噻吗洛尔与普萘洛尔治疗高血压病与心绞痛的疗效比较

劳累性心绞痛38例采用噻吗洛尔2.5-5mg, tid,共4wk;另12例采用普萘洛尔10-20mg, tid,共4wk。结果:前者显效率为79％,显著高于后者42％(P<0.05)。高血压病(Ⅰ,Ⅱ期)37例采用噻吗洛尔治疗,方法同上;另13例采用普萘洛尔20-40mg, tid,疗程亦4wk。结果:2组均有显著降压疗效(P<0.01),噻吗洛尔治疗后1h即获显效,普萘洛尔须24h才获显效。噻吗洛尔7％(5/75)、普萘洛尔4％(1/25)治疗后发生窦性心动过缓,前者被迫停药,后者未停药。     

糖尿病增大无症状心肌缺血发生率

用常规心电图及动态心电图监测的方法，分别观察３０例糖尿病人和３０例非糖尿病人无症状心肌缺血的发生率。发现无症状心肌缺血在糖尿病组显著高于非糖尿病组（Ｐ〈０．０５），部分糖尿病人有严重心肌缺血却无胸痛症状，可能与其植物神经功能损害引起痛阈提高、血中内啡肽水平增高导致痛觉敏感性下降有关，用动态心电图监测可提高无症状心肌缺血的检出率。     

低分子肝素治疗不稳定性心绞痛临床观察

目的:观察低分子肝素治疗不稳定性心绞痛病人的疗效。方法:不稳定性心绞痛病人80例,随机分为两组:治疗组(40例),给予阿司匹林和抗心绞痛常规治疗下,加低分子肝素5000U,每12h一次,连用14d,对照组(40例),给予阿司匹林和抗心绞痛常规治疗。结果:治疗组与对照组在改善心绞痛症状及心电图表现方面总有效率分别为87.5％、70.0％(P<0.05),两组均未发生心脏事件。结论:低分子肝素是一种有效安全的治疗不稳定性心绞痛的药物。     

用反相HPLC分析一例HbF变异体—HbF—新疆[~Aγ~T25(B7)Gly→Arg]

在1989年乌鲁木齐市进行的脐带血筛选中,我室又发现了一例异常胎儿血红蛋白(HbF)。理化性质测定证明该变异体为一轻度不稳定Hb。经反相高效液相色谱法(HPLC)等方法测定证明该变异体为HbF-新疆[~Aγ~T25(B7)Gly→Arg]。胡怀钰曾于1986年首次发现该变异体,并命名。与前例比较,本例除分析方法部分不同外,两例先证者的临床症状亦稍有差别。本例的先证者在半岁前患有轻度贫血,而首例先证者未见关于贫血的报道。     

地尔硫静脉滴注治疗冠心病心绞痛

目的：观察地尔硫Ｚｈｕｏ注射液静脉滴注治疗冠心病心绞痛的疗效。方法：８６例心绞痛患者分为两组，其中治疗组４６例，用地尔硫Ｚｈｕｏ５０ｍｇ加入５％葡萄糖液２５０ｍｌ中静滴，１次／ｄ，连续１０ｄ；对照组４０例用丹参液１６ｍｌ加入５％葡萄糖液２５０ｍｌ中静滴，１次／ｄ，连续１０ｄ。结果：治疗组症状控制总有效率９８％，患者心电图改善率６１％，明显高于对照组的３７％和２８％，地尔硫Ｚｈｕｏ改善心功能效果明显     

心绞痛患者血小板功能改变及丹参对其影响

本实验观察了心绞痛患者血小板环核苷酸水平,血浆TXB_2、6酮PGF_(10)深度、血小板内外5—HT含量及血小板聚集性的变化以及丹参治疗前后各指标的改变。结果表明,心绞痛患者血小板聚集性血浆5—HT和血浆TXB_2水平明显增高,而血小板内5—HT、血浆6—酮—PGF_(10)水平则明显低于对照组。丹参能增加血小板内cAMP水平,降低血浆5—HT水平,对血小板聚集性有抑制作用。     

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.     

急性冠脉综合症与补体激活

目的： 评价各种类型急性冠脉综合症 (ACS) 病人补体激活的情况和补体激活与心肌损伤的关系。方法： 研究对象分为ACS组110例和正常对照组18人。 ACS组包括ST段抬高型心肌梗死（STEMI）51例，非ST段抬高型心肌梗死（NSTEMI）28例和不稳定性心绞痛（UA）31人。检测病人和正常对照健康人血浆C₃和C₄，CK-MB和肌钙蛋白T (TnT)浓度。结果： STEMI和 NSTEMI病人峰值C₃ 水平［分别为（1 525±302） mg/L和（1 516±289）mg/L］ 和C₄［分别为（423±123） mg/L和（396±68） mg/L］水平高于UA病人和对照组的C₃［分别为（1 275±172） mg/L和（1 072±196） mg/L,P<0.01］ 和C₄［分别为（356±91）mg/L和（182±73） mg/L,P<0.01］。UA病人的 C₃ ［(1 275±172） mg/L］和C₄ ［（356±91） mg/L］均高于对照组（P<0.01）。 ACS病人C₃和C₄水平在住院的前7 d均有明显的变化（P<0.01）。ACS病人峰值C₃和C₄水平与峰值CK-MB（分别为r=0.51和r=0.46，P<0.01）和肌钙蛋白T（分别为r=0.48和r=0.39，P<0.01）呈正相关。结论： ACS病人血浆C₃和C₄均明显升高。C₃和C₄水平与ACS的联系提示补体激活与心肌坏死有关。     

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.