血浆vaspin浓度与不稳定型心绞痛的相关性研究

目的:腹腔脂肪型丝氨酸蛋白酶抑制剂(vaspin)是新发现的脂肪因子,对代谢性疾病具有预防作用.该研究旨在探讨血浆vaspin浓度与冠心病及不稳定型心绞痛的关系.方法:经血管造影诊断明确的冠心病患者88例(其中稳定型心绞痛47例,不稳定型心绞痛41例),同期入院的103例无心脏疾病的患者作为对照.测量患者血浆中vaspin的浓度,记录临床一般情况及血脂、血糖、高敏C反应蛋白等指标.并根据冠状动脉的病变支数来评定冠心病严重程度.结果:不稳定型心绞痛的血浆vaspin浓度(0.43±0.38)μg/L较稳定型心绞痛(0.91±0.95)μg/L显著降低(P<0.01).在冠心病患者中血管病变支数与血浆vaspin浓度负相关(r=-0.350,P<0.01).ROC曲线分析血浆vaspin对冠心病有鉴别价值(AUC=0.684,P<0.001),对不稳定型心绞痛也有鉴别价值(AUC=0.640,P=0.024).结论:不稳定型心绞痛患者具有较低的血浆vaspin浓度;低血浆vaspin浓度与冠心病严重程度呈相关.     

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.     

Ischaemia related ventricular arrhythmias in patients with variant angina pectoris

Twenty-three patients with variant angina were studied by Holtermonitoring both to assess the incidence of serious ventriculararrhythmias (a risk factor of sudden death in variant angina),during ischaemic episodes and to examine the time-relation ofthe arrhythmias to ST changes. Serious ventricular arrhythmias were observed in 12/23 patients(52%). In the 23 patients, a total of 491 episodes of ST segmentelevation were recorded during 954 h of Holter monitoring; seriousventricular arrhythmias were found in only 46 ischaemic episodes(9.4%). Six out of 12 patients showed serious ventricular arrhythmiasat the onset of ischaemic episodes or during maximal ST elevation(phase 1), one patient during return or immediately after returnof ST to baseline (phase 2) and five patients during both phases.Thirty-three out of 46 ischaemic episodes (76%) showed seriousventricular arrhythmias during phase 1, eight (17%) during phase2, and five (11%) during both phases. Serious ventricular arrhythmias were neither related to previousmyocardial infarction nor to the presence of serious ventriculararrhythmias during inter-crisis periods, whereas a good relationshipwith severity of ischaemic episodes, as assessed by the magnitudeand duration of ST elevation, was found. A modest relationshipwith anterior ST elevation was also found. In conclusion: (1) serious ventricular arrhythmias occur ina high percentage of variant angina patients, but in only asmall proportion of ischaemic episodes; (2) serious ventriculararrhythmias are related to the severity of ischaemia and occurpredominantly at the onset of ischaemic episodes and/or duringmaximal ST elevation; in only a few cases do they occur duringresolution of ischaemic episodes.     

Comparison of plasma serotonin levels in patients with variant angina pectoris versus healed myocardial infarction

Patients with variant angina pectoris showed greater serotonin plasma levels than did control subjects and patients with healed myocardial infarction. The levels also tended to be greater in those with >1 episode/month than in those with fewer episodes. Moreover, patients with variant angina pectoris also had greater levels of nitrite and nitrate plasma levels than did control subjects or patients with healed myocardial infarction, partly, perhaps, as a compensatory mechanism.     

Treatment of variant angina pectoris with perhexilene maleate.

Three patients with variant angina pectoris resistant to therapy with nitrates and propranolol were treated with perhexilene maleate. Two patients had normal coronary arteries with documented coronary artery spasm, while the third patient had a fixed coronary artery obstruction. In all three patients, attacks of variant angina pectoris disappeared following institution of therapy with perhexilene maleate. When the dose of this drug was decreased to 100 mg per day or less, symptoms reappeared in all patients. Reinstitution of therapeutic doses of perhexilene maleate once again resulted in complete control of symptoms. Perhexilene maleate is therefore a useful agent for the treatment of variant angina pectoris.     

变异型心绞痛发作时的特点分析及预后

目的分析变异型心绞痛(VAP)发作时的特点,探讨其临床意义及预后。方法采用模拟胸导CM5、CM3、CM1记录24h动态心电信息。通过回放记录:①VAP发作时的ST段抬高的时期和持续时间;②VAP发作时ST段抬高部位及ST段最高升幅和抬高极期时的心率;③VAP发作时出现的心律失常及时期;④VAP发作前1h及发作后1h的心率变异性.结果8例VAP患者共发作26例次ST段显著抬高。VAP发作多在22∶00～8∶00,每次持续时间平均(3.5±2.5)min;ST段抬高最显著部位3例在CM5,5例在CM3,反复发作患者ST段改变各自几乎在同一部位;ST段最高升幅平均(8.1±3.7)mm,心率平均(83±20)/min。8例患者有5例伴发心律失常;26例次有13次出现心律失常,其中室早、室速为42%,多数发生在闭塞期;2次室速在再灌注期,1例并院外猝死。发作时1h心率变异性SDNN、SDANN较发作前1h有显著增高(P<0.05)。7例随访4个月至5年无心脏事件发生。结论VAP发作几乎都在后半夜至清晨,冠状动脉痉挛易在各自的部位反复出现,历时短暂,不伴有缺血加重现象;VAP发作时室性心律失常发生率高,可能与大的冠脉痉挛有关,再灌注期并发的高危性室速易致猝死;VAP发作时交感神经兴奋性增高;VAP患者经及时有效治疗预后良好。     

Correlation of plasma propranolol concentration with therapeutic response in patients with angina pectoris.

The therapeutic response to propranolol was evaluated in patients with documented coronary artery disease at doses varying from 40 to 320 mg/day. Therapeutic response was quantified by evaluating exercise performance on a treadmill and then related to plasma propranolol concentration. Plasma propranolol was defined in terms of beta-adrenergic blockade by comparison with dose (concentration) response curves in normal subjects. Individual therapeutic benefit occurred at doses which averaged 144 +/- 21 mg/day and at concentrations which averaged 30 +/- 7 ng/ml. There was a wide variation between both dose and concentration among the patients at maximum therapeutic response, but when the plasma propranolol was related to pharmacologic activity, the maximum therapeutic response was observed between 64 to 98% of total blockade. Despite the increased exercise performance in these patients, the double product of heart rate and systolic blood pressure was always less, suggesting either an alteration of the relation between myocardial oxygen consumption and the double product during propranolol or a reduction on oxygen delivery to the myocardium as the result of beta-adrenergic blockade of the coronary vasculature.     

Eosinophil counts and plasma fibrinogen in patients with vasospastic angina pectoris

Epidemiologic studies have suggested a relation between white blood cell (WBC) counts and the incidence of coronary heart disease. However, the relation between vasospastic angina pectoris (VAP) and WBC counts remains to be elucidated. To clarify the relation between differential and WBC counts in VAP, we compared the hematologic values, blood chemical values, plasma fibrinogen levels, C-reactive protein levels, and coronary risk factors in patients with spontaneous attacks of VAP (n = 39) with those in patients with stable effort angina pectoris (EAP, n = 35) and in control subjects (n = 19). Patients with VAP were further divided into mild VAP (n = 22) and severe VAP groups (n = 17). There were no differences in the coronary risk factors, body temperature, total WBC counts, and C-reactive protein levels among the control, EAP, mild VAP, and severe VAP groups, except that the high-density lipoprotein cholesterol in the EAP group was significantly lower than that in the control group (p <0.01). In contrast, the eosinophil counts were significantly higher in the severe VAP group than in the other 3 groups (p <0.01). Plasma fibrinogen levels were also significantly higher in the severe VAP group than in the other 3 groups (p <0.05). The follow-up study for differential and WBC counts in patients with VAP (n = 23) demonstrated that, after medical therapy, the eosinophil counts were significantly decreased to the some level as those in the control group (p <0.0001). Thus, the eosinophil counts and plasma fibrinogen levels could predict the severity of VAP. Furthermore, a follow-up study in patients with VAP suggests that coronary vasospasm could result in an increase in eosinophil counts.     

变异型心绞痛心律失常特点的临床分析

目的 探讨变异型心绞痛（variant angina pectoris,VAP）患者,心绞痛发作时伴发各种类型心律失常的临床特点及其发生机制。方法 临床观察88例VAP患者,均采用18导联心电图或CM5或CMaVF导联系统进行24h动态心电图监测,记录VAP患者心肌缺血时间的长短、伴发心律失常的有无、类型及发作时相,并均行冠状动脉造影检查,明确有无冠状动脉病变以及病变部位。结果 88例VAP患者心肌缺血发作时有48例患者发生心律失常,发生率为54．5％。快速和缓慢心律失常均有发生。V1－V3或V4－V5导联ST段抬高时,室性心律失常多见。其中室性心动过速9例,室性期前收缩21例,心室颤动2例。Ⅱ、Ⅲ、aVF导联ST段抬高时常见缓慢心律失常,如窦性心动过缓、窦性停搏及房室阻滞。48例发生心律失常的患者中,缺血持续时间平均为9．2min,而在40例未发生心律失常的患者中,缺血持续时间平均为3．4min;42例患者（87．5％）的心律失常发生在缺血闭塞期,6例患者（12．5％）的心律失常发生在缺血再灌注期。结论 （1）VAP可并闭塞期和再灌注期心律失常,以前者为多;（2）右冠状动脉痉挛引起Ⅱ、Ⅲ、aVF导联ST段抬高时,易造成缓慢心律失常;而左前降支冠状动脉痉挛引起V1－V3或V4－V6导联ST段招高时,则易发生室性快速心律失常;（3）VAP发作时心肌缺血持续时间的长短与心律失常发生具有相关性,且直接影响预后。     

Provocation of coronary spasm by dopamine in patients with active variant angina pectoris

The effects of dopamine on arteries are different depending on the dose, route of administration, and receptor population. Its administration can cause vasodilation by stimulation of dopaminergic receptors, vasoconstriction by stimulation of alpha-adrenergic and serotonergic receptors, and even spasm of cerebral arteries when given intracisternally in dogs. The ability of dopamine to provoke coronary spasm was assessed in 18 patients with active vasospastic angina in whom this amine was infused at rates of 5, 10, and 15 micrograms/kg/min for periods of 5 min each. The 12-lead electrocardiogram and blood pressure (cuff) were monitored throughout the whole test. In nine patients dopamine caused angina and ischemic electrocardiographic changes suggestive of coronary spasm: ST segment elevation in six patients and ST segment depression in the absence of important coronary stenoses in the remaining three. Infusion of dopamine was repeated during coronary angiography in three patients with positive test results: this provoked occlusive coronary spasm with ST segment elevation in two patients and nonocclusive spasm with ST segment depression in the remainder. In conclusion, infusion of dopamine provokes coronary spasm in a sizeable proportion of patients with active vasospastic angina. Its administration may be detrimental in patients susceptible to coronary spasm, such as those with acute myocardial infarction.     

Effects of phentolamine and atropine on angina pectoris induced by handgrip test in patients with variant angina

In 19 patients with variant angina, handgrip test as an isometric exercise was performed in 3 conditions on different successive days in the early morning: in the control, after administration of phentolamine (0.3 mg/kg) and after administration of atropine sulfate (0.04 mg/kg). Angina associated with ST-segment elevation on the electrocardiogram was induced in 5 patients (26%) in the control condition, in 14 (74%) after phentolamine and in 5 of 16 (31%) after atropine. All anginal events but 1 occurred after the cessation of the exercise and were not associated with the significant increase of rate-pressure products. These attacks were considered to be due to coronary spasm. The frequency of the induction of angina was significantly higher after phentolamine than in the other 2 conditions (p less than 0.01). It is concluded that the attack can be induced by the handgrip exercise in a sizable number of patients with variant angina, and that the administration of phentolamine increases the incidence of angina induced by handgrip exercise. The mechanism or mechanisms by which coronary spasm is induced by handgrip exercise remains to be elucidated.     

Elevated plasma adiponectin concentrations in patients with liver cirrhosis correlate with plasma insulin levels

Abstract: Background: Adiponectin is a hormone secreted by adipocytes and has anti‐diabetic and anti‐atherogenic properties. Hypoadiponectinemia is associated with insulin‐resistant diabetes and liver dysfunction. The aim of this study was to determine plasma adiponectin and insulin levels in patients with liver cirrhosis. Methods: Adiponectin and insulin levels were determined in 38 patients with cirrhosis and 30 healthy controls, and were correlated with various clinical and biochemical parameters. Patients included 21 with Child A, eight Child B, and nine with Child C liver cirrhosis. Results: Log adiponectin and insulin levels were significantly elevated in patients with cirrhosis compared with the control. In liver cirrhosis, the level of adiponectin increased proportionately with the Child's classification score. In control subjects, plasma adiponectin correlated inversely with insulin levels. In contrast, plasma adiponectin correlated positively with insulin levels in patients with liver cirrhosis. Plasma adiponectin levels did not correlate with age, sex, body mass index, total bilirubin, aspartate aminotransferase, and fasting blood sugar levels in both groups, while alanine aminotransferase correlated negatively with adiponectin in control subjects as reported previously. Conclusion: Our results of high plasma adiponectin in patients with liver cirrhosis could reflect an imbalance between its production by adipocytes and metabolism in the liver.     

Prominent negative U wave in variant angina pectoris

The extremely prominent negative U wave occasionally appears during a cardiac attack in variant angina pectoris. The clinical profile of the negative U wave was therefore studied in 80 patients with variant angina pectoris (VA) and 33 controls with resting angina pectoris (RA). The prominent negative U wave appeared in 55 of the patients with VA (68.8% of patients) and in 10 of the patients with RA (30.3%); thus, there was a significant difference in the appearance of the wave between the 2 groups of patients (p less than 0.001). The leads in which the negative U wave appeared were mostly consistent with those in which the ST segment was elevated. The negative U wave began to appear at about the time when ST-segment elevation began to improve; the wave then gradually became very prominent and then eventually disappeared. The patients with VA and also those with RA on whose ECGs the negative U wave appeared during exercise testing also had negative U waves during spontaneous episodes of angina. An investigation of the frequency of appearance of ST deviation and negative U waves during exercise testing, regardless of the type of angina pectoris, disclosed that the negative U wave appeared in 14 of 20 patients with ST-segment elevation (70% of patients), while the negative U wave appeared in only 52 of 519 patients with either no ST change or ST-segment depression (10.4%); thus, there was a significant difference in the appearance of the negative U wave between these 2 groups (p less than 0.001). Coronary cinearteriography failed to disclose any apparent difference between the appearance of the negative U wave and the presence of stenosis. The prognosis of VA and RA in patients with negative U waves was less favorable compared to those without negative U waves. In particular, we noted that of the 10 patients with RA associated with negative U waves, 4 died. Although the mechanism of the negative U wave is not yet known, we believe that the above findings contribute to its elucidation.     

Decreased plasma concentrations of adiponectin in patients with slow coronary flow

Adiponectin has multiple protective effects on vascular endothelium through anti-inflammatory and anti-atherogenic properties. Recent data suggested that endothelial activation and inflammation may contribute to the pathogenesis of slow coronary flow (SCF). Therefore, we investigated whether adiponectin plasma concentrations were decreased in patients with SCF compared to subjects with normal coronary flow. The study population consisted of 35 patients with angiographically documented SCF in all three coronary arteries and 35 sex- and age-matched cases with normal coronary flow. Coronary flow rates of all participants were determined by Thrombolysis in Myocardial Infarction (TIMI) frame count. Plasma adiponectin concentrations were measured by an enzyme-linked immunosorbent assay method using commercially available adiponectin kits. There were no statistically significant differences between the patients with SCF and the subjects with normal coronary flow in terms of demographic characteristics and cardiovascular risk factors (P > 0.05). Plasma adiponectin concentrations of patients with SCF were found to be significantly lower than those with normal coronary flow (4.77 ± 3.86 mg/ml vs 10.8 ± 6.60 mg/ml, P = 0.001, respectively). Plasma adiponectin levels were correlated significantly and inversely with mean TIMI frame count in patients with SCF (r = −0.441, P = 0.008). Furthermore, the Receiver Operator Characteristics curve of adiponectin concentrations showed that an adiponectin <4.6 mg/ml is associated with SCF with a sensitivity of 68.6%, specificity of 82.9%, positive predictive value of 80.0%, and negative predictive value of 72.5%. Our findings suggest that endothelial inflammation may play a role in the pathogenesis of SCF phenomenon.     

Decreased circulating protective adiponectin level is associated with angiographic coronary disease progression in patients with angina pectoris

Adipocyte cytokines regulate glucose metabolism and insulin resistance and adiponectin is thought to have a protective effect against atherosclerosis. Studies have shown that adiponectin expression is decreased in obese subjects and those with metabolic syndrome or diabetes mellitus. The purpose of this study was to investigate the relationship between circulating adipocyte cytokine concentrations and angiographic coronary artery disease (CAD) progression in patients with chest pain. Patients with stable angina pectoris who underwent repeat coronary angiograms and had serum samples at the time of first catheterization between March 1999 and January 2004 were enrolled. A modified Gensini scoring system was used to define angiographic coronary artery progression between the index and follow-up angiograms. Those who had significant angiographic progression of coronary lesions were classified into the progression group (N = 55). Those who did not have CAD progression were classified into the non-progression group (N = 102). Univariate analysis showed that CAD progression was associated with male gender (93% vs. 78%, p = 0.038), higher baseline total cholesterol (187 ± 43 vs. 173 ± 39 mg/dl, p = 0.037) and higher baseline fasting blood glucose (128 ± 57 vs. 110 ± 40 mg/dl, p = 0.037). Patients in the progression group had a significantly lower serum adiponectin level (14.3 ± 7.9 vs. 18.9 ± 13.2 μg/ml, p = 0.007) than, but resistin (28.9 ± 13.4 vs. 34.4 ± 26.0 ng/ml, p = 0.142) and leptin (7.4 ± 4.6 vs. 7.7 ± 6.5 ng/ml, p = 0.675) levels similar to, those in the non-progression group. In a multivariate binary logistic regression model, male gender (odds ratio 4.283, p = 0.015), higher serum cholesterol (odds ratio 1.010, p = 0.032) and lower serum adiponectin (odds ratio 0.959, p = 0.030) were all significant independent predictors of CAD progression. In conclusion, we found that a decreased circulating level of adiponectin is associated with angiographic CAD progression in patients with angina pectoris.     

Labetalol in normotensive patients with angina pectoris

Summary Labetalol, an alpha-beta-blocker, has been shown to have vasodilating as well as beta-blocking properties. From the theoretical point of view such a drug is likely to be beneficial in the treatment of angina pectoris. There are very few studies investigating the effects of labetalol in normotensive patients with angina pectoris. The three major controlled trials that have been published show that labetalol reduces angina frequency and prolongs exercise duration. In one study the effects of labetalol in anginal subjects using ambulatory monitoring was performed and showed a reduction in silent ischemia as well as a reduction in angina pectoris. Thus labetalol would appear to be an effective antianginal agent. Further studies are necessary to determine if the anti-anginal effect is entirely due to the beta-receptor-blocking activity of the drug or whether labetalol's vasodilating property has important additional benefit.