速避凝治疗不稳定性心绞痛的临床观察

目的 评价速避凝治疗不稳定性心绞痛（ＵＡ）的临床疗效。方法 将筛选的８０例ＵＡ患者随机分成治疗组（４０例,皮下注射速避凝注射剂）和对照组（４０例,静点前列腺素Ｅ１注射剂）。治疗期间两组均不用其他除脂、降压及血管扩张剂。心绞痛发作程度较重且频繁时,可临时给硝酸甘油片舌下含化,并做记录。结果 治疗后心绞痛发作情况及心电图改变两组对照经ｔ检验,差异有显著性至非常显著性。治疗组总有效率为８５％,对照组总有     

Additional value of thallium-201 SPECT to a conventional exercise test for the identification of severe coronary lesions after an episode of unstable coronary artery disease

The additional value of thallium-201 SPECT to a conventional exercise test for the identification of patients with severe coronary lesions was evaluated in 170 men, one month after an episode of unstable coronary artery disease. Severe coronary lesions at coronary angiography — defined as three vessel disease, left main stenosis or proximal left anterior descending artery stenosis as part of two vessel disease — were observed in 45.9%. In the SPECT image, the left ventricular myocardium was divided into nine segments and each segment was classified as either normal (=0), reduced uptake (=1) or uptake defect (=2). The sum of gradings in all segments post-exercise was denoted SPECT score. The patients were divided into nine different groups regarding ST-depression during exercise (no ST-depression, ST-depression in 1–2 leads or 3 leads) and SPECT score (no SPECT score, 1–3 scores or 4 scores). Severe coronary lesions were, in 68% identified by SPECT score 4 and in 65% by ST-depression in 1 lead at exercise test. The specificity for identification of severe coronary lesions was, for both tests, 65%. SPECT score 4 and/or ST-depression in 3 leads identified 82% of the patients with severe coronary lesions with a specificity of 63%. Furthermore, SPECT score 3 identified more patients with isolated proximal left anterior descending artery stenosis than ST-depression alone at exercise test.     

Optimizing the treatment of unstable angina

Unstable angina and non-Q-wave myocardial infarction (MI) are at the center of the spectrum of myocardial ischemia, which ranges from stable angina to acute Q-wave MI. In addition to clinical evaluation, cardiac specific markers such as troponin T or I can assist in early diagnosis, triage, and risk stratification. Antithrombotic therapy with aspirin and heparin have been shown to improve the outcome of patients with acute ischemic syndromes. Thrombolytic therapy does not appear to be beneficial in these syndromes. Antiischemic therapy remains an important component of the overall therapy. A strategy of early coronary angiography and revascularization leads to a similar long-term outcome as compared with a more conservative strategy of revascularization for recurrent ischemia, but the early invasive strategy is more expeditious as a large number of conservatively treated patients have recurrent ischemia. At present, many new antithrombotic agents are under active investigation, with the hope that they will lead to further improvement in the clinical outcome of patients with acute ischemic syndromes.     

Venous plasma levels of endothelin-1 are not altered immediately after nitroglycerin infusion in healthy subjects

Endothelin-1 and nitric oxide play an important regulatory role in the control of vascular smooth muscle tone. Nitroglycerin (NTG), a nitric oxide donating drug, may inhibit endothelin production. In this double-blind placebo-controlled crossover study, plasma levels of endothelin-1 were measured before and immediately (5–30 s) after 80 min infusion of NTG (glyceryl trinitrate) or saline in 12 healthy subjects. On two different days separated by at least 1 week, NTG in four different doses, 0.015, 0.25, 1.0, and 2.0 g·kg^–1·min^–1, or placebo (isotonic saline) was infused successively for 20 min each dose. During the infusion blood pressure and heart rate were measured. NTG infusion significantly decreased systolic blood pressure from 112.4 to 103.4 mmHg and pulse pressure from 39.3 to 29.5 mmHg. Heart rate increased from 62.7 to 73.1 beats·min^–1. No changes in endothelin-1 plasma levels were induced by NTG infusion (2.4 pg·ml^–1 before NTG vs. 2.7 pg·ml^–1 after NTG) and placebo infusion also did not affect plasma endothelin-1. It is concluded that venous plasma levels of endothelin-1 are not altered immediately after NTG infusion.     

血清铁蛋白,血清铁与冠心病及其有关危险因素关系的临床研究

目的：研究血清铁蛋白（ＳＦ）、血清铁（ＳＩ）与冠心病（ＣＨＤ） 之间的关系以及ＳＦ、ＳＩ与ＣＨＤ有关危险因素的相关关系。方法：测定４３ 例心肌梗塞（ＭＩ）,４４ 例心绞痛（ＡＰ） 患者的ＳＦ、ＳＩ、血脂、血糖（ＢＧ）、血压、腰臀比（ＷＨＲ） 、体重指数（ＢＷＩ）水平,与４０ 例健康对照组进行分析。结果：ＡＰ组、ＭＩ组男、女、总体ＳＦ水平分别明显高于对照组（Ｐ＜ ０．０５～０．００１）,但女性升高不如男性明显;ＳＦ水平与ＷＨＲ、甘油三脂（ＴＧ）、低密度脂蛋白（ＬＤＬ）呈正相关（ｒ＝ ０．４６,０．３４,０．４４）,与高密度脂蛋白（ＨＤＬ）呈负相关（ｒ＝ － ０．３３）。结论：体内ＳＦ增加是ＡＰ、ＭＩ的主要易发因素之一;ＳＦ水平受营养因素特别是某些脂代谢及腹部脂肪分布的影响     

心肌肌钙蛋白T对梗死后心绞痛病人预后的判断价值

目的探讨心肌肌钙蛋白Ｔ（ｃＴｎＴ）对梗死后心绞痛（ＰＡ）病人预后的判断价值。②方法急性心肌梗死（ＡＭＩ）发生１０ｄ后,连续２０ｄ检测１２６例ＰＡ病人血清ｃＴｎＴ和肌酸磷酸激酶同工酶ＭＢ（ＣＫ－ＭＢ）,随访０．５年,观察心脏事件（再梗死、猝死或严重心力衰竭）的发生率。③结果连续２０ｄ检测,ｃＴｎＴ均正常（ｃＴｎＴ≤０．２μｇ／Ｌ）者２６例,随访期内只有１例发生心脏事件;ｃＴｎＴ升高≤１０次者５１例,随访期内发生心脏事件１２例,其中非Ｑ波心肌梗死４例,Ｑ波心肌梗死８例;ｃＴｎＴ升高＞１０次者４９例,随访期内发生心脏事件２９例,其中非Ｑ波心肌梗死２０例,Ｑ波心肌梗死９例。特别是非Ｑ波心肌梗死后的ＰＡ病人,其心脏事件的发生率明显高于Ｑ波心肌梗死（χ２＝１５．３２,Ｐ＜０．００１）。ＣＫ－ＭＢ升高者１３例,随访期内发生心脏事件５例。④结论血清ｃＴｎＴ监测可以判断ＰＡ病人的预后,ｃＴｎＴ持续升高者,预后不良。     

复方丹参、黄芪注射液治疗不稳定型心绞痛临床观察

目的观察复方丹参、黄芪注射液治疗不稳定型心绞痛的临床疗效;方法61例不稳定型心绞痛患随机分为两组,对照组采用常规西药治疗;治疗组在对照组的基础上,加用复方丹参注射液20ml,黄芪注射液20ml加入5％葡萄糖250ml中静脉滴注,每日1次,两组均2周为1个疗程,对其结果做统计学赴理;结果治疗组在总的临床疗效方面和心电图缺血性S—T段恢复以及症状控制时间上,均明显优于西药对照组(总有效率分别为93.55％和73．33％,P<0.05);结论复方丹参、黄芪注射液联用治疗不稳定型心绞痛疗效显,并与抗心绞痛西药有协同治疗作用。     

急性心肌梗死和稳定型心绞痛血小板GPⅡb,GPⅢa动态变化的比较研究

目的：观察急性心肌梗死（ＡＭＩ）和稳定型心绞痛（ＳＡＰ）血液中血小板表面糖蛋白ＧＰⅡｂ和ＧＰⅢａ的动态变化,探讨急性心肌缺血前、后血小板的活性。方法：６１例住院的心病患者,其中ＡＭＩ３２例,ＳＡＰ２９例,采用竞争性酶联免疫方法比较ＡＭＩ及ＳＡＰ患者发病后２４ｈ,第２天、第３天、１财２周时血中血汀反ＧＰⅡｂ和ＧＰⅢａ的含量动态变化,并进行统计学分析,结果：ＳＡＰ组ＧＰⅡｂ和ＧＰⅢａ在上述５个时间段分     

梗死前心绞痛发作对急性心肌梗死近期预后的影响

目的：评价急性心肌梗死发病前４８小时内的心绞痛发作对急性心肌梗死近期预后的影响。方法：将８７１例急性心肌梗死前４８小时内有心绞痛组３７８例,梗死前无心绞痛４９３例,对两组住院期间的并发症和病死率进行比较分析,结果：发生心绞痛组的心肌梗死范围较小,住院期间病率、心力衰竭、心源性休克、室速的发生率均低于梗死前无心绞痛组。末溶栓组和溶栓未再通组,梗死前有心绞痛发作者的近期预后较无心绞痛者好,而两组溶栓冠     

A comparison of nisoldipine and nifedipine, in combination with atenolol, in the management of myocardial ischaemia

The effects of the addition of slow-release nifedipine 20 mgtwice daily and nisoldipine 10 mg twice daily to atenolol monotherapywere compared in a double-blind placebo-controlled study of24 patients with chronic stable angina pectoris. Neither nisoldipinenor nifedipine was associated with significant subjective benefitat these doses. Two hours post-dosing, exercise capacity improvedafter both nisoldipine (duration+37 s, P<0.01; time to angina+67s, P<0.01; time to sign ST depression+60 s, P<0.01) andnifedipine (duration +21 s, ns; time to angina+56 s, P<0.05;time to significant ST depression+49 s P<0.05) However, thisimprovement was not maintained 12 h post-dosing. Ambulatorymonitoring did not demonstrate a sign reduction in the amountof silent or total ischaemia following the addition of eithernifedipine or nisoldipine to atenolol monotherapy. There wasno significant difference between nifedipine and nisoldipinein any parameter tested. In conclusion, like slow-release n 20 mg, the effective durationof anti-ischaemic action of nisoldipine 10 mg is less than 12h. Since several patients experienced vasodilatory unwantedeffects, more frequent administration rather than larger individualdoses may be desirable to achieve a clinical response.