Coronary angioscopy in patients with unstable angina pectoris

To visualize intracoronary lesions in patients with different clinical expressions of coronary disease, we performed coronary angioscopy during coronary-artery bypass surgery in 10 patients with unstable angina and 10 patients with stable coronary disease. We examined a total of 32 vessels, using flexible fiberoptic angioscopes. Twenty-two vessels had no acute intimal lesion; three had complex plaques, six had thrombi, and one had both. Coronary angiography correctly identified the absence of complex plaque and thrombus in 22 vessels, but it detected only one of four complex plaques and one of seven thrombi. On angioscopy, none of the 17 arteries in the patients with stable coronary disease had either a complex plaque or thrombus. In the "offending" arteries of the patients with unstable angina, all three patients with accelerated angina had complex plaques and all seven with angina at rest had thrombi. We conclude that angioscopy frequently reveals complex plaques or thrombi not detected by coronary angiography. Our observations suggest that anginal syndromes that are refractory to medical treatment can be caused by unstable pathologic processes in the intima. Ulceration of plaques may increase the frequency and severity of effort angina, and the subsequent development of partially occlusive thrombi may cause unstable rest angina.     

Skeletal muscle training in chronic heart failure

Patients with heart failure are limited in their ability to tolerate exercise. Recent research has suggested that this limitation cannot be entirely attributed to cardiac or lung impairment but rather that changes in peripheral muscles may play an important role. There are objective similarities between heart failure and muscular deconditioning. Deficiencies in peripheral blood flow and skeletal muscle function, morphology, metabolism and function are present in both conditions. Moreover, an exaggerated activity of the receptors sensitive to exercise‐derived metabolic signals (muscle ergoreceptors and peripheral and central chemoreceptors) leads to early and profound exercise‐induced fatigue and dyspnoea. These muscle afferents contribute to the ventilatory, haemodynamic and autonomic responses to exercise both in physiological and pathological conditions, including chronic heart failure. Against this background, a skeletal muscle origin of symptoms in heart failure has been proposed. The protective effects of physical training have been described in many recent studies: training improves ventilatory control, skeletal muscle metabolism and autonomic nervous system activity. The exercise training appears to induce its beneficial effects on skeletal muscle both directly (on muscle function, histological and biochemical features) and indirectly (by reducing the activation of the muscle afferents). The metabolic mediators of these muscle afferents may become a potential target in the future therapy of heart failure symptoms.     

Myoglobin release in patients with angina pectoris following short-term ischaemia by pacing to angina

Thirteen patients with severe stable angina pectoris were studied by coronary sinus catheterization. In all patients, severe chest pains were produced by atrial pacing. The chest pains had disappeared within 10 min after pacing. Simultaneous arterial (a) and coronary sinus (cs) blood samples were taken before, during and after pacing and analyzed for myoglobin and lactate. The a-cs difference of myoglobin tended to become more negative after pacing, although the change was not significant. However, the change in negative direction post-pacing of the a-cs myoglobin difference was quantitatively correlated with the change in negative direction of the a-cs lactate difference during pacing in the individual patients. This suggests that short-term myocardial ischaemia without signs of established myocardial infarction may provoke myocardial myoglobin release.     

Skeletal muscle training in chronic heart failure.

Patients with heart failure are limited in their ability to tolerate exercise. Recent research has suggested that this limitation cannot be entirely attributed to cardiac or lung impairment but rather that changes in peripheral muscles may play an important role. There are objective similarities between heart failure and muscular deconditioning. Deficiencies in peripheral blood flow and skeletal muscle function, morphology, metabolism and function are present in both conditions. Moreover, an exaggerated activity of the receptors sensitive to exercise-derived metabolic signals (muscle ergoreceptors and peripheral and central chemoreceptors) leads to early and profound exercise-induced fatigue and dyspnoea. These muscle afferents contribute to the ventilatory, haemodynamic and autonomic responses to exercise both in physiological and pathological conditions, including chronic heart failure. Against this background, a skeletal muscle origin of symptoms in heart failure has been proposed. The protective effects of physical training have been described in many recent studies: training improves ventilatory control, skeletal muscle metabolism and autonomic nervous system activity. The exercise training appears to induce its beneficial effects on skeletal muscle both directly (on muscle function, histological and biochemical features) and indirectly (by reducing the activation of the muscle afferents). The metabolic mediators of these muscle afferents may become a potential target in the future therapy of heart failure symptoms.     

Reproducibility of coronary haemodynamics and cardiac metabolism during pacing-induced angina pectoris

The reproducibility of coronary sinus blood flow (CSBF) (thermodilution technique) and myocardial metabolism (exchange of oxygen, lactate, free fatty acids, glucose, citrate, glutamate and alanine) during two identical pacing periods separated by 45 min were studied in eight patients with chronic coronary artery disease. The mean of the individual difference (delta-values) between values during the first (T1) and second (T2) test, at corresponding times (rest, pacing and after 3-5 min of recovery), were calculated and expressed as a percentage of the resting level of each parameter in order to assess their reproducibility. All patients experienced angina pectoris during both pacing sessions, and pacetime to onset of symptoms did not differ between the tests. Group values for haemodynamics and exchange of metabolites were acceptably reproducible throughout the period under study. Mean delta-values of CSBF ranged from 10% to 16% and myocardial oxygen uptake from 14% to 22% in relation to the resting levels. In contrast, mean delta-values of metabolites ranged from 5% to 136% in relation to the respective A-V differences during the study. The greatest variation occurred during pacing and of all the metabolites lactate exchange varied most. A spontaneous variation in the degree of ischaemia during repeat stress tests might be the major reason for the metabolite variability. Changes in CSBF, however, tended to correlate inversely to the delta-aortocoronary sinus differences of substrates during pacing. Precision of chemical analysis and blood sampling technique were of minor importance for the variability. Since lactate exchange varied most, the study suggests that additional measurements should be made of more metabolites when assessing the efficacy of therapy by means of myocardial metabolism.     

不稳定型心绞痛患者树突状细胞功能的研究

目的：研究不稳定型心绞痛患者(UAP)树突状细胞(DC)的功能。方法：分离14例UAP和11例正常人外周血单个核细胞(PBMC)，在含粒细胞巨噬细胞集落刺激因子(GM-CSF)和白介素4(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CD 86(B7-2)的表达；混合淋巴反应(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。结果：与正常组比较，UAP者DC表面CD 86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，TNF-α)增多，抑炎细胞因子(IL-10)减少。结论：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发病的原因。     

ST depression and left ventricular haemodynamics during exercise in patients with angina pectoris

The mechanism of ischaemic ST depression and the cause of its low sensitivity to coronary artery stenosis are not well understood. Of 30 patients with severe stable effort angina, 19 (63%) showed ischaemic ST depressions after exercise (the STAE group) and 11 did not. The highest load during the symptom-limited exercise test and the heart rate on that load did not differ between the two groups. The clinical characteristics and angiographic findings were also similar, but the findings at heart catheterization differed during exercise (in supine). Although the load was similar, the stroke index was significantly lower (38 vs. 53 ml/m2 BSA) and the left ventricular end-diastolic pressure rose to a significantly higher value in the STAE group (40 vs. 32 mmHg). When STAE occurred, they were exclusively or concomitantly present in chest lead 5. These findings suggest that ischaemic STAE may not reflect regional ischaemia but the consequent left ventricular dysfunction. The mechanism may, for example, be that a sufficiently elevated left ventricular diastolic pressure causes a global subendocardial ischaemia.     

曲美他嗪对冠心病稳定性劳力型心绞痛患者心肌缺血的影响

目的探讨曲美他嗪对冠心病(CHD)稳定性劳力型心绞痛患者心肌缺血的影响。方法选择在1周的时间内经2次运动试验,结果为阳性,且运动持续时间变异低于10%的CHD稳定性劳力型心绞痛患者40例,在原有治疗不变的情况下,加用曲美他嗪20mg每日3次,治疗12周。治疗前后均行平均运动试验,观察用药前后下述指标的变化:①用药前后每周心绞痛发作的次数;②每周硝酸甘油片的用量;③心率及心率与收缩压的乘积;④运动诱发心绞痛发作所需的时间;⑤运动后ST段下降1mm所需的时间;⑥运动持续时间;⑦总工作量。结果曲美他嗪应用12周后,患者每周心绞痛发作次数及硝酸甘油片的用量无明显下降(P<0.05);而对心率及心率与收缩压的乘积的影响无统计学显著意义(P>0.05)。与试验前相比,运动耐量和总工作量显著提高(P<0.01),至心绞痛发作时间及ST段下降1mm的时间均明显延长(P<0.01)。不良反应较少。结论曲美他嗪对CHD稳定性劳力型心绞痛患者能增加运动耐量,改善运动诱发心绞痛的心肌缺血,且安全有效,易于耐受。     

SELDI-TOF-MS技术检测心绞痛患者血浆蛋白指纹图谱的研究

目的： 采用表面增强激光解析/电离飞行时间质谱（SELDI-TOF-MS）技术检测心绞痛患者血浆蛋白质指纹图谱,从中筛选出特异的分子标志物。方法: 应用SELDI-TOF-MS技术及金属离子螯合（IMAC-3）蛋白质芯片对20例心绞痛患者和29例正常对照者血浆样本进行检测,借助生物信息学工具（非线性的支持向量机,SVM）提出心绞痛的诊断模型,并运用留一交叉验证法来评估该模型的判别效能。结果: 用SELDI-TOF-MS技术筛选出由3个有显著差异的蛋白质峰［质荷比（m/z）分别为2 667.3、5 914.0和6 890.5］组合构建的诊断模型,可将20例心绞痛患者和29例正常人全部正确分组,诊断特异性和灵敏度均为100%。结论: SELDI-TOF-MS技术在心绞痛的诊断中具有较高灵敏度和特异性,发现的蛋白质峰可能在心绞痛的发病中起一定作用,血浆中分子标志物的发现有助于心绞痛的早期诊断。