Zusammenfassung
Insgesamt sind kardiogene Hirnembolien für 30% aller Hirninfarkte verantwortlich; bei Patienten bis zum 40. Lebensjahr werden Häufigkeiten bis zu 50% angegeben. Zur Routineabklärung eines Hirninfarkts zählen daher immer das möglichst frühzeitige Elektrokardiogramm (Herzrhythmusstörung?), die Langzeit-EKG-Ableitung sowie die transösophageale Echokardiographie (TEE). Schon der notfallmäßig hinzugezogene Neurologe sollte palpatorisch feststellen, ob eine Herzrhythmusstörung vorliegt und diese im Rahmen der Ultrachalldiagnostik dokumentieren. Klinisch läßt sich der Hirninfarkt durch kardiogene Hirnembolie nicht zuverlässig von Hirninfarkten anderer Genese unterscheiden. Es sollten jedoch eine begleitende Bewußtseinsstörung sowie isolierte kortikale Symptome (Aphasie, Apraxie, Neglekt, Gesichtsfelddefekt) an diese Genese denken lassen [33]. Das Rezidivrisiko kardiogener Hirnembolien ist stets erhöht, wenn eine kardiale Erkrankung nachweisbar ist (absolute Arrhythmie bei Vorhofftimmern, Herzklappenerkrankung, Herztumoren) sowie bei Nachweis von kardialen Thromben, bei AT-III-Mangel und bei Dehydratation [65]. Grundsätzlich stellt der Nachweis einer kardialen Emboliequelle eine Indikation zur Antikoagulation dar, die bei einem akuten Hirninfarkt mittels PTT-wirksamer Heparinisierung und im Verlauf (etwa nach 1 Woche) mittels oraler Antikoagulation erfolgt (PTT = partielle Thromboplastinzeit).
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Berlit, P. (2001). Internistische Ursachen zerebrovaskulärer Erkrankungen. In: Hartmann, A., Heiss, WD. (eds) Der Schlaganfall. Steinkopff, Heidelberg. https://doi.org/10.1007/978-3-642-57629-4_4
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