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DOI: 10.1055/s-2003-42986
Antikoagulation beim Schlaganfall
Indikationen im Spannungsfeld zwischen Evidenz und EmpirieAnticoagulation in strokeEvidence-based and empirical indicationsPublication History
                     eingereicht: 24.2.2003
                     
                     akzeptiert: 6.8.2003
                     
Publication Date:
16 October 2003 (online)

Zusammenfassung
Der Einsatz von Heparin, Heparinoiden und Vitamin-K-Antagonisten zur Akutbehandlung bzw. Prävention von Schlaganfällen wird heutzutage kontrovers diskutiert. Bei Vorhofflimmern und -flattern wird eine orale Antikoagulation insbesondere bei Hochrisikopatienten befürwortet. Als weitere Indikationen werden Erkrankungen mit hohem kardialen Embolierisiko (z. B. mechanische Herzklappen und intrakardiale Thromben), symptomatische Dissektionen hirnversorgender Arterien, Basilaris- und Sinusvenen-Thrombose sowie Erkrankungen mit vorwiegend genetisch bedingter Thrombophilie angesehen. Da für viele Befundkonstellationen das Verhältnis von Nutzen und Risiko einer Antikoagulation bislang nicht durch aussagekräftige Studien geklärt ist, sollten therapeutische Entscheidungen unter Berücksichtigung des individuellen Risikoprofils und der spezifischen Pathophysiologie der abgelaufenen zerebralen Ischämie getroffen werden.
Summary
Therapeutic benefit of heparin, heparinoids and Vitamin-K-antagonists in acute stroke as well as in stroke prevention is still a controversial issue. In patients with atrial fibrillation and flutter, oral anticoagulation is recommended when further high risk factors are present. Most experts agree that anticoagulation therapy is useful in disorders with increased cardiogenic embolisation risk (e. g. mechanical valves and intracardiac thrombus), symptomatic dissection of brain-supplying arteries, thrombosis of the basilar artery, sinus venous thrombosis, and in thrombophilia. Since for many clinical constellations controlled randomized studies differentially assessing the benefits and the risks of anticoagulation are lacking, therapeutic decisions have to be based on the patients individual risk profile and pathophysiology of cerebral ischemia.
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Dr. U. Walter
         Klinik und Poliklinik für Neurologie, Universität  Rostock
         
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