Dipyridamole technetium 99m sestamibi myocardial tomography as an independent predictor of cardiac event-free survival after acute ischemic events

Background  

A total of 137 consecutive patients with recent uncomplicated myocardial infarction (n=31) or unstable angina (n=106) were studied to determine the relative prognostic value of predischarge clinical risk stratification and intravenous dipyridamole stress sestamibi (MIBI) myocardial tomography in patients unable to exercise maximally after an acute ischemic coronary event.     

葛根素冻干粉针治疗不稳定型心绞痛的短期疗效观察--附30例报告

目的观察葛根素冻干粉针(麦普宁)治疗不稳定型心绞痛(Unstable angina pectoris.UAP)的临床疗效.方法将60例UAP患者随机分为治疗组30例和对照组30例.对照组采用常规治疗.治疗组在常规治疗的基础上加用葛根素冻干粉针400mg加入5%葡萄糖液250ml中静脉滴注,疗程均为14d.结果治疗组的总有效率(93%)优于对照组(66%),差异有统计学意义(P＜0.05).治疗组治疗前后心电图12导联中ST段下降导联数(NST)及12导联中ST段压低数值总和(ΣST)均有明显改善(P＜0.05),随访心绞痛患者6～18个月,未发现明显不良反应.结论葛根素冻干粉针剂能有效减少心绞痛发作,应用简单、监测方便,可降低心肌梗死发生率.     

灯盏花素合力源精纯溶栓酶治疗不稳定型心绞痛30例

目的 :观察灯盏花素、力源精纯溶栓酶治疗不稳定型心绞痛 (UAP)的临床疗效。方法 :将 6 0例 UAP患者随机分为治疗组和对照组各 30例。治疗组给予灯盏花素、力源精纯溶酶加常规抗心绞痛治疗 ;对照组仅给予常规抗心绞痛治疗。分别观察 2组治疗前后的心绞痛发作及硝酸甘油用量的变化 ,检测静息心电图和血液流变学指标。结果 :治疗组在缓解心绞痛总有效率 (93.33% )、改善异常心电图及血液流变学指标、降低硝酸甘油用量〔(0 .4 5± 0 .15 ) m g/ d〕等方面均显著优于对照组。结论 :灯盏花素联合力源精纯溶栓酶治疗 U AP疗效优于常规西药治疗。     

祛瘀消斑胶囊治疗不稳定型心绞痛及对其血浆Fib、DD的影响

目的　观察祛瘀消斑胶囊治疗不稳定型心绞痛及对其血浆Fib和DD水平的影响。方法　对 4 0例不稳定型心绞痛患者随机分为常规西药加祛瘀消斑胶囊治疗组 (治疗组 )和常规西药治疗组 (对照组 ) ,治疗组与对照组各 2 0例。采用相应药物治疗 4周后 ,观察 2组患者的临床疗效、心电图改善及硝酸酯类药物的停减率 ,以及血浆Fib、DD水平变化 ,并进行比较分析。结果　治疗组可显著改善心绞痛症状 ,与对照组比较有显著性差异 (P <0 .0 5 ) ,2组患者心电图改善情况及硝酸酯类药物减停率无显著性差异 (P >0 .0 5 )。治疗组降低Fib、DD水平 ,与对照组比较有显著性差异 (P <0 .0 5 )。 2组均未出现明显不良反应。结论　祛瘀消斑胶囊可显著降低不稳定型心绞痛患者Fib、DD水平 ,联合西药治疗不稳定型心绞痛 ,疗效优于单用西药 ,且安全可靠。     

Additional molsidomine in refractory unstable angina pectoris

Summary In a prospective single-blind study we examined the effects of additional molsidomine in 20 patients (63±10 years; 15 males, 5 females) with unstable resting angina (3 attacks/24 hours) refractory to triple therapy (nitrates, calcium antagonists, and beta blockers) combined with heparin or aspirin. All but one patient had coronary artery disease documented by coronarography (n=17) or by recent myocardial infarction (n=3). Two patients had angiographically documented severe coronary spasms. Patients entered the study if coronary bypass surgery or PTCA could not be performed within 3 days after angiography (n=9) or was not feasible due to anatomical or technical reasons (n=6), concomitant malignant disease (n=2), or age greater than 75 years (n=3). All patients received molsidomine orally 12 to 24 mg/day. In 15 of the 20 patients molsidomine was given i.v. initially, starting with 20 mg i.v., followed by infusion of 1 to 4 mg/hour. Heart rate and blood pressure did not change significantly, and eight patients had a slight decrease of systolic and diastolic blood pressure. Severe adverse effects did not occur, and moderate headaches were reported by five patients. In 13 patients, unstable angina could be stabilized, and they remained free of resting angina; five had a marked reduction of the frequency of anginal attacks. In two patients, molsidomine was without demonstrable beneficial effects. After a follow-up of 4 weeks, nine patients were free of symptoms after bypass surgery or PTCA, 10 continued to have angina NYHA class II or III, and one patient died due to acute myocardial infarction and cardiogenic shock 4 days after starting additional molsidomine. We conclude that molsidomine is well tolerated and has a marked beneficial effect in patients with refractory unstable angina. Molsidomine should therefore be considered for routine therapy of unstable angina, especially in those patients who are suspected of tolerance to nitrate therapy.     

Direct molecular diagnosis of myotonic dystrophy

Hecht BK, Donnelly A, Gedeon AK, Byard RW, Haan EA, Mulley JC. Direct molecular diagnosis of myotonic dystrophy. Clin Genet 1993: 43: 276–285. © Munksgaard, 1993 Myotonic dystrophy (DM) arises from an unstable trinucleotide (CTG_n) repeat sequence within the DM locus at 19q13.3. Twenty-three myotonic dystrophy families containing 205 persons with no symptoms, minimal manifestations, classic DM or congenital DM were investigated to validate the application of the pM10M6 probe to direct molecular diagnosis. Affected family members had been diagnosed clinically and the unaffected family members had been assigned carrier probabilities close to either zero or 100%, using closely linked flanking markers. Southern analysis identified all 89 DM gene carriers as having expansions of the unstable element. PstI detected all small expansions of the repeat sequence as easily seen discrete bands; but large expansions were usually seen as diffuse smears, sometimes difficult to distinguish from lane background. EcoRI concentrated these diffuse smears, associated with somatic instability, into discrete bands which were easy to detect; but it did not resolve the smaller expansions present in 9 (10%) of the DM carriers. It is essential that PstI and EcoRI gels are run in parallel to detect all DM gene carriers. The extent of expansion of CTG correlated with age of onset and disease severity. Biopsies of various fetal tissues from two terminated pregnancies confirmed the diagnosis obtained by CVS and revealed no heterogeneity between tissues at this developmental stage. Further expansion occurred during the culture of CVS cells, indicating that direct prenatal diagnosis needs to be carried out on CVS tissue rather than on cultured cells. The intergenerational change of the repeat sequence from DM parent to DM offspring showed a significant parental sex difference for those parents with large expansions. Contraction of the unstable element was observed in the three males carrying the largest expansions and could explain why congenital DM is exclusively of maternal origin.     

Soluble Antiapoptotic Molecules and Immune Activation in Chronic Heart Failure and Unstable Angina Pectoris

Programmed myocyte cell death and activation of the immune system have been shown to occur in patients with congestive heart failure. Besides, unstable angina episodes are likely to be associated with immune activation. Our aim was to evaluate the role of changes in circulating levels of soluble Fas (sFas), suggestive of an enhanced inhibitory response to ongoing apoptosis, and soluble IL2 receptor (sIL2-R), indicative of T-lymphocyte activation, in chronic heart failure and unstable angina pectoris. Thirty patients affected by chronic heart failure (20 idiopathic and 10 ischemic cardiomyopathy) and 13 patients with unstable angina were evaluated. Twenty healthy individuals matched for age and gender were used as controls. A complete biochemical determination of indexes of myocardial damage including cardiac troponin I (cTnI) and creatine kinase (MB/CK) was performed. The results demonstrated that mean levels of sFas and sIL2-R were significantly increased in patients affected by chronic heart failure and unstable angina and were not associated with changes in renal function or with serum levels of cTnI. Highest values of sFas were found in NYHA class IV patients (IV NYHA class = 7.39 ± 0.52 vs. controls = 1.34 ± 0.12 ng/ml; P < 0.01) and more elevated in idiopathic than in ischemic cardiomyopathy (3.64 ± 0.40 vs. 1.82 ± 0.37 ng/ml; P < 0.01). Moreover, in chronic heart failure patients sFas and ejection fraction were negatively correlated (P = 0.01), whereas sFas and sIL2-R were positively correlated (P < 0.01). In unstable angina patients too, sFas and sIL2-R appeared to be correlated (P = 0.03); whereas sFas (angina group = 3.18 ± 0.39 vs. controls = 1.34 ± 0.12 ng/ml; P < 0.01) and sIL2-R (angina group = 0.46 ± 0.11 vs. controls = 0.00 UI/ml; P < 0.01) were higher in angina group than in controls. In most of the cases, the increase of sFas was associated with comparable changes in sIL2-R serum levels, indicating that the activation of Fas system is strictly associated with autoimmune–inflammatory reactions. This phenomenon, both in chronic heart failure and in unstable angina, occurs in the absence of biochemical evidences of myocardial damage and seems to parallel the activation of T cell. Soluble Fas could have a role in sustaining inflammatory response and in prolonging the detrimental effects correlated with it in chronic heart failure and angina pectoris.     

心痛安颗粒剂对不稳定性心绞痛患者血小板功能及凝血系统的影响

目的 :观察心痛安颗粒剂对不稳定性心绞痛患者血小板和凝血系统的作用。方法 :6 0例不稳定性心绞痛患者随机分为心痛安组 (30例 ,常规西药加心痛安颗粒剂治疗 )与对照组 (30例 ,单用常规西药治疗 ) ,观察治疗前后血小板最大聚集率 (Ma% )血小板 α颗粒膜糖蛋白 (GMP- 140 )和 D-二聚体 (D- D)的变化。结果 :治疗后 ,心痛安颗粒组的 Ma% ,GMP- 140和 D- D经治疗后明显下降 ,下降幅度明显大于对照组。结论 :心痛安颗粒剂可能通过抑制血小板聚集、活化和纤维蛋白合成而发挥治疗不稳定性心绞痛的作用。     

低分子肝素治疗不稳定型心绞痛33例疗效观察

目的：探讨低分子肝素治疗不稳定型心绞痛的疗效及安全性,方法：不稳定型心绞痛33例,经内科常规药物治疗疗效不佳,加用低分子肝素0．4ml,2次／d腹壁皮下注射,疗程10d。结果：低分子肝素治疗后总有效率93．9％,心绞痛发作次数,持续时间,硝酸甘油用量均显著减少（P＜0．01）,全血粘度,血浆粘度和纤维蛋白原均明显降低（P＜0．05）,无发生急性心肌梗塞和猝死,无出血不良反应,结论：低分子肝素治疗不稳定型心绞痛安全,有效。     

果糖治疗不稳定性心绞痛的临床疗效

目的　观察果糖治疗不稳定性心绞痛的疗效 .方法　 138例患者随机分为果糖组 (70例 )和对照组 (6 8例 ) ,观察心绞痛发作次数 ,12导联心电图变化和心脏事件发生次数(心肌梗死、猝死、严重的心律失常 ) .结果　心绞痛发作次数 :果糖组和对照组明显低于治疗前 (P<0 .0 1) ,治疗后果糖组也明显低于对照组 [(0 .6 8± 0 .5 7)次· d- 1 vs(1.0 4± 0 .81)次· d- 1 ,P<0 .0 1];12导联心电图改善的比较 :果糖组 (4 9/70例 )明显优于对照组 (36 / 6 8例 ,P<0 .0 5 ) ;心脏事件发生上 ,果糖组明显低于对照组 (8/ 70例比 17/ 6 8例 ,P <0 .0 5 ) .结论　果糖治疗不稳定性心绞痛有明显的临床疗效