Anticoagulation therapy for cardiogenic emboli to brain
Anticoagulation therapy for cardiogenic emboli to brain
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心源性脑栓塞的抗凝治疗
作者：
F. Yatsu;J. Mohr
肝素能否抗凝心源性栓塞引起的缺血性中风尚无科学依据。必须权衡不抗凝治疗时栓塞复发的风险与引发出血性梗塞或明显血肿的风险。然而，目前还没有对照前瞻性研究确定来自公认的心脏来源的栓塞性梗塞后复发中风的风险，更不用说来自不明部位的栓塞（所谓的“非来源”栓塞）。甚至还没有确定肝素的最佳剂量。我们知识上的这些差距并没有平息人们对急性抗凝治疗可能导致出血的传统担忧。幸运的是，不知情地使用抗凝剂治疗小型深部血肿或皮层下“狭缝”血肿（仅凭临床理由误诊为缺血性中风）的旧有风险已不再是一个严重的问题，因为 CT 已常规用于急性中风。当 CT 显示没有出血迹象时，许多神经科医生现在大胆地使用抗凝治疗次最大缺血性中风，尽管其他人仍然反对这种治疗。在本期《神经病学》中，那些倾向于立即抗凝治疗的人将从 Furlan 等人和 Koller 的文章中得到安慰。这两篇论文都表明，接受充分抗凝治疗的心源性栓塞患者随后的早期再栓塞明显少于接受不充分或未接受抗凝治疗的患者。他们的研究结果表明了治疗时机的重要性，因为再栓塞可能在初始事件后不久发生。不能安全地推迟抗凝治疗的决定。这些论文没有提供关于肝素急性抗凝价值的明确答案，因为这两项研究都不是前瞻性或随机的。然而，这些报告应该起到重新唤醒辩论的重要作用，并可能促进对该主题长期被忽视和急需的前瞻性调查。在设计该问题的前瞻性研究时，必须密切关注治疗方法和栓塞的来源。在“肝素故事”的复杂性中，肝素的有效性和作用存在重要差异，这取决于药物的来源（肺或胃肠道）或物种以及多种分子形式。2此外，令人不安的证据表明，肝素可能通过增强血栓素A、合成或中和前列环素来矛盾地诱导血栓形成，并可能引发血栓〜血细胞减少症。〜l2此外，再栓塞的风险可能会根据栓子的来源而有所不同，这可能会混淆在不可比病例中显示肝素化有效性的尝试。栓子的来源包括一些心律失常，尤其是心房颤动、心肌梗塞和血液学异常（提示血小板过度聚集、高凝状态和粘度增加）。 ’~~~但是还需要更多的研究来帮助确定栓塞复发的风险以及在这种情况下引起的中风的大小。然而，归根结底，Furlan 等人和 Koller 的论文向从业者传达的“要点”信息非常明确：在前瞻性研究即将推出之前，在没有脑出血的情况下，可以毫不犹豫地登上立即和最佳抗凝脑部心源性栓塞的潮流，并期望防止再栓塞。进一步的研究应该有助于“微调”这种做法。
Whether to anticoagulate ischemic strokes due to cardiogenic emboli with heparin is still unsettled scientifically. The risks of recurrent emboli without anticoagulation must be balanced against the risks of provoking hemorrhagic infarction or frank hematoma. However, no controlled prospective study has yet established even the risk of recurrent strokes after embolic infarction from a recognized cardiac source, let alone from unidentified sites (so-called “nonsource” embolism). Not even the optimal dose of heparin is established. These gaps in our knowledge have not calmed the traditional fears that acute anticoagulant therapy may cause hemorrhage. Fortunately, the old risk of unwitting use of anticoagulants to treat small deep hematomas or subcortical “slit” hematomas, misdiagnosed on clinical grounds alone as ischemic stroke, is no longer a serious concern because CT is used routinely in acute stroke. Many neurologists are now emboldened to use anticoagulation for submaximal ischemic strokes when CT shows no sign of hemorrhage, although others still hold back such therapy.’ In this issue of Neurology, those inclined toward prompt anticoagulation will draw comfort from the articles by Furlan et a1 and Koller. Both papers show that patients with cardiogenic emboli who receive adequate anticoagulant therapy have significantly less subsequent early re-embolization than patients receiving inadequate or no anticoagulant treatment. Their findings show the importance of timing of therapy, because re-embolization may occur soon after the initial event; the decision to anticoagulate cannot be deferred safely. These papers do not provide the definitive answer about the value of acute anticoagulation with heparin because neither study was prospective or randomized. However, these reports should serve the important function of reawakening debate and may catalyze the long neglected and much needed prospective investigation of this subject. In designing a prospective study of this problem, close attention must be paid to the therapy and the source of the emboli. Among the unfolding intricacies of the “heparin story” are important differences in effectiveness and action of heparin that depend on the source of the agent (lungs or gastrointestinal tract), or the species, and the multiple molecular forms.2 Furthermore, disturbing evidence suggests that heparin may paradoxically induce thrombosis, perhaps by enhancing thromboxane A, synthesis or neutralizing prostacyclin, and may initiate thromb~cytopenia.~ l2 In addition, the risk of re-embolization may vary according to the source of the emboli, and this may confound attempts to show the effectiveness of heparinization in noncomparable cases. Sources of emboli include some cardiac arrhythmias, especially atrial fibrillation, myocardial infarcts, and hematological aberrations suggesting hyperaggregability of platelets, hypercoagulability, and increased visc ~ s i t y . ’ ~ ~ ~ But more studies are needed to help determine the risk of recurrence of embolization and the size of the stroke caused in such cases. In the final analysis, however, the “take-away” message of the papers by Furlan et a1 and Koller for practitioners is abundantly clear: until prospective studies are forthcoming, the bandwagon for immediate and optimum anticoagulation of cardiogenic emboli to the brain can be boarded without reluctance, in the absence of brain hemorrhage, with the anticipation of preventing reembolization. Further studies should assist in the “fine tuning” of this practice.
影响因子：
39.2
作者：
Lovett,JL;Sandok,BA;Giuliani,ER;Nasser,FN
通讯作者：
Nasser,FN