急性冠脉综合征患者强化抗栓治疗研究进展

急性冠脉综合征（ACS）是冠心病的严重类型,ACS患者不仅病死率较高,还存在缺血事件（如缺血性卒中、心肌梗死）复发风险。血小板聚集及血栓形成是导致ACS的重要原因。为降低缺血事件的发生风险,临床推荐ACS患者接受阿司匹林联合强效P2Y12抑制剂的双联抗血小板治疗12个月。然而在标准双联抗血小板治疗下,ACS患者残余缺血风险（经抗栓治疗后仍残留的缺血事件发生风险）仍旧较高。因此为进一步降低缺血事件发生风险,临床对强化抗栓方案的研究也逐渐增多。本文通过总结强化抗栓治疗方案的作用机制及其最新研究进展,发现延长双联抗血小板治疗时间、三联抗血小板治疗、双通道抑制（抗血小板联合抗凝治疗）等强化抗栓治疗方案可降低缺血事件发生风险,为进一步指导临床个体化抗栓治疗及明确最佳抗栓策略提供了参考。     

Platelet proteins as autoantibody targets in idiopathic thrombocytopenic purpura

Idiopathic thrombocytopenic purpura (ITP), caused by autoantibodies directed against certain platelet antigens, is the most common entity of the immune thrombocytopenias. ITP is an acquired disorder and can affect both children and adults. However, the clinical syndromes of ITP are distinct between children and adults. Childhood (acute) ITP characteristically is acute in onset, occurs within 1-2 weeks of an infection, usually of viral origin, resolves spontaneously within 6 months. Adult (chronic) ITP has an insidious onset and rarely resolves spontaneously. Over the last decade considerable new information has accumulated as to the pathophysiological mechanisms of immune thrombocytopenias. In addition, most of the knowledge on this disorder has been obtained from studies of adult patients with chronic ITP. The present work gives an updated overview of the platelet autoantigens and the molecular immunological reactions in ITP.     

丹参片在冠状动脉支架介入治疗后应用的初步观察

目的观察丹参片与抗血小板药物联合应用对冠状动脉支架介入治疗后血栓等术后冠状动脉事件的预防作用。方法选择支架植入成功的冠心病患者82例,随机分为治疗组(42例)和对照组(40例),两组均服用支架植入术常规用抗血小板药,治疗组加用丹参片,每次4片,每日3次。采用双缩尿法、激光散射比浊法和流式细胞术检测两组患者行支架植入术前、术后即刻和术后30 d时的血浆纤维蛋白原(Fg)、C反应蛋白(CRP) 和血小板膜糖蛋白((3P)Ⅱb／Ⅲa、P选择素(CD62P)的变化。结果与对照组比较,治疗组血浆CRP显著下降 (P<0．05),GPⅡb／Ⅲa和CD62P也有降低的趋势。经6个月临床随访,治疗组心绞痛复发5例(11．9%),未发生支架术后再狭窄;对照组心绞痛复发21例(52．5％),支架术后再狭窄9例,心肌梗死3例;治疗组心绞痛复发率显著低于对照组(P<0．05)。结论丹参片与抗血小板药联合应用能预防冠状动脉支架血栓等术后冠状动脉事件,且疗效优于单用抗血小板药。     

他汀类与抗血小板药联合用药对缺血性脑血管病患者颈动脉粥样硬化的干预作用

目的:探讨缺血性脑血管病患者联合应用他汀类及抗血小板药对颈动脉粥样硬化和脑血管事件的干预作用。方法:选择146例缺血性脑血管病合并颈动脉粥样硬化患者,将其随机分为治疗组和对照组。治疗组74例,应用氟伐他汀(每晚40mg)和拜阿斯匹灵(100mg/d),对照组72例,仅给拜阿斯匹灵(100mg/d)。共随访2年,分别在治疗前,治疗后6月、12月、18月、24月检测血脂,颈动脉内-中膜厚度,颈动脉斑块积分。结果:治疗组平均颈动脉内-中膜厚度和颈动脉斑块积分,治疗前分别为(1.22±0.19)mm和4.4±2.5,治疗后分别为(0.87±0.15)mm和2.8±1.1,治疗前后比较差异具有显著性(P<0.01)。随访结束时,治疗组缺血性脑血管病复发率9.5%,与对照组复发率(26.3%)相比明显下降。结论:联合应用他汀类及抗血小板药能延缓和逆转缺血性脑血管病患者颈动脉粥样硬化的进展,对缺血性脑血管病的复发有很好的预防作用,且不增加脑出血发生率。     

Role of antiplatelet therapy in cardiovascular disease I: acute coronary syndromes

The acute coronary syndromes (ACS), consisting of ST-segment elevation myocardial infarction (STEMI), non-STEMI (NSTEMI), and unstable angina, remain a leading cause of death in the United States. Through the process of atherothrombosis, underlying atherosclerosis can progress to an acute ischemic coronary event. This disease mechanism is also common to ischemic

stroke and peripheral arterial disease. As ACS is a heterogeneous disease, accurate patient diagnosis and risk categorization is essential. Treatment approaches for both STEMI and NSTEMI ACS consist of a combination of surgical intervention and pharmacotherapy, with antiplatelet agents such as clopidogrel, aspirin and glycoprotein IIb/IIIa receptor antagonists playing an essential role.     

Role of Ticlopidine on Adriamycin-Induced Nephropathy

The effect of ticlopidine on rats with adriamycin nephropathy was observed during 26 weeks. In the ticlopidine-treated nephrotic animals (TNG), proteinuria was less than in the untreated nephrotic animals (NG), but this difference was significant only at week 6 (TNG = 47.27 ± 16.52 versus NG = 100.08 ± 13.83 mg/24h, p < 0.01) and week 26 (TNG =157.00 ± 28.73 versus NG = 217.00 ± 21.73 mg/24h, p < 0.01) after ADR injection. NG presented severe tubulointerstitial abnormalities with a tubulointerstitial lesion index of 3+. No diffience in glomerular lesions was observed among the groups (NG median = 6%. TNG median = 4% and TCG median = 2%). The tubulointerstitial lesion index of TNG was less intense (median = 2+) but not different from those of the control groups (CG median = 1+; TCG median = 0+) nor NG (median = 3+). We concluded that the treatment with ticlopidine produced some partially beneficial effects but did not prevent the devdopment of adriamycin-induced nephropathy.