替罗非班对急性冠状动脉综合征患者肝剂量及血小板的影响

目的：探讨对急性冠状动脉综合征患者在常规治疗基础上联合替罗非班强化抗血小板治疗对肝素抗凝剂量及血小板数量和功能的影响。资料和方法：选择因急性冠状动脉综合征入院的患者共64例，分为双联抗血小板和肝素抗凝的常规治疗组(n=36)和在此基础上联合使用替罗非班组(n=28)，以达到肝素抗凝使激活的部分凝血时间延长2倍为标准，比较两组肝素使用剂量、ADP诱导的血小板聚集率及血小板数量变化情况。结果：替罗非班组肝素用量（500±120U/h）显著低于常规组(760±148U/h, P<0.01)，用药后两组的血小板聚集率均显著低于用药前(P<0.01)，但替罗非班组降低更显著(P<0.01)，替罗非班组用药后血小板降低(P<0.05)。结论：联合应用替罗非班可降低肝素抗凝剂量，显著抑制血小板聚集活性，并呈降低降低血小板数量的趋势。     

动脉粥样硬化的抗栓和抗凝治疗

在由动脉粥样硬化引起的冠心病、缺血性脑卒中和外周动脉病中,抗血小板和抗凝治疗是主要的措施之一.抗血小板治疗可以减少血小板聚集,防治斑块上形成白色血小板血栓,肝素或低分子量肝素则可以防止白色血栓基础上进一步形成红色血栓完全阻塞动脉.阿司匹林、氯吡格雷是目前最常用的抗血小板药物,而肝素或低分子量肝素是目前最常用的抗凝药物.     

高血压合并冠心病患者抗凝和抗血小板治疗的选择

<正> 抗血小板治疗和抗凝治疗统称为抗栓治疗,常用抗血小板药物包括阿司匹林、氯吡格雷和血小板膜糖蛋白(GP)Ⅱh/Ⅲa受体拮抗剂,常用抗凝药物包括低分子肝素、肝素以及华法林。高血压是冠心病最重要的危险因素之一,抗栓治疗是冠心病预防中的主要手段。多年来,对于哪些高血压患者应该应用抗栓药物一直存在争议。合并冠心病的高血压     

不同途径应用低分子肝素对血小板活性的影响及阿司匹林的干预作用

目的:探讨不同途径应用低分子肝素(LMWH)对血小板活性的影响,并观察联用常规剂量100 ms/d的阿司匹林对该影响的干预作用.方法:107例患者依据用药途径不同分为静脉达肝素钠组(n=29)、皮下达肝素钠组(n=27)、静脉达肝素钠加阿司匹林组(n=25)和皮下达肝素钠加阿司匹林组(n=26).分别采用酶联免疫双抗体夹心法(ELISA)和流式细胞技术检测静脉及皮下应用低分子肝素后血小板活化指标:血小板α颗粒膜糖蛋白-140(GMP-140)、血管性假血友病因子相关抗原(vWF:Ag)及血小板膜糖蛋白Ⅱb/Ⅲa(GPⅡb/Ⅲa)受体复合物的变化,并观察联用常规剂量阿司匹林干预后上述指标的变化.结果:不同途径应用低分子肝素对血小板激活的影响:血小板膜糖蛋白Ⅱb/Ⅲa水平:静脉达肝素钠组注射0.5 h后和皮下达肝素钠组注射2天后均较其注射前升高,差异均有统计学意义(P<0.05).血小板α颗粒膜糖蛋白-140水平:静脉达肝素钠组注射0.5 h后较其注射前升高,差异有统计学意义(P<0.05).阿司匹林对不同途径应用低分子肝素激活血小板的干预作用:静脉达肝素钠加阿司匹林组和皮下达肝素钠加阿司匹林组,血小板膜糖蛋白Ⅱb/Ⅲa水平、血小板α颗粒膜糖蛋白-140水平,2组各时间点较注射前差异无统计学意义(P>0.05);而血管性假血友病因子相关抗原水平,静脉达肝素钠加阿司匹林组注射0.5 h后较其注射前下降,差异有统计学意义(P<0.05).结论:静脉或皮下应用低分子肝素均可以激活血小板,且联用常规剂量100 mg/d的阿司匹林能够有效抑制由低分子肝素引起的血小板活性增高.     

第492例——反复血栓形成, 血小板减低

患者女性, 43岁。因反复血栓形成2年余, 血小板(PLT)减低1年余就诊。患者临床表现为反复动静脉血栓形成、少见部位血栓及抗凝治疗中新发血栓, 伴有进行性加重的血小板减少。外院及我院多次筛查抗核抗体、抗可溶性抗原抗体、抗磷脂抗体谱均为阴性。病程中糖皮质激素冲击及静脉免疫球蛋白(IVIG)曾使血小板升至正常, 骨髓巨核细胞成熟障碍, 支持免疫性血小板减低。入院后筛查易栓症的病因, 同时予肝素静脉泵入抗凝, 利妥昔单抗600 mg 1次;IVIG 20 g/d×3 d;口服艾曲波帕50 mg/d治疗。以上治疗3周后, 血小板减少无明显改善, 期间仍有新发血栓。后易栓症基因筛查回报PROS1基因杂合突变, MTHFR基因型为TT型, 发现少量IgGκ型M蛋白, 但仍不足以解释如此顽固的血栓倾向。在排除肿瘤、肝素诱导的血小板减少症等之后最终诊断血清阴性抗磷脂综合征可能性大。后续加用地塞米松20 mg/d×4 d, 联合口服西罗莫司2 mg/d加强免疫抑制, 抗凝方案过渡为低分子肝素后出院。1个月后电话随访, 患者颅内静脉窦血栓所致的头痛症状好转, PLT升至(20～30)×109/L, 无新...     

盐酸替罗非班致极重度血小板减少一例分析

替罗非班是一种可逆性血小板糖蛋白Ⅱb/Ⅲa受体拮抗剂,可引起血小板减少症.现有文献报道替罗非班所致的极重度血小板减少症较少.下文报道一例经皮冠脉PCI术后应用替罗非班(商品名欣维宁,武汉远大制药集团有限公司,批号为H-20041165)导致的极重度的血小板减少症.     

替罗非班对急性冠状动脉综合征肝素剂量及血小板的影响

目的探讨替罗非班对急性冠状动脉综合征患者肝素剂量及血小板计数和功能的影响。方法选择因急性冠状动脉综合征入院患者64例，分为常规治疗组36例和替罗非班组28例，常规治疗组使用抗血小板药和肝素抗凝；替罗非班组在上述基础上联合使用替罗非班，以达到肝素抗凝使激活的部分凝血时间延长2倍为标准，比较两组肝素用量、二磷腺苷（ADP）诱导的血小板聚集及血小板数。结果替罗非班组肝素用量（500±120）U／h显著低于常规组（760±148）U／h，差异有统计学意义（t=7.558，P〈0．01），用药后两组的血小板聚集率均显著低于用药前（P〈0．01），但替罗非班组降低更显著（P〈0．01），替罗非班组用药后血小板数降低（P〈0.05）。结论联合应用替罗非班可降低抗凝肝素剂量，显著抑制血小板聚集，并呈降低血小板数的趋势。     

肝素诱导的血小板减少症

接受抗凝剂治疗或预防栓塞的病人,最常使用肝素,而肝素诱导的血小板减少症(heparin-inducedthrombocytopenia,HIT)是肝素治疗的并发症,此并发症与肝素预期的治疗效果相反。1什么是HIT?通常,肝素预防血栓栓塞,不影响血小板,由于肝素触发免疫系统,HIT导致血小板数降低(血小板减少症)。HIT可出现2种明显的类型:非免疫和免疫介导。非免役介导HIT:最常出现,血小板数轻微减少,对身体无害。免疫介导HIT:较少出现,但很危险。免疫介导HIT引起血小板数明显降低,但尽管血小板数很低,HIT病人仍有栓塞的危险。病人使用肝素后,在肝素和特殊的血…     

基因分型导向抗血小板治疗的曙光——深度解析TAILOR PCI研究

阿司匹林联合氯吡格雷双联抗血小板治疗(dual antiplatelet therapy,DAPT)是接受经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)患者术后的标准治疗[1-2]。氯吡格雷仍然是目前使用最广泛的P2Y12抑制药[3]。然而,由于基因变异,大约三分之一的患者对氯吡格雷无或低反应,需要接受新型P2Y12抑制药治疗(例如替格瑞洛或普拉格雷)[4-5]。因此,如何根据基因类型量身定制抗血小板治疗方案一直是临床研究的热点[6-7]。     

2012年急性冠状动脉综合征抗栓治疗热点聚焦

<正>近年来急性冠状动脉综合征(ACS)抗栓治疗领域取得了较大进展,包括新型抗血小板药物普拉格雷和替卡格雷挑战了氯吡格雷一枝独秀的局面,经皮冠状动脉介入治疗(PCI)术前氯吡格雷的负荷剂量不再是300 mg,而是增加至600 mg;Ⅱb/Ⅲa受体拮抗剂静脉给药仍为标准途径。抗栓     

Coronary Sarcoidosis Presenting as Acute Coronary Syndrome

Sarcoidosis is a systemic disorder of uncertain etiology characterized by noncaseating granulomatous inflammation. The disease often involves the heart on autopsy, but the antemortem diagnosis of cardiac sarcoidosis is frequently missed. Cardiac involvement usually includes granulomatous inflammation or fibrosis of the myocardium, conduction system, or pericardium. We now describe a case of epicardial coronary involvement by sarcoidosis, where the diagnosis was made by surgical biopsy of the coronary artery in an African American man presenting with acute coronary syndrome and recurrent symptomatic restenosis following coronary intervention. The case extends the spectrum of common cardiac syndromes that cardiac sarcoidosis can masquerade as and highlights the importance of maintaining a high index of suspicion for early recognition and instituting specific treatment that might improve prognosis. A review of the literature also suggests the need for improvement in diagnostic approaches and prospective clinical trials to establish the best management strategy for this disease. Copyright © 2009 Wiley Periodicals, Inc.     

Coronary Atherosclerotic Precursors of Acute Coronary Syndromes

Background

The association of atherosclerotic features with first acute coronary syndromes (ACS) has not accounted for plaque burden.

Coronary Thromboembolism with Fatal Outcome Following Coronary Angiography

ABSTRACT A case of fatal thromboembolic occlusion of the left coronary artery at selective coronary arteriography is described. The course of events and the findings at autopsy suggest that thrombotic material was deposited on one intravascular catheter and transferred to a second catheter inserted over the same guide wire. Contrast injection through the second catheter into the left coronary ostium resulted in immediate and fatal occlusion of the two major branches of the left coronary artery.     

Coronary embolism

The literature on coronary embolism is reviewed and the rarity of such an occurrence emphasized. Cases in which the source of the embolism is not found at autopsy should not be accepted as proved cases of coronary embolism. Three cases of coronary embolism are reported. In one, the source of the embolus was a thrombus in the femoral vein; there was also a patent foramen ovale. In the second case, the source of the embolus was a mural thrombus in the right coronary artery, occurring on the basis of an atheromatous ulcer. The embolus had lodged in the distal part of this artery at the origin of the posterior descending branch. In the third instance, the source of the embolus which had occluded the mouth of the right coronary artery was a thrombus occurring on an atheromatous ulcer in the region of the sinus of Valsalva. In all three instances the patients died suddenly.     

Coronary microembolization

Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndromes and during coronary interventions. Atherosclerotic plaque rupture does not always result in complete thrombotic occlusion of the entire epicardial coronary artery with subsequent acute myocardial infarction; however, in milder forms it may result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation. The present report summarizes the available morphologic evidence for coronary microembolization in patients who died of coronary artery disease, especially sudden death. The report then goes on to address the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes and heart failure. Finally, the report presents the available clinical evidence for coronary microembolization, highlights its key features--arrhythmias, contractile dysfunction, infarctlets and reduced coronary reserve--and addresses prevention by mechanical protection devices and glycoprotein IIb/IIIa antagonism.