用肌氨肽苷治疗不稳定型心绞痛 5 2例 ,现将观察结果报道如下。1　资料与方法1.1　一般资料　选择我院 2 0 0 1年 10月— 2 0 0 2年 12月收入院的不稳定型心绞痛病人 98例 ,符合 1979年WHO关于《缺血性心…     

冠心病患者循环内皮祖细胞与血管内皮功能的变化

目的:探讨冠心病患者循环内皮祖细胞(EPCs)数量及功能变化与血管内皮舒张功能的关系。方法:将58例患者分为对照组(20例)、稳定性心绞痛组(11例)、不稳定性心绞痛组(27例)。采用高分辨率二维超声检测肱动脉血流介导的内皮依赖性血管舒张功能(FMD)及硝酸甘油介导的非内皮依赖性血管舒张功能(NMD);用密度梯度离心法从外周血获取单个核细胞,将其接种在人纤维连接蛋白包被培养板,培养7天后贴壁细胞进行细胞化学分析,激光共聚焦显微镜鉴定异硫氰酸荧光素标记荆豆凝集素I和DiI标记的乙酰化低密度脂蛋白双染色阳性细胞为正在分化的EPCs,采用二苯基四氮唑嗅盐比色法、改良的Boyden小室和黏附能力测定实验观察内皮祖细胞的增殖能力、迁移能力和黏附能力。结果:①稳定性心绞痛组与不稳定性心绞痛组的FMD均明显低于对照组,有显著性差异(P<0．05～0．01),而稳定性心绞痛组的FMD较不稳定性心绞痛组也降低,有显著性差异(P<0．05);3组间NMD差异无统计学意义(P>0．05)。②稳定性心绞痛组、不稳定性心绞痛组较对照组循环EPCs数量明显减少,且黏附、迁移及增殖能力也明显下降,均有极显著性差异(P<0．01);不稳定性心绞痛组较稳定性心绞痛组EPCs数量及迁移能力无差异(P>0．05),但黏附和增殖能力降低(P<0．05)。③直线相关性分析发现不稳定性心绞痛组EPCs的数量及功能均与FMD呈正相关(P<0．05),而稳定性心绞痛组仅EPCs黏附功能与FMD呈正相关(P<0．05)。结论:冠状动脉EPCs数量及功能下降与血管内皮依赖性舒张功能障碍一致,提示当冠心病患者血管内皮功能受损而又缺乏足够有效的EPCs时,可能影响冠心病的病情程度及临床表现。     

停用辛伐他汀对冠心病及冠心病危险因素患者血管内皮功能的影响

目的 观察在冠心病及冠心病危险因素患者中,停用辛伐他汀治疗对血管内皮功能的影响,并探讨相应作用机制。方法 入选33例血清胆固醇（Tc）水平未达标的冠心病及冠心病危险因素患者,分别于基线水平、停药前（即辛伐他汀20mg治疗4周后）及停用辛伐他汀1周时,采用高分辨超声技术检测肱动脉血流介导性扩张（FMD）评估血管内皮依赖性舒张功能,并测定一氧化氮（NO）、血浆内皮素（ET）、6-酮-前列腺素F1α（6-keto-PGF1α）和血栓素B2（TXB2）的水平及主要血脂参数的变化。结果 辛伐他汀治疗4周后可有效降低冠心病及冠心病危险因素患者TC、低密度脂蛋白胆固醇（LDL-C）水平,并明显改善患者肱动脉内皮依赖性舒张功能（FMD）。然而,停用辛伐他汀治疗1周后,所有患者肱动脉内皮依赖性舒张功能均较停药前明显下降（4．82士0．71）％与11．51±0．87％,P〈0．01）,甚至低于未服用辛伐他汀时的基线水平（4．82±0．71％与5．89±0．65％,P〈0．01）,其中冠心病患者停药后FMD下降幅度较仅有冠心病危险因素患者更显著（65．6％与56．3％,P〈0．01）。停药1周后,患者血清NO水平较停药前及基础值均明显降低,而血浆ET水平升高。血浆TXB,水平在停药前后无明显变化。此外,停药后患者血清LDL-C水平虽较治疗4周时有所升高,但仍未恢复至基线水平。停药后肱动脉FMD的变化仅与血清NO降低幅度呈正相关关系（r=0．674。P=0．004）,而与血清LDL-C水平变化无明显相关性（r=-0．414,P=0．083）。结论 在TC水平未达标的冠心病及冠心病危险因素患者中突然终止辛伐他汀治疗可在1周内完全逆转该药对血管内皮功能的改善作用,甚至还可能导致血管内皮功能进一步恶化。并且这种撤药反应随基础疾病的严重性增加。停药所致血管内皮功能损害可能与血管内皮源性的NO减少有关,是非胆固醇依赖性作用。     

肌氨肽苷治疗冠心病心力衰竭的疗效观察

我们应用肌氨肽苷与硝酸酯类药物治疗冠心病所致心力衰竭，进行疗效对比观察。     

注射用肌氨肽苷治疗急性冠脉综合征的临床用药观察

目的观察注射用肌氨肽苷治疗急性冠脉综合征(ACS)的临床效果。方法将58例ACS患者随机分为注射用肌氨肽苷治疗组(观察组)和常规治疗组(对照组),每组29例。对照组给予常规的硝酸酯类药物和阿司匹林、氯吡格雷抗凝治疗,观察组在常规治疗基础上加用肌氨肽苷。结果 ACS治疗中加用肌氨肽苷,能有效改善患者症状及心电图。结论 ACS治疗中加用肌氨肽苷疗效好。     

叶酸对冠心病患者支架术后血管内皮功能的影响

目的 探讨叶酸能否改善冠心病患者支架术后的血管内皮功能.方法 共184例冠心病患者,在行冠状动脉支架术后,随机分为叶酸治疗（20 mg/d）92例和对照组92例.随访6个月,观察两组同型半胱氨酸水平.以超声测定肱动脉血流介导的舒张功能（FMD）变化来评价血管内皮功能,并观察两组间的差别.结果 叶酸治疗组血浆同型半胱氨酸水平低于对照组[（8.83±3.33）μmol/L比（13.18±5.08）μmol/L,P＜0.01].叶酸治疗后,FMD由（4.72±1.73）%增加至（8.54±1.45）%,P＜0.01.结论 叶酸治疗可能通过降低同型半胱氨酸以外的途径改善血管内皮功能,对介入治疗后的冠心病患者发挥潜在益处.     

肌氨肽苷治疗脑梗死32例临床观察

目的探讨肌氨肽苷治疗脑梗死的疗效.方法将我院收治的脑梗死患者64例,随机分为治疗组32例,给予肌氨肽苷治疗20d,对照组32例,给予胞二磷胆碱治疗20d,其余治疗基本相同.结果总有效率:治疗组93.8%,对照组81.3%;治愈率:治疗组34.3%,对照组31.3%,治疗组疗效优于对照组.结论肌氨肽苷治疗脑梗死临床效果好、疗效显著.     

肌氨肽苷治疗不稳定型心绞痛的疗效

目的:评价肌氨肽苷注射液对不稳定型心绞痛的疗效。方法:80例不稳定型心绞痛患者随机分为两组,治疗组:以肌氨肽苷8ml加入5%葡萄糖液250ml中静滴治疗;对照组:以硝酸甘油(NTG)20mg加入5%葡萄糖液250ml中静滴治疗。结果:肌氨肽苷组临床疗效总有效率95.2%,NTG组总有效率73.7%(P<0.05)。两组均能减小二项乘积(RPP,收缩压×心率)及ECG的∑ST(P<0.05),但肌氨肽苷组减少∑ST更著(P<0.05),且肌氨肽苷能改善左室射血分数等心功能指标(P<0.05)。结论:肌氨苷比NTG更有效地改善不稳定型心绞痛患者的症状,心电图缺血和心功能。     

辛伐他汀对冠心病患者血管内皮功能作用的时效关系

目的探讨辛伐他汀改善冠心病患者血管内皮功能的时效关系。方法共入选30例确诊冠心病患者,每天服用辛伐他汀20mg,进行1年随访。采用超声法检测血流介导的肱动脉内皮依赖性舒张功能(flow mediated dila-tion,FMD),同时观察血脂水平、肝肾功能、血糖以及心肌酶学的变化。结果完成50周随访的25例冠心病患者,辛伐他汀(20mg/d)服后2周、4周、8周、12周及50周可分别使患者血清总胆固醇(TC)降低18.9%、24.3%、29.0%、30.1%、29.4%,低密度脂蛋白胆固醇(LDL-C)降低20.1%、26.8%、34.7%、36.0%、35.2%。辛伐他汀治疗可显著改善冠心病患者的血管内皮功能,FMD较治疗前明显增加,2周:64%,4周:95%,8周:123%,12周:179%,52周:142%(2周、4周P<0.05;8周、12周、52周P<0.01)。FMD的改善与血清TC和LDL-C降低水平无显著相关,而与基础FMD有关。所有患者耐受性好,无明显不良反应。结论辛伐他汀治疗冠心病患者2周时,血管内皮功能即有改善,8~12周达高峰,长期治疗能产生持续的血管内皮功能改善。     

辛伐他汀对冠心病患者血管内皮功能作用的量效关系

目的探讨不同剂量(5mg,10mg,20mg)的辛伐他汀对冠心病患者血管内皮功能的作用及其量效关系。方法共入选80例冠心病患者,随机分为4组:对照组(不服用辛伐他汀),辛伐他汀5 mg组、辛伐他汀10 mg组、辛伐他汀20 mg组、每组20例,治疗8周。采用超声法检测血流介导的肱动脉内皮依赖性舒张功能(FMD),同时观察血脂水平的变化。结果辛伐他汀治疗8周后,5 mg、10 mg、20 mg呈剂量依赖性显著降低血总胆固醇(分别降低9%,18%,29%)和低密度脂蛋白胆固醇水平(分别降低12%、24%、35%),不同剂量组间P<0.05。对照组治疗8周后血脂水平无明显变化(P>0.05)。5 mg、10 mg、20 mg的辛伐他汀均可显著改善FMD[5mg:(3.41±2.99)%VS(7.46±5.11)%;10mg:(3.76±3.01)%比(7.98±4.92)%;20mg:(3.59±3.47)%比(8.09±6.10)%;P均<0.01]。但三组之间FMD的变化值比较无显著差异(P>0.05),且FMD的改善与血TC、LDL-C水平的降低不相关。对照组FMD虽有轻度增加,但无统计学意义。辛伐他汀治疗后肱动脉内径、肱动脉对硝酸甘油的反应均无显著改变。结论辛伐他汀5 mg、10 mg、20 mg治疗8周后,可显著改善冠心病患者血管内皮功能,但该作用无明显的量效关系,可能独立于调脂作用之外。     

阿司匹林和西洛他唑对冠心病合并糖尿病患者血小板聚集活性的影响

目的:探讨阿司匹林对冠心病合并糖尿病患者血小板聚集活性的影响;西洛他唑对血小板聚集活性作用是否有类似改变。方法:入选的冠心病患者中合并与合并2型糖尿病患者各45例。根据其口服药物又分为阿司匹林组、西洛他唑组和联合用药组,每组各15例。记录患者基本情况并测定血小板聚集活性、血浆血栓素(TX)B2、6-K-前列腺素(PG)F1a和髓过氧化物酶(MPO)水平,并进行统计分析。结果:(1)多元逐步回归分析显示血糖是影响血小板聚集的独立因素(R=0.914,P<0.01);(2)方差分析显示糖尿病患者血小板聚集活性、血浆TXB2、MPO水平较非糖尿病患者明显增高,6-K-PGF1a水平降低(P<0.001);(3)非糖尿病患者阿司匹林组和西洛他唑组血小板聚集活性和TXB2没有明显差异,西洛他唑组血浆6-K-PGF1a水平高于阿司匹林组,而MPO水平低于阿司匹林组(P<0.001);糖尿病患者西洛他唑组血小板聚集活性、TXB2和MPO水平低于阿司匹林组,而6-K-PGF1a水平高于阿司匹林组(P<0.05~0.001)。结论:对冠心病合并糖尿病患者西洛他唑较阿司匹林可以更有效地抑制血小板聚集。     

Thrombopoietin and platelet aggregation in patients with stable coronary artery disease

Thrombopoietin (TPO) may facilitate platelet activation and aggregation. However, data on the impact of TPO on platelet aggregation in patients with stable coronary artery disease (CAD) are scarce. We aimed to investigate associations between TPO and platelet aggregation and activation in patients with stable coronary artery disease (CAD). We studied 900 stable CAD patients. Serum TPO was assessed by ELISA. Platelet aggregation was evaluated using the Multiplate Analyzer (agonists: arachidonic acid [AA] and collagen) and the VerifyNow Aspirin Assay. Platelet activation was evaluated by soluble (s)P-selectin. Cyclooxygenase-1 inhibition was evaluated by serum thromboxane B₂ (TXB₂). We found that TPO correlated weakly with platelet aggregation evaluated by Multiplate using AA (r = ?0.09, p = 0.01) and collagen as agonists (r = ?0.03, p = 0.43) and by VerifyNow (r = 0.07, p = 0.03). We found no correlation between TPO and sP-selectin (r = ?0.01, p = 0.70). Independent predictors of AA-induced platelet aggregation by Multiplate included high levels of sP-selectin and serum TXB₂, high platelet count, increasing age and body mass index, female sex, and active smoking. Independent predictors of TPO included low AA-induced platelet aggregation by Multiplate, high levels of hs-CRP, active smoking, and high platelet aggregation evaluated by VerifyNow. In conclusion, TPO levels did not correlate with platelet activation and only weak associations were found between TPO and platelet aggregation, suggesting that TPO did not substantially facilitate platelet aggregation in stable CAD patients.     

抵克力得对冠心病患者血小板聚集功能的影响及意义

目的:探讨冠心病患者血小板聚集功能和抵克力得的影响。方法:选择体检正常者、不稳定心绞痛(UAP)和急性心肌梗死(AMI)患者各20例,测定三组血小板聚集功能和后两组服用抵克力得后,由二磷酸腺苷(ADP)、肾上腺素(EP)诱导的血小板聚集功能的变化。结果:UAP组和AMI组血小板聚集率明显高于对照组(P<0.001); 服抵克力得后血小板聚集率均明显降低(P<0.001)。结论:冠心病患者血小板聚集功能明显增强,抵克力得对它有明显抑制作用。     

High platelet reactivity is associated with vascular function in patients after percutaneous coronary intervention receiving clopidogrel

Background

In the present study, we evaluated the association of platelet reactivity with vascular function in patients after percutaneous coronary intervention receiving clopidogrel treatment.

Methods

We enrolled 150 patients with stable CAD receiving clopidogrel regimen (75 mg/d), 1 month after percutaneous coronary intervention. Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) as an index of arterial wave reflections. High on treatment platelet reactivity (HPR) was evaluated using VerifyNow Assay. VerifyNow reports its results in P2Y12 reaction units (PRU), and the diagnostic cutoff value is 230 PRU. Patients were evaluated prospectively up to 24 months. The primary end point was a composite of death from cardiovascular causes, nonfatal major cardiovascular events and hospitalization for cardiovascular causes.

Results

There was no difference in the basic clinical and demographic characteristics between subjects with HPR and non-HPR. Subjects with high on treatment platelet reactivity and PRU > 230 had significantly increased PWV (8.81 ± 2.25 m/s vs. 7.69 ± 1.95 m/s, p = 0.001) and AIx (25.27 ± 8.67% vs. 20.87 ± 10.57%, p = 0.04) compared to subjects with PRU ≤ 230. PWV was also associated with PRU (r = 0.23, p = 0.02). HPR was associated with significantly increased risk of primary end point [HR = 5.38, 95%CI:(1.15, 26.04), p = 0.03].

Conclusions

Increased platelet reactivity is associated with impaired arterial stiffness in patients after percutaneous coronary intervention receiving clopidogrel treatment, highlighting another clinical factor implicated in individual platelet response to antiplatelet therapy. Moreover, increased platelet reactivity is associated with adverse outcome in these patients.     

冠心病患者血清血管内皮生长因子水平与冠状动脉病变程度的关系

目的 :探讨冠心病 (CHD)患者血清血管内皮生长因子 (VEGF)水平与冠状动脉病变的关系。方法 :采用酶联免疫吸附法 (ELISA)检测了 12 4例经冠状动脉造影证实有一支以上主要冠状动脉狭窄≥ 5 0 %的CHD患者血清VEGF水平 ,并作相关分析。结果 :CHD组血清VEGF水平明显高于正常对照组〔(2 93.2± 12 6 .3)ng/L∶(12 0 .1± 31.5 )ng/L ,P <0 .0 1〕 ,双支和三支血管病变患者血清VEGF水平高于单支组〔(2 83.4± 85 .0 )ng/L ,(398.1± 10 5 .5 )ng/L∶ (191.7± 2 7.3)ng/L ,P <0 .0 1〕 ,随着血管狭窄程度的加重 ,血清VEGF水平升高越明显 ,两者呈显著正相关 (r =0 .78,P <0 .0 0 1) ,CHD并发高血压和 (或 )糖尿病对血清VEGF水平无显著影响 (P >0 .0 5 )。结论 :CHD患者血清VEGF水平升高 ,其升高程度与冠状动脉病变程度有良好的相关性     

Role of circulating vascular endothelial growth factor and hepatocyte growth factor in patients with coronary artery disease

Vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) are thought to stimulate endothelial cell proliferation and induce angiogenesis in vivo. However, the precise mechanism responsible for VEGF and HGF release in patients with coronary artery disease is still unknown. We studied serum concentrations of VEGF and HGF in 20 patients with acute myocardial infarction (AMI), 20 patients with stable angina pectoris (AP) who had reversible perfusion defects on stress myocardial scintigraphy, and 16 patients with old myocardial infarction (OMI) who had no reversible defects on stress myocardial scintigraphy. The control group consisted of 20 patients with atypical chest pain who had angiographically normal coronary arteries. Serum VEGF and HGF concentrations were measured by enzyme-linked immunosorbent assay. Both the serum VEGF and HGF concentrations in the early stage of myocardial infarction in the patients with AMI were higher than those in the patients with AP and with OMI, and control patients. The VEGF concentration in the patients with AP was higher than in the patients with OMI, whereas the HGF concentration did not differ in the patients with AP and OMI. The VEGF concentration in AMI patients who had had preinfarction angina on admission was higher than that of patients who had had no preinfarction angina, whereas the HGF concentration did not differ between the two groups of patients. These results suggest that the serum VEGF concentration may reflect myocardial ischemia to a greater degree than the serum HGF concentration. Received June 9, 2000 / Accepted September 30, 2000