1981 年 12 巻 1 号 p. 53-56
Atrial fibrillation is one of the most frequent causes of arterial embolism to the brain. The pathogenesis of these embolisms has been considered to be caused by abnormal hemorheological dynamics. Paroxysmal atrial fibrillation with tachycardia (PaT) is one of the typical arrhythmias which disturb stable hemodynamics.
In our two patients with PaT cerebral embolisms recurrently developed. One had five such episodes of stroke during six months, the cardinal symptom of the first episode was visual agnosia, the second left hemiparesis, the third left hemianopsia, the fourth motor aphasia and the fifth right hemiparesis. All of them were associated with attacks of PaT. The fifth episode of stroke developed just after the recovery from PaT due to administration of β-blocker. In every attack of PaT, a momentary increase of plasma β-thromboglobulin (β-TG) was found, which is a platelet specific protein, liberated during intravascular aggregation and release reaction of platelet.
The other case suffered from cerebral embolism with dysarthria, dysphagia and right hemiparesis just after the recovery from PaT by digitalisation, and plasma β-TG was also increased during every attack of PaT.
Including these two cases, plasma β-TG was measured in 11 patients with PaT during attacks and was compared with that at normal sinus rhythm. Plasma β-TG was 64.6±36.6ng/ml (n=20) during attacks of PaT and remained 35.2±20.0ng/ml (n=13) at normal sinus rhythm (p<0.05). This high level of plasma β-TG during attacks was thought to reflect accelerated intravascular aggregation of platelet in PaT.
From these results it was suggested that an increased coagulability can be induced by PaT and that administration of antiplatelet drugs is also desirable in the treatment of PaT and atrial fibrillation.