阿托伐他汀对不稳定型心绞痛患者树突状细胞功能的影响

目的 研究不稳定型心绞痛患者(UAP)树突状细胞(DC)的功能及阿托伐他汀对其的影响。方法 将27例UAP分为常规治疗组(12例)和常规加阿托伐他汀治疗组(15例),分别于治疗前及治疗后2周取血分离外周血单个核细胞,在含粒细胞巨噬细胞集落刺激因子和白细胞介素(IL)4的培养条件下制备DC。用流式细胞仪检测DC表面共刺激分子CD86(B7-2)的表达;混合淋巴细胞反应(MLR)检测DC对同种异体T淋巴细胞的刺激能力;ELISA法测定MLR上清液中的细胞因子;探讨CD86表达与冠心病危险因素及C反应蛋白(CRP)的相关性。结果 与正常对照组比较,UAP者DC表面CD86的表达明显增高;对T淋巴细胞刺激的能力增强;经DC刺激的淋巴细胞分泌致炎细胞因子(IL-1β,IL-6,肿瘤坏死因子α)增多,抑炎细胞因子(IL-10)减少;用药前CD86的表达与血LDL-C水平正相关;阿托伐他汀抑制DC功能的同时显著降低血CRP水平;且CD86与CRP水平正相关。结论 (1)UAP者DC的功能亢进,由此启动的T淋巴细胞的增殖和炎性细胞因子分泌可能是UAP者动脉斑块不稳定的原因,(2)LDL-C可能是其刺激因素;(3)阿托伐他汀抑制斑块炎症的机制之一是其对DC的抑制。     

Hemodynamic observations in patients with unstable angina pectoris

Brachial and pulmonary arterial pressures were monitored for 48 hours in 26 patients with unstable angina pectoris and documented occlusive coronary artery disease. The circulatory response during 56 episodes of spontaneous anginal pain permitted the division of responses into three distinctive hemodynamic subsets. Patients in group I had an increased heart rate only with the spontaneous attack of angina; patients in group II had associated increases in brachial arterial pressure and slight increases in heart rate during the episodes of pain; patients in group III demonstrated increases in both brachial and pulmonary arterial diastolic pressures with minimal changes in heart rate. Resting hemodynamic data during pain-free periods were normal in 25 of 26 patients. Patients in all groups who had more than one episode of pain had similar hemodynamic responses to the first and later episodes. Although myocardial hypoxemia appears to be responsible for the spontaneous attack of angina, the hemodynamic responses to the attack varied but were highly specific for any one patient.Our observations suggest that there may be various pathogenic mechanisms for “spontaneous” or resting angina in patients with occlusive coronary artery disease but that the mechanism and associated hemodynamic changes may be specific for individual patients.     

Glutathione reductase levels in patients with unstable angina

Experimental evidence suggests that free-radical damage and antioxidant defense may play an important role in the pathogenesis of coronary heart disease. We have examined the association between plasmatic glutathione reductase (GR) levels and the prognosis of patients with unstable angina. We have evaluated 37 patients, under the age of 75, diagnosed with unstable angina and 19 healthy volunteers. The patients were divided into two groups: the first group--10 patients with unstable angina with readmission in the following 6 months--and the second group--27 patients with unstable angina and favourable evolution. GR was measured in dynamics during hospitalization period. After discharge, the patients were monitored and the following data were recorded: months of follow-up, death due to cardiovascular cause and onset of major cardiovascular events. In patients with unstable angina there was a statistically significant higher increase of GR on admission to the values of the control group (p < 0.0001). Subsequently, plasmatic levels begin to decline, so that at discharge, the GR is similar to the control group. Plasmatic levels of GR were statistically significantly lower in patients with unstable angina without cardiovascular event than in patients with readmission in the following months (p < 0.05). In conclusion, patients who experienced unstable angina and without cardiovascular events during follow-up had lower GR plasmatic levels and that GR activity was an independent predictor of cardiovascular events during follow-up.     

Plasma thioredoxin levels in patients with unstable angina

Plasma levels of human thioredoxin are indicative of the responses against oxidative stress. We measured the plasma thioredoxin levels in patients with unstable angina in order to examine the relationships between subsequent clinical course and plasma thioredoxin levels before and after treatment for unstable angina. Blood was sampled both on admission and after treatment in 44 patients with unstable angina. In addition, blood samples were obtained from 41 patients with stable exertional angina and 41 patients with chest pain syndrome after admission. The plasma levels of thioredoxin were the highest in the unstable angina group among three groups (p<0.001). Treatment of unstable angina decreased the plasma thioredoxin levels (p<0.01). We divided the patients with unstable angina into two groups according to the plasma thioredoxin levels on admission and after treatment. There was a significant difference in Braunwald's classification between the high thioredoxin and the low thioredoxin group on admission, as analyzed by the chi2 test with Yates's correction (p<0.05). Moreover, there was a significant difference in incidence of recurrent anginal attacks at rest between the high thioredoxin and the low thioredoxin group after treatment, as analyzed by the chi2 test with Yates's correction (p<0.001). The present study demonstrated that plasma thioredoxin levels are significantly increased in patients with unstable angina compared to those with stable exertional angina and chest pain syndrome. Thioredoxin levels were associated with recurrent myocardial ischemia in patients with unstable angina.     

Enoxaparin in unstable angina patients with renal failure

The dosage of the subcutaneous low molecular weight heparin enoxaparin in unstable angina patients undergoing coronary angiogram and coronary angioplasty depends clearly on the renal function. It should be significantly reduced to 64% of the standard dose (1 mg/kg per 12 h) in patients with severe renal failure (creatinine clearance<30 ml/min) to provide a safe anticoagulant profile.     

曲美他嗪治疗不稳定型心绞痛的疗效分析

目的　观察曲美他嗪与传统药物相结合治疗对冠心病不稳定型心绞痛患者心肌缺血的保护作用。方法　将 60例冠心病不稳定型心绞痛患者随机分成两组 ,治疗组 3 0例 ,除用硝酸酯类、β-阻滞剂等传统药物治疗外 ,加用曲美他嗪 2 0 mg,每日 3次口服。对照组 3 0例接受传统药物治疗 ,连续观察 4周。观察两组患者心绞痛发作次数、心电图缺血性 ST-T的疗效及血压、心率的变化。结果　治疗组心绞痛发作次数较对照组明显减少分别为 [( 3 .2± 1.4)次 ,( 5 .7± 1.6)次 ]两组比较 P<0 .0 5 ,心电图缺血性 ST-T改善的疗效明显好于对照组 ,P<0 .0 5 ,而两组的心率、血压变化无明显差异。结论　曲美他嗪作为一种影响代谢的药物 ,对改善心肌缺血有良好的效果 ,且方法简便 ,疗效显著 ,安全可靠 ,易于接受。     

替罗非班治疗老年不稳定型心绞痛临床观察

目的 探讨血小板糖蛋白Ⅱb/Ⅲa受体拮抗剂替罗非班治疗老年不稳定型心绞痛的有效性和安全性.方法 将＞60岁＜80岁确诊为不稳定型心绞痛（高危组）的138例患者随机分为2组,对照组66例给予阿司匹林、氯吡格雷、低分子肝素、硝酸酯类及其他常规治疗,试验组72例在以上治疗基础上加用替罗非班,48 h持续静脉泵入.观察两组心绞痛症状缓解情况和心电图ST段变化,记录用药后48 h、1周、1个月心脏不良事件包括顽固性心绞痛、心肌梗死、心源性猝死及出血等不良反应发生.结果 与对照组相比,试验组心绞痛缓解有效率高,心电图压低ST明显改善（P＜0.05）,心脏不良事件发生率降低.两组均无严重不良反应,轻微出血反应试验组略高于对照组,但无统计学意义.结论 在阿司匹林、氯吡格雷、低分子肝素基础上加用替罗非班治疗老年不稳定型心绞痛安全、有效.     

不稳定性心绞痛患者循环内皮祖细胞与血管内皮功能的变化

目的探讨不稳定性心绞痛患者外周血循环内皮祖细胞(EPCS)与血管内皮功能的变化。方法采用高分辨率血管超声法检测30例不稳定性心绞痛患者与30例正常者作对照组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);流式细胞仪测定外周血中CD34+单个核细胞的水平;外周血分离单个核细胞一定条件下培养2周,免疫组织化学技术鉴定培养贴壁细胞表面标志CD34的表达;倒置荧光显微镜鉴定贴壁细胞FITC-UEA-I和DII-ACLDL双染色阳性细胞为正在分化的EPCS。结果不稳定性心绞痛组FMD明显低于对照组[(5·85±3·04)%比(8·81±4·48)%,P<0·05];NMD在两组中差异无统计学意义[(13·60±5·03)%比(14·18±4·50)%,P>0·05];CD34+细胞水平明显高于对照组[(0·13±0·05)%比(0·09±0·04)%,P<0·05];FMD与CD34+细胞水平呈负相关(R=-0·385,P<0·05)。培养的贴壁细胞免疫组化显示CD34阳性,倒置荧光显微镜显示这些贴壁细胞FITC-UEA-I和DII-ACLDL双染色阳性。结论不稳定性心绞痛患者CD34+细胞增加和血管内皮功能受损,提示循环EPCS增加可能是对急性冠状动脉缺血和内皮损伤的代偿反应。     

Serial ambulatory monitoring in patients with unstable angina pectoris

We performed a prospective study by dual-channel ambulatory monitoring performed for 24 to 72 hours immediately after hospitalization for unstable angina. The incidence of ST-segment depression or elevation or ventricular tachycardia or complex premature ventricular complexes (PVCs) in 42 consecutive patients with unstable angina due to coronary artery disease (39 by coronary arteriography) was investigated. During ambulatory monitoring, 28 of 42 patients (67%) exhibited ST-segment depression or elevation, 13 of 42 patients (31%) had ventricular tachycardia or complex PVCs, and 31 of 42 patients (74%) had either ST-segment depression or elevation, ventricular tachycardia, or complex PVCs. Ventricular tachycardia or complex PVCs occurred in 10 of 20 patients (50%) with abnormal left ventricular function and in 3 of 22 patients (14%) with normal left ventricular function (p less than 0.025). We found that 72 hours of ambulatory monitoring was not more useful than 48 hours in detecting the incidence of ST-segment depression or elevation, ventricular tachycardia, or complex PVCs. Ambulatory monitoring did not help in clinically differentiating patients with left main or 3-vessel disease from 1-vessel or 2-vessel disease. In addition, ambulatory monitoring did not help in predicting which patients with unstable angina would require coronary artery surgery.     

Thoracic epidural anaesthesia in patients with unstable angina pectoris

The effect of high thoracic epidural anaesthesia with intermittentepidural bolus injections of bupivacaine (2.5 or 5 mg ml^-1)was studied in 28 patients with unstable angina pectoris. Themajority of the patients had a history of previous acute myocardialinfarction(s) and/or angina pectoris and severe coronary arterydisease. All patients were treated wth nitroglycerin infusionfor gt;24 h and were included in the study if they had chestpain, not caused by acute myocardial infarction, at bed restor recurrent anginal pain at rest < 2 days after infarction.4.4 ± 0.3 ml of bupivacaine induced a blockade of theupper seven sympathetic segments ( Th_1-7) for 98 ± 9min.Heart rate decreased significantly from 70 ± 3 to 64± 3 beats min^-1 while blood pressure was unaffected bythoracic epidural anaesthesia. In 27 patients (96%) the anaesthesiainduced complete analgesia. Nitroglycerin infusion was discontinueddefinitely within 3 h in 26 patients (93%) and pain was thereaftercontrolled by means of thoracic epidural anaesthesia as thesole treatment in 23 patients (82%) and as the major treatmentin 25 patients (89%). Twenty-one patients (75%) were fully mobilizedand stabilized. Treatment with thoracic epidural anaesthesialasted for 6.0 ± 1.1 days. The number of daily epiduralinjections decreased significantly with time from 2.7 ±0.3the first day to 0.9 ± 0.3 the fourth day (P>0.01,n = 19). Two patients developed acute myocardial infarctionduring the anaesthesia treatment period, and one of these patientsdied. Exercise stress testing was performed on eight patients threeto five days after the start of thoracic epidural anaesthesia.At a comparable workload, ST-segment depression was significantly(P>0.05) less pronounced during anaesthesia ( – 0.6± 0.1 mm) compared with control ( – 1.3 ±0.2mm). The respective heart rate values were 95 ± 7and 107 ± 7 beats min ^-1 (P > 0.05), while systolicor diastolic blood pressure did not differ between the two conditions. We conclude that blockade of cardiac sympathetic afferents andefferents by means of thoracic epidural anaesthesia can effectivelytreat pain and stabilize patients with unstable angina pectorisrefractory to medical treatment. Furthermore, thoracic epiduralanaesthesia attenuates stress-induced myocardial ischaemia;thus, it may be an efficient supplementary treatment for thecontrol of pain and for stabilizing patients with unstable anginapectoris during diagnostic procedures and prior to coronarysurgery or angioplasty.     

Cardiac multidetector-row computed tomography in patients with unstable angina

Ideally, information on coronary artery stenosis and left ventricular (LV) function is obtained in patients who have unstable angina to allow optimal risk stratification. The value of multidetector-row computed tomography (MDCT) was evaluated for a simultaneous assessment of coronary artery disease and global/regional LV function using a single acquisition. Twenty-five patients who had unstable angina underwent a single multidetector-row computed tomographic acquisition using a 4-slice multidetector-row computed tomographic system. Based on retrospective electrocardiographic gating, images and cine movies were reconstructed, which allowed 2 independent observers to analyze the 9 major coronary artery segments and global/regional LV function. Conventional angiography (with quantitative analysis) and echocardiography served as standards of reference, which were performed /=50%) coronary artery stenosis was detected with sensitivities, specificities, and positive and negative predictive values of 95%, 91%, 85%, and 97% for observer 1 and 89%, 87%, 79%, and 94% for observer 2, respectively; the interobserver kappa value was 0.73. MDCT showed excellent agreement with echocardiography for regional wall motion (90%; kappa = 0.88) and LV ejection fraction (correlation 0.95%, mean difference 0.7 +/- 3.9). Thus, MDCT can simultaneously assess coronary artery disease and LV function in patients who have unstable angina. High accuracies in excluding significant coronary artery disease and in confirming normal LV function were observed, suggesting potential clinical use for screening of patients who present with symptoms of unstable angina.     

Coronary artery thrombosis in patients with unstable angina.

This report describes the clinical course, coronary artery anatomy, and ventricular function of 16 patients in whom coronary artery thrombosis was detected at the time of cardiac catheterisation. All patients had an unstable clinical course in which accelerated angina occurred a mean of four weeks (range four days to 12 weeks) before catheterisation, and four patients had recent subendocardial myocardial infarction. In all patients severe coronary artery disease was documented at catheterisation. Fifteen patients had segmental wall motion abnormalities involving the left ventricular wall that was supplied by the coronary artery in which there was thrombus. Three patterns of coronary artery thrombus were noted: (1) Thrombus proximal to high-grade coronary artery stenosis; (2) thrombus distal to high-grade coronary artery stenosis; and (3) thrombus in segments of the arterial tree in which there was no high-grade coronary artery stenosis. Though the precise cause of the coronary artery thrombosis in our patients is unknown, it may have been a result of stasis, a ruptured atherosclerotic plaque, or coronary spasm. The common clinical course with unstable angina of acute onset suggests the possibility that the thrombus may have been responsible for the abrupt change in clinical condition or may have been a contributing factor in the patients' course.     

Circulating endothelial progenitor cells in patients with unstable angina: association with systemic inflammation.

BACKGROUND: Endothelial progenitor cells (EPC) are present in peripheral blood and can develop a functional endothelial phenotype. The number and function of circulating EPCs are altered in atherosclerosis, diabetes, and after myocardial infarction and EPCs have been shown to promote postnatal angiogenesis and vasculogenesis. We investigated the number and adhesive properties of EPCs from patients with unstable angina and no evidence of cardiac necrosis. METHODS AND RESULTS: Patients were selected with unstable angina (n=29) and no evidence of cardiac necrosis, and controls with stable angina (n=12) and atherosclerotic risk factors, medication use, and coronary vessel involvement similar to patients. Circulating EPC numbers were determined by colony-forming unit assay and their adhesive properties were evaluated by EPC capacity to bind immobilised fibronectin. High-sensitivity C-reactive protein (hsCRP) was determined in all patients. Circulating EPCs were significantly increased in patients with unstable as compared with stable angina (24.5+/-2.6 vs. 13.3+/-2.9, respectively). Seven unstable angina patients followed up for 3 months after clinical stabilisation exhibited a reduction of close to 50% in circulating EPC numbers. The adhesive capacity of EPCs from patients with unstable and stable angina did not differ. A positive correlation was found between systemic CRP levels and circulating EPC numbers, but not their adhesive capacity. CONCLUSION: Patients with unstable angina and no evidence of cardiac necrosis exhibited increased circulating EPCs. Systemic inflammation, in addition to recognised growth factors, could play a role in the peripheral mobilisation of EPCs in patients with anginal syndromes.