急性冠脉综合征患者外周血MCP-1和IL-18水平变化的临床意义

目的探讨急性冠脉综合征患者外周血单核/巨噬细胞趋化蛋白1(MCP-1)和白细胞介素18(IL-18)水平变化的意义及其相关性。方法酶联免疫吸附法测定30例急性冠脉综合征患者(急性冠脉综合征组),30例稳定型心绞痛患者(稳定型心绞痛组)及29例胸痛、胸闷等症状予以冠脉造影正常的患者(对照组)外周血MCP-1和IL-18水平的变化,并分析冠状动脉的病变情况。结果①急性冠脉综合征组MCP-1水平[(151.84±29.66)pg/ml]显著高于稳定型心绞痛组[(128.49±16.97)pg/ml,P<0.001]和对照组[(112.11±10.36)pg/ml,P<0.01],并且稳定型心绞痛组和对照组比较有统计学意义(0.0010.05)。④急性冠脉综合征组外周血MCP-1和IL-18呈明显正相关(r=0.519,P<0.01)。结论外周血MCP-1和IL-18水平可以判断冠心病的严重程度,能预测急性冠脉综合征发生的危险性,但与冠状动脉的病变程度无明显关系,MCP-1和IL-18的正相关提示因子间相互作用可能共同促进冠脉综合征的发生和发展。     

银蒺胶囊对心绞痛(血瘀证)患者内皮素的影响及其疗效

目的:观察银蒺胶囊对心绞痛(血瘀证)患者外周静脉血内皮素(ET)含量的影响及其临床疗效。方法:43例患者被随机分为两组:治疗组,银蒺胶囊45mg,3次/日;对照组,阿斯匹林75mg,1次/日;两组均予以常规扩冠治疗,疗程1个月。结果:治疗后,治疗组患者临床症状改善有效率85.7％,心电图改善有效率53.7％,外周静脉血ET含量由治疗前的95.59±10.58pg/ml降至77.44±9.35pg/ml,治疗前、后有显著差异(P<0.01),且其降低幅度18.51±6.75pg/ml,较对照组显著(P<0.01)。结论:银蒺胶囊可以改善冠心病心绞痛(血瘀证)患者的症状,降低血浆ET含量。     

冠心病免疫激活的一个指标—新蝶呤

目的　探讨新喋呤与冠心病发病机制的可能关系。方法　前瞻性地对 16例正常献血员测定了外周静脉血清新蝶呤水平并测定了 2 0例经冠状动脉造影证实的冠心病患者外周静脉血及冠状窦血清新蝶呤水平 ,且与冠状动脉造影进行了相关分析。结果　冠心病患者外周静脉血及冠状窦血新蝶呤水平均显著高于正常人 (分别为 (14 .78± 7.17)nmol/L、(2 0 .0 4± 14 .73)nmol/L和 (8.32± 4 .70 )nmol/L ,均P <0 .0 1) ;且两者均随着冠心病患者血管病变支数增加而升高得更明显 ,两者均与血管病变支数呈正相关 (r =0 .4 80 ,P <0 .0 1) ;(r =0 .810 ,P <0 .0 1)。结论　在冠心病患者中有新蝶呤水平显著升高 ,免疫激活可能参与了冠心病的病理生理过程。新蝶呤是冠心病免疫激活的一个新指标。     

出血性脑卒中患者血浆内皮素和血清超氧化物歧化酶研究

应用放射免疫分析法(RIA)测定55例出血性脑血管疾病患者血浆内皮素(ET)和血清超氧化物歧化酶(SOD)水平,结果表明:脑出血和蛛网膜下腔出血(SAH)患者的血浆ET和血清SOD均明显高于对照组,ET分别为68.32±12.12pg/ml、59.45±10.24pg/ml及45.69±9.12pg/ml,SOD分别为526.18±202.12ng/ml、498.18±168.85ng/ml及374.12±161.21ng/ml(P<0.01或P<0.05).相关回归分析显示两者具有相关性,提示ET和SOD与出血性脑卒中的病理改变有密切关系.     

急性冠脉缺血综合症患者血浆内皮素和内啡肽的变化及意义

目的 :观察急性冠脉缺血综合征 (ACIS)几种血浆介质的变化及意义。方法 :6 5例 ACIS患者被分为 AMI组(4 3例 ) ,不稳定型心绞痛组 (2 2例 ) ,于其发病后 12、 14、 48小时和 2 0天检查血肌酸激酶同工酶 (CK- MB)、内皮素 (ET)、β内啡肽 (β- EP)水平。结果 :ET峰值 :AMI组、心绞痛组分别为发病 12小时的 2 88.4± 80 .6 pg/ml,2 45 .1± 6 3.4pg/ml;β- EP峰值 :AMI组为 2 4小时的 2 10 .9± 5 0 .2 pg/ml,心绞痛组为 12小时的 15 4.2± 47.6 pg/ml;CK-MB>15 0 U/L 组 :β- EP2 40 .5± 42 .6 pg/ml,ET30 2 .4± 5 8.1pg/ml,明显高于 CK- MB<10 0 U/L组的 (P<0 .0 5 )。心功能 级患者 :β- EP 2 48.6± 2 7.3pg/m l,ET 311.6± 45 .2 pg/ml,明显高于心功能正常组 (P<0 .0 5 )。结论 :(1) ACIS发病后 β- EP在 2 4小时达到峰值 ,升高程度与心肌缺血坏死程度有关 ,它是 AMI后心衰的病理性介质之一 ;(2 ) ACIS发病后 ET迅速升高 ,12小时达到峰值 ,是急性损伤时的一种内源性致病因子 ,能诱发冠状动脉痉挛和血小板聚集。     

心衰患者伴肝脏肿大时血浆内皮素水平的变化

检测24例重度心衰(NYHAⅢ～Ⅳ)患者和20例健康对照者的血浆内皮素(ET)浓度,发现前者明显高于后者(102.4±26.3pg/ml,55.5±17.4pg/ml,P<0.001)。心衰病人伴肝大者(n=11)较无肝大者(n=13)血浆ET浓度显著降低(82.8±13.6pg/ml,121.5±21.1pg/ml,P<0.001)。其机制可能是钠水潴留致ET浓度稀释。     

冠心病患者血浆神经肽Y水平的临床观察

选择符合WHO诊断标准的急性心肌梗塞(AMI)21例,心绞痛(AP)19例,应用放射免疫法动态观察血浆神经肽Y(NPY)含量变化,并以21例正常人作对照.结果显示:对照组NPY水平为 75.1±30.4Pg/ml,AMI组发病第1天NPY含量达峰值,为136.7±66.5pg/ml,显著高于正常组(P<0.05).发病第3天开始下降,第1周末趋于正常,为77.4±48.4pg/ml,与正常组比较无显著差异.AP组于心绞痛发作期NPY含量为159.3±98.5pg/ml,亦显著高于对照组(P<0.05);经治疗2周症状缓解后复查血浆NPY含量下降至118.9±54.3pg/ml,前后比较有显著差异(P<0.05).冠心病伴高血压者血浆NPY含量为186.9±103.1Pg/ml,显著高于不伴高血压者(111.7±45.5pg/ml,P<0.01);既往有吸烟史的冠心病患者,血浆NPY含量为181.8±193.1pg/ml,显著高于无吸烟史者(122.0±65.6pg/ml,P<0.05).提示:NPY水平在冠心病发病初期显著升高,其升高可能由于心肌缺血急性期交感神经兴奋性提高、释放活性增强所致,而高血压及吸烟可能也产生对NPY释放的影响.NPY参与了冠心病的发病机理及病理生理过程.     

冠心病患者内皮素水平的变化及其与冠脉病变的关系

目的：探讨冠心病患者血浆内皮素（ET）水平变化与冠状动脉病变的关系.方法：选择2012年12月至2013年12月在我院心内科住院确诊的冠心病患者130例,其中稳定型心绞痛（SAP）、不稳定型心绞痛（UAP）各40例,非ST段抬高型心肌梗死（NSTEMI）、ST段抬高型心肌梗死（STEMI）各25例;多支血管病变58例,单支病变72例.冠状动脉造影正常者50名为非冠心病正常对照组.检测各组ET浓度并进行比较分析.结果：（1）冠心病各组血浆ET水平均显著高于非冠心病对照组（P均＜0.01）;STEMI组、NSTEMI组血浆ET水平显著高于UAP组和SAP组[（95.6±14.7） pg/ml、（89.6±11.2） pg/ml比（67.2±8.5） pg/ml比（35.7±5.8） pg/m门,且UAP组显著高于SAP组（P均＜0.01）,STEMI组和NSTEMI两组间比较无显著差异（P＞0.05）;（2）冠心病组中多支血管病变组血浆ET水平显著高于单支血管病变组[（81.3±12.6） pg/ml比（64.5±10.3） pg/ml],P＜0.01.结论：冠心病患者血内皮素水平显著升高,其检测对于观察病情、判断预后有重要临床意义.     

冠心病心绞痛患者血浆内啡肽水平与心功能的关系

目的探讨冠心病心绞痛患者β-内啡呔(β-EP)的血浆水平变化规律及其与心功能变化的关系及意义.方法观察42例冠心病心绞痛患者血浆β-EP水平和心功能指标的变化.结果不同临床心功能分组患者β-EP水平有明显差异,心衰Ⅱ～Ⅲ组β-EP水平高于心衰Ⅰ组,分别为218.5±65.2和138.5±44.6 pg/ml.不同β-EP水平分组患者心脏彩色多普勒心功能有明显差异,β-EP水平＞200pg/ml组患者的射血分数(EF)和心输出量(C())分别为0.47±0.20%和3.47±0.20l/min,β-EP水平＜100pg/ml组患者分别0.62±0.14%和5.62±0.14 l/min;组间比较差异显著.结论β-EP与心功能变化有相关性.β-EP水平过高是心衰的病理介质之一.β-EP监测是分析判断病情及预后的一项重要参考指标.     

不稳定型心绞痛患者氧化型低密度脂蛋白自身抗体水平增高的探讨

目的探讨血清氧化型低密度脂蛋白自身抗体(anti-Ox-LDL)水平与冠心病患者病变稳定性及病变程度的关系.方法根据临床诊断标准和冠状动脉造影检查结果,将76名患者分为对照组、不稳定型心绞痛组和稳定型心绞痛组三组,采用ELISA法测定血清anti-Ox-LDL浓度.结果不稳定型心绞痛组血清anti-Ox-LDL水平[(491.19±307.01)mU/ml]明显高于稳定性心绞痛和对照组,而稳定型心绞痛组anti-Ox-LDL水平[(242.18±95.91)mU/ml]与对照组[(304.57±170.96)mU/ml]比较差异无显著性.Logistic回归分析发现血清anti-Ox-LDL水平与不稳定型心绞痛呈正相关(χ2=7.146,P=0.008,OR=0.989).冠心病多支血管病变组血清anti-Ox-LDL水平[(453.19±285.93)mU/ml]明显高于单支血管病变组和对照组,而单支血管病变组anti-Ox-LDL水平[(283.71±197.36)mU/ml]与对照组比较差异无显著性.结论血清anti-Ox-LDL水平不仅反映冠心病患者病变的严重程度,而且可以评价冠心病斑块的稳定性.     

Interleukin-18: a strong predictor of the extent of coronary artery disease in patients with unstable angina

The aim of this study was to confirm that plasma interleukin (IL)-18 level is associated with the extent of coronary artery disease in unstable angina patients. Previous studies have shown that patients with unstable angina have significantly higher plasma IL-18 levels than healthy volunteers. However, the association between IL-18 and the extent of coronary artery atherosclerosis in patients with unstable angina remains unclear. Plasma concentrations of IL-18 and high-sensitivity C-reactive protein (hs-CRP) were measured in 166 consecutive patients admitted for coronary arteriography. One hundred and eighteen patients with unstable angina had coronary artery disease (coronary artery disease group; severity score: 2.32 ± 1.47; Gensini score: 31.3 ± 25.9), and 48 patients with coronary risk factors and without coronary artery lesions served as the risk control group. Plasma levels of IL-18 were higher in the coronary artery disease group than in the risk control group (P = 0.062). Additionally, plasma levels of IL-18 were significantly higher in 77 coronary artery disease patients with severity score ≥2 than in the risk control group (242.3 ± 110.6 vs 209.8 ± 120.3 pg/ml, P = 0.016). By univariate analysis, log-transformed plasma IL-18 concentration was positively correlated with coronary artery disease severity score (r = 0.244, P = 0.009). By multiple regression analyses, the association between coronary artery disease severity score and IL-18 remained significant (β = 0.733, P = 0.017) when controlling for age, diabetes mellitus and left ventricular ejection fraction. Additionally, coronary artery disease severity score was greater in the highest tertile (>246 pg/ml) of plasma IL-18 levels than in the middle (176–246 pg/ml) and the lowest (<176 pg/ml) tertiles (2.79 ± 1.52 vs 2.05 ± 1.08 vs 2.13 ± 1.66, P = 0.028). Of note, plasma hs-CRP level had no significant correlation with coronary artery severity. Plasma IL-18 level is associated with the extent of coronary artery disease in unstable angina patients, suggesting the link between IL-18 and coronary artery atherosclerosis in these patients.     

Change of plasma leukotriene c4 during myocardial ischemia in humans

Changes in leukotriene C4 levels during different degrees of myocardial ischemia in humans were examined by comparing radioimmunoassay measures of leukotriene C4 plasma levels obtained during transient and prolonged myocardial ischemia. Leukotriene C4 levels in systemic arterial and coronary sinus blood were determined in patients with chronic stable angina before and after myocardial ischemia induced either by exercise (supine bicycle ergometer exercise stress testing; n = 14; age, 52 ± 8 years) or by coronary occlusion during angioplasty (n = 14; age 53 ± 7 years). Temporal changes of leukotriene C4 were also followed in arterial and pulmonary artery blood within 24 h after the onset of chest pain (acute phase), and 1 day, 1 week, and 1 month later in 22 patients with acute myocardial infarction (AMI) (12 patients with thrombolytic therapy, age 61 ± 10 years; 10 patients without thrombolytic therapy, age 60 ± 11 years). Clinical characteristics, including coronary risk factors and the severity of coronary artery disease, were not significantly different among the groups. Exercise-induced myocardial ischemia and coronary occlusion did not induce any significant leukotriene C4 changes in the chronic stable angina patients, whereas AMI patients had significantly higher plasma leukotriene C4 levels in both arterial and pulmonary artery blood in the acute phase compared with those of chronic stable angina patients (arterial blood, 471 ± 164 pg/ml and 477 ±235 pg/ml vs. 275 ± 254 pg/ml or 240 ± 66 pg/ml, p< 0.05; pulmonary artery blood in AMI, 543 ± 162 pg/ml vs. 234 ± 125 pg/ml or 225 ±64 pg/ml, coronary sinus blood in chronic stable angina, p < 0.05). These results suggest that leukotriene C4 is involved more in prolonged myocardial ischemia than in transient myocardial is chemia, and that leukocyte function might play a significant role in the pathogenesis of patients with AMI.     

经皮腔内冠状动脉成形术对冠心病患者血和尿内皮素的影响

为调查冠心病和内皮素之间存在的联系，并评价经皮腔内冠状动脉成形术过程中各种刺激因素对内皮素水平的影响，观察了15名采取经皮腔内冠状动脉成形术成功的患者股动脉血及尿液的内皮素水平，并与10名健康人作对照。结果发现冠心病患者血、尿基础内皮素值高于正常（P＜0．01）。经皮腔内冠状动脉成形术后股动脉血中内皮素水平无显著增加，尿中内皮素水平却增加3～6倍（P＜0．01），且持续24h以上。收缩期主动脉压力与尿中基础内皮素水平呈正相关（r=0．87，P＜0．01，n=15）。结果表明冠状动脉粥样硬化时内皮素水平高于正常。经皮腔内冠状动脉成形术过程中的血管损伤引起水后内皮素释放，尿内皮素值能较敏感地反映出经皮腔内冠状动脉成形术后内皮素的增加。     

Decreased plasma urotensin Ⅱ levels inversely correlate with extent and severity of coronary artery disease

Objective To determine the plasma urolensin Ⅱ(UII) levels in various types of coronary heart disease and to clarify how the plasma UII levels correlate with the clinical presentation, extent and severity of coronary artery atherosclerosis (CAD). Methods: One hundred and three aged patients undergoing elective diagnostic coronary angiography for proven or clinical suspected coronary heart disease were enrolled in this study. The extent and severity of coronary artery disease were evaluated by vessel score and Gensini score, respectively. Plasma UII levels were measured by radioimmunoassay. Results: The plasma UII levels in the patients with modest to severe coronary stenosis (3.03±0.34 pg/ml, 1.83±0.67 pg/ml) were significantly lower than that in subjects with normal coronary artery (4.80±1.11 pg/ml, P<0.001). The plasma UII levels in patients with coronary heart disease were also significantly lower than that in patients with insignificant coronary stenosis (P < 0. 001). Compared to patients with stable angina pectoris, plasma UII levels in patients with acute coronary syndrome were significantly decreased (1.89±0.51 pg/ml vs 2.42±0.77 pg/ml, P < 0.001). Plasma UII levels were found to be negatively correlated with the severity of coronary artery stenosis (r = -0.488, P<0.001), as well as the vessel score (r = -0.408, P<0.05) in the patients with CAD. Conclusion: Significant inverse correlations exist between the plasma UII levels, and the extent and severity of coronary artery stenosis. These findings suggest that plasma UII contribute to the development and progression of coronary artery stenosis, and may be a novel marker to predict clinical types, as well as the extent and severity of coronary artery disease in the patients.     

Plasma immunoreactive endothelin concentration correlates with severity of coronary artery disease in patients with stable angina pectoris and normal ventricular function

Objectives. The present study tested the hypothesis that plasma immunoreactive endothelin concentration correlates with the severity and extent of coronary atherosclerosis.Background. Plasma endothelin-1 concentration is increased in patients with unstable coronary syndromes and advanced atherosclerosis. This finding, together with other clinicopathologic observations, suggests that endothelins may participate in the atherogenic process. However, the relation between plasma immunoreactive endothelin and coronary artery disease in patients with stable angina pectoris remains controversal.Methods. Ninety consecutive patients undergoing coronary angiography for the investigation of exertional chest pain and 49 normal control subjects were prospectively studied. Eleven patients had normal coronary angiographic findings (group I), 65 had coronary artery stenoses (group II), and 14 had coronary artery disease plus symptoms indicating atheroma in other vascular territories (group III). Computerized angiography was used to determine the extent, severity and morphology of coronary stenoses. Plasma immunoreactive endothelin was measured by radioimmunoassay.Results. Mean (± SD) plasma endothelin concentration (pg/ml) was significantly higher in patients than in control subjects (7.29 ± 4.07 vs. 3.48 ± 1.29, p < 0.0001). Endothelin levels were higher in patients of group III than in those of groups II and I (9.43 ± 5.48, 7.20 ± 3.72 and 4.94 ± 2.89, respectively, p = 0.02). In patients of group II, plasma endothelin correlated with the maximal degree of stenosis in each patient (r = 0.25, p = 0.04) and with the number of stenoses with ≥70% diameter narrowing (r = 0.36, p = 0.002). The highest plasma endothelin levels were found in patients with total occlusions (8.65 ± 3.78 vs. 6.46 ± 3.51, p = 0.02).Conclusions. Plasma immunoreactive endothelin concentration is increased in patients with chronic stable angiuya. The highest levels occur in patients with severe stenoses and total coronary occlusion.     

Increased plasma endothelin levels in angina patients with rapid coronary artery disease progression.

AIMS: To investigate the association between plasma endothelin levels and rapid coronary artery disease progression, as assessed by quantitative angiography. METHODS AND RESULTS: Changes in diameter were assessed in 224 coronary stenoses of 92 consecutive patients (62 men) with chronic stable angina pectoris who were on a waiting list for routine coronary angioplasty and underwent coronary angiography on two occasions: the first (diagnostic) angiogram was carried out at study entry and the second 5.5+/-3.0 months later, immediately prior to coronary angioplasty. A digital quantitative angiographic analysis system was used to assess differences in stenosis diameter between the first and second angiogram. Plasma immunoreactive endothelin levels were estimated by radioimmunoassay at study entry. Rapid coronary artery disease progression occurred in 29 (31.5%) patients according to pre-established criteria: 12 (41%) had a > or =10% diameter reduction of at least one pre-existing stenosis > or =50%, 10 (34%) had a > or =30% diameter reduction of a pre-existing stenosis <50%, 5 (17%) patients developed a new stenosis and 2 (7%) had progression of a lesion to total occlusion by the second angiogram. Baseline demographic, clinical and angiographic data were similar in patients with and without stenosis progression. Plasma endothelin levels were significantly higher in patients with rapid disease progression than in those without (5.7+/-2.0 pg. ml(-1)vs 3.9+/-1.6 pg. ml(-1), P<0.001). Multiple logistic regression analysis revealed that endothelin was an independent predictor of disease progression (P=0.001). Moreover, endothelin levels above 4.26 pg. ml(-1)(the median of the total endothelin concentrations) were associated with a sixfold increase in the risk of developing rapid stenosis progression. CONCLUSIONS: Plasma endothelin is raised in patients with coronary artery disease progression and may be a marker of risk of rapid stenosis progression. Endothelin may also play a pathogenic role in this process.     

Comparison of plasma concentrations of thromboxane B2 in Prinzmetal's variant angina and classical angina pectoris

We have reported that thromboxane B₂ is present in plasma of Prinzmetal's angina patients measured by radioimmunoassay but is below detection limits, <0.5 pmol/ml, in normals. To determine whether this metabolite of thromboxane A₂ (a coronary vasoconstrictor) is present in the peripheral blood in classical angina pectoris, we studied 14 patients with fixed obstructive coronary artery disease (2.5 lesions per patient) in whom angina was induced by atrial pacing. Thromboxane B₂ at rest was barely detectable (0.537±0.16 pmol/ml), but rose during pacing (0.747±0.18 pmol/ml) and was maximal (p<0.05) 5–10 min after pacing (1.237±0.36 pmol/ml). In eight variant angina patients, resting levels of thromboxane B₂ were not statistically different during spontaneous angina and angina-free intervals (2.837±0.56 and 1.577±0.34 pmol/ml), but the mean 5–10 min after angina was higher than during angina (6.41 7±1.46 pmol). The means of preanginal, anginal, and postanginal samples were all higher than the corresponding means of the classical angina group, and thromboxane B₂ levels in variant angina patients in the absence of angina, during angina, and 5–10 min after angina were all significantly higher (p<0.025) compared to the classical angina group measured prior to pacing. Unlike the case with variant angina, thromboxane B₂ is indetectable in classical angina pectoris patients at rest. Furthermore, spontaneous angina in variant angina or pacing-induced angina in classical angina pectoris are both followed by increased thromboxane B₂, although the latter responses are smaller. The role of these phenomena in the pathogenesis of coronary artery spasm and ischemia remains to be clarified.     

Cardiac Release and Kinetics of Endothelin After Uncomplicated Percutaneous Transluminal Coronary Angioplasty

This study was designed to assess the release kinetics of endothelin after percutaneous transluminal coronary angioplasty (PTCA) and to prove the coronary endothelium as the source of the endothelin release. Twenty-seven patients with single-vessel coronary artery disease underwent PTCA. Endothelin, troponin T, myoglobin, and creatine phosphokinase paired blood samples were withdrawn from the coronary sinus and a peripheral vein before the balloon maneuver and at 1, 5, 10, 30, 45 minute(s), and at 1, 2, 3, 6, 12, and 24 hour(s) after the last balloon maneuver. Myocardial ischemia was monitored by means of cardiac lactate metabolism and 12-lead electrocardiogram. Thirteen patients who underwent a diagnostic cardiac catheterization served as a control group. In the left coronary artery, PTCA (n = 19) endothelin concentrations increased from 4.1 pg/ml as a common mean baseline level before intervention to 13.9 ± 2.6 pg/ml (mean ± SD) in the coronary sinus and 7.9 ± 2.2 pg/ml (mean ± SD) in the peripheral vein at 1 minute after the intervention (p <0.001). The levels remained elevated for 3 hours with higher coronary sinus than peripheral venous concentrations due to persistant cardiac endothelin release. PTCA of the right coronary artery (n = 8) also led to an instantaneous endothelin increase from a mean concentration of 4.4 before intervention to 8.3 pg/ml after intervention with identical coronary sinus and peripheral venous levels (p <0.001). Endothelin levels gradually decreased to normal within 6 hours. No patient developed a measurable myocardial ischemia or a myocardial infarction. In the control group all parameters remained unchanged. Uncomplicated PTCA was followed by a significant cardiac endothelin release that seems to indicate endothelial injury and not myocardial ischemia.     

Endothelin-1 in patients with coronary heart disease undergoing cardiac catheterization

Objectives. This study examined the possible association between endothelin and coronary atherosclerosis and evaluated the synthesis and release of endothelin in the presence of various stimuli that occur during cardiac catheterization.Background. Circulating endothelin has been reported to be increased in diffuse atherosclerosis and acute myocardial infarction. However, the relation between coronary artery disease and endothelin release remains unclear.Methods. We measured the plasma and urinary concentrations of endothelin immunoreactivity in 45 patients and 10 healthy control subjects.Results. In group IA (n = 9), simultaneous blood sampling in the coronary sinus and femoral artery during coronary angioplasty of the left anterior descending coronary artery demonstrated no immediate changes in plasma immunoreactive endothelin-1 (ir-ET-1) levels. In 11 patients in group IB undergoing coronary angioplasty of a major artery, we did not detect changes in peripheral plasma concentrations of ir-ET-1 within 24 h, but urinary ir-ET-1 levels increased from 9.2 ± 2.3 to 18.6 ± 4.9 pg/mg of creatinine a few hours after coronary angioplasty (mean ± SEM, p < 0.05). This increase in urinary endothelin excretion persisted 24 h later. Group II patients (n = 12) had coronary angiography without coronary angioplasty. Levels of both plasma and urinary ir-ET-1 did not change during the 24-h follow-up period. There was no relation between the severity of coronary atherosclerosis and the plasma or urinary concentrations of ir-ET-1. Systolic aortic pressure correlated with basal urinary excretion of endothelin (r = 0.54, p = 0.03, n = 15). In group III (n = 13), levels of ir-ET-1 in patients undergoing right heart catheterization without angiography did not differ from those in the control group.Conclusions. The presence or the severity, or both, of coronary atherosclerosis is not associated with a detectable increase in endothelin release. The diagnostic procedures of Catheterization do not modify endothelin concentrations in plasma and urine. Vascular stretch or injury, or both, during coronary angioplasty increases urinary ir-ET-1 levels a few hours after the procedure. This increase persists for at least 24 h but is not detectable by brief sampling of peripheral or coronary sinus blood.     

Cardiac Release and Kinetics of Endothelin After Severe Short-Lasting Myocardial Ischemia

Objectives. The aim of this study was to investigate the release kinetics of endothelin after induced short-lasting myocardial ischemia.Background. Endothelin is an endothelium-derived vasoactive peptide. Unequivocal proof of its cardiac release in ischemic syndromes has not yet been demonstrated.Methods. A coronary sinus study with atrial pacing was performed in 23 patients with coronary artery disease. Endothelin (ET), cardiac troponin-T (TnT), myoglobin (Mb) and creatine kinase (CK) samples were withdrawn from the coronary sinus and a peripheral vein before and 1, 5, 10, 30 and 45 min and 1, 2, 3 and 6 h after pacing. The appearance of angina pectoris, abnormal cardiac lactate metabolism and ST segment depression were further criteria for myocardial ischemia.Results. In the study group, pacing stress induced severe ischemia (mean duration ± SD 6.1 ± 1.2 min), with a maximum of 0.34 ± 0.12-mV ST segment depression in 21 of 23 patients and angina pectoris in 22 of 23. The maximal cardiac lactate production was 42.8 ± 17.3% (p < 0.03). TnT and CK levels in the total group were normal; in 14 of 23 patients a transient elevation of Mb with a maximum after 3 h was detected (86.4 ± 27.1 μg/liter, p < 0.03). The ET concentrations increased significantly (p < 0.001) in the coronary sinus (from 4.6 ± 0.8 [baseline] to 12.9 ± 2.7 pg/ml at 1 min after cessation of pacing) and the peripheral vein, respectively (from 4.7 ± 0.7 [baseline] to 8.3 ± 2.1 pg/ml at 1 min). ET further remained elevated for 1 h with persisting higher coronary sinus than peripheral venous concentrations, indicating cardiac ET release. In a control group of 18 patients without heart disease, all variables were unchanged.Conclusions. Short-lasting severe myocardial ischemia was associated with significant ET release of cardiac origin that lasted up to 1 h.