Thrombolytic therapy-associated acute myocardial infarction in patients with acute ischemic stroke: A treatment dilemma

Acute myocardial infarction (AMI) is uncommon in the acute phase of acute ischemic stroke (AIS) and occurs in approximately 1% of the population. Here, we report a paradoxical case of AMI during tissue plasminogen activator (t-PA) infusion for AIS. We review and analyze the previously reported cases. We found that only patients with AMI which occurred after thrombolytic therapy for AIS who received an adequate combination of anticoagulation plus percutaneous coronary intervention survived their events. Several mechanisms have been proposed for the development of AMI after thrombolytic therapy. These mechanisms include fragmented intra-cardiac thrombus, intensified platelet aggregation that may lead to an increased potential for intra-cardiac thrombus formation, and a reduction in clot-associated plasminogen that may lead to a paradoxical hypercoagulable state of the coronary arteries. Currently, there is no consensus regarding this specific scenario. We propose that the therapeutic benefit and the potential risk of hemorrhagic complications should be further investigated and individualized. In patients who receive thrombolytic therapy for AIS and who then develop post-thrombolytic AMI, we suggest that the maximum treatment for the subsequent AMI be instituted promptly to avoid short-term mortality.     

不同剂量的首剂肝素在维持性血液透析患者中的抗凝效果

目的探讨不同剂量的首剂肝素在维持性血液透析患者中的抗凝效果。方法 62例维持性血液透析患者随机分为A、B两组,A组30例,B组32例。肝素抗凝方法:A组每次透析开始时从静脉端给予首次剂量肝素28~32 mg(约0.5 mg/kg),维持期用肝素泵每小时追加肝素6~10mg;B组每次透析开始时从静脉端给予首次剂量肝素14~20 mg(约0.3 mg/kg),维持期用肝素泵每小时追加肝素8~12 mg;同时监测2组患者0、0.5、2、3.5及4 h活化凝血时间(activated clotting time,ACT)及变化曲线,观察治疗过程中管路和透析器凝血情况,治疗后穿刺点压迫止血平均时间、组织器官24 h内出血情况以及在线KT/V情况。结果 2组患者首剂肝素量及维持期肝素用量存在显著性差异,而肝素总量无差异。2组均能顺利完成血液透析,A组透析充分性更好。A组血液透析治疗0.5及2 h ACI较B组明显延长,而在透析3.5及4 h时ACT明显缩短,2组比较均有显著性差异(P0.01);2组ACT 0.5与3.5 h自身比较,A组有明显下降趋势(P0.05),B组无明显差异。2组患者透析器凝血情况、穿刺点压迫时间、透析治疗后24 h内组织器官出血情况比较A组优于B组,差异有统计学意义(P0.01)。结论选择合适剂量的首剂肝素及维持期肝素用量是血液透析顺利进行的关键,首剂肝素用量为28~32 mg(约0.5 ng/kg)时抗凝效果好、透析充分性好,透析后患者出血机会少。     

双向冲水法在无肝素血液透析中的应用效果

目的探讨双向冲水法用于无肝素血液透析中对患者透析器及静脉壶凝血程度、透析时间的影响。方法选取2018年12月至2019年12月于医院行无肝素血液透析的62例患者,按随机数字表法分为两组,各31例。对照组予以传统冲水法,观察组予以双向冲水法,比较两组透析器及静脉壶凝血程度、透析时间。结果两组透析器凝血程度比较,差异无统计学意义(P>0.05);观察组静脉壶凝血程度低于对照组,差异有统计学意义(P<0.05);观察组透析时间长于对照组,差异有统计学意义(P<0.05)。结论双向冲水法可降低无肝素血液透析患者静脉壶凝血程度,延长透析时间,增强透析效果。     

宫腔内灌注粒细胞集落刺激因子联合低分子肝素在薄型子宫内膜患者冻融胚胎移植周期中的研究

目的:探讨宫腔内灌注粒细胞集落刺激因子(G-CSF)联合低分子肝素(LMWH)对薄型子宫内膜患者冻融胚胎移植(FET)周期中的临床疗效。方法:选取2018年6月-2019年10月于山西医科大学第一医院进行FET助孕治疗的薄型子宫内膜患者175例,根据患者自身意愿分为3组,A组:63例患者仅接受激素替代治疗;B组:52例患者接受激素替代治疗+宫腔内G-CSF灌注;C组:60例患者接受激素替代治疗+宫腔内G-CSF灌注+皮下注射LMWH。对3组患者的子宫内膜厚度、子宫内膜血流阻力指数(RI)、搏动指数(PI)、周期取消率、胚胎种植率、临床妊娠率、早期流产率、异位妊娠率等指标进行比较。结果:在内膜转化日,与A组相比,B、C组子宫内膜厚度、Ⅱ+Ⅲ型血流比例均增加,RI、PI均降低(P<0.05)。治疗结局方面,与A组相比,B、C组胚胎种植率、临床妊娠率增加,周期取消率降低,差异有统计学意义(P<0.05);B、C组间比较差异无统计学意义(P>0.05);C组早期流产率较B组降低,差异有统计学意义(P<0.05)。结论:在FET周期中宫腔内灌注G-CSF可提高薄型子宫内膜患者的子宫内膜厚度,改善子宫内膜的血流情况,提高胚胎种植率及临床妊娠率,注射LMWH可降低早期流产率。     

肝素联合低分子肝素预防动静脉内瘘术后早期血栓形成

摘 要 目的： 研究肝素联合低分子肝素对预防动静脉内瘘（AVF）术后早期血栓形成的影响。方法: 采用前瞻性研究方法,将299例行AVF术的患者随机分为两组,对照组患者术后给予低分子肝素5 000 IU皮下注射qd×7 d;观察组术中在游离动脉端与静脉端分别推注1 500 u肝素钠,术后给予低分子肝素5 000 IU皮下注射qd×7 d。观察两组患者术后1周和4周AVF血栓形成率及药品不良反应（ADR）发生情况。结果: 术后1周,对照组和观察组的AVF血栓形成率分别为3.4%和0;术后4周分别为4.8%和0.67%,观察组均明显低于对照组（P<0.05）。两组ADR发生率差异无统计学意义（P>0.05）,未发生严重不良反应。结论: 肝素联合低分子肝素可降低AVF术后早期血栓形成率,提高手术成功率,安全性较好。     

尿激酶治疗血栓栓塞性疾病的效果研究

目的：研究尿激酶治疗血栓栓塞性疾病的临床效果。方法选取湛江市第二中医医院2012年6月—2014年6月收治的195例血栓栓塞性疾病患者,根据治疗方法不同分为两组,111例采用尿激酶治疗的患者设为尿激酶组,84例采用低分子肝素治疗的患者设为肝素组,比较两组效果和不良反应。结果尿激酶组肺栓塞（ PE）患者总有效率为78.44%,深静脉血栓形成（ DVT）患者总有效率为96.67%;肝素组 PE患者总有效率为60.98%, DVT患者总有效率为81.40%。两组比较差异有统计学意义（ P<0.05）。治疗后2周尿激酶组膝下15cm和膝上15cm健、患肢周径差均小于肝素组（ P<0.05）。尿激酶组不良反应发生率为5.41%,肝素组为2.38%,无黏膜或其他脏器出血病例,两组不良反应发生率比较,差异无统计学意义（ P>0.05）。结论尿激酶溶栓可提高血栓栓塞性疾病患者的疗效,且不良反应少。     

Absence of nitroglycerin-induced heparin resistance in healthy volunteers.

A previously described nitroglycerin-induced heparin resistance could not be verified by in-vitro experiments or in a randomized, double-blind, crossover trial in healthy volunteers. A clinically relevant attenuation of the anticoagulant effect of a heparin bolus (40 U.kg-1) by a concomitant infusion of nitroglycerin (100 micrograms.min-1) was absent. Activated partial thromboplastin time was not significantly different under nitroglycerin infusion as compared to placebo after heparin injection. Concentrations and activities of antithrombin III and heparin cofactor II remained unchanged during nitroglycerin infusion. An interaction of these two frequently combined drugs in patients with active thromboembolic disease or after a prolonged concomitant intravenous administration cannot be ruled out. Since this is of clinical importance, further studies must clarify a possible nitroglycerin-induced heparin resistance.