1986 Volume 17 Issue 2 Pages 167-169
In twenty patients with ischemic cerebrovascular disease fibrinopeptide A (FPA) and fibrinopeptide Bβ 15-42 (Bβ 15-42) were serially assayed in cerebrospinal fluid (CSF) and in plasma.
After plasma FPA levels began to be elevated, it took a peak from 5th to 14th day after stroke (p<0.05), and gradually returned to control level. Bβ 15-42 levels in plasma were constantly elevated at least during first three weeks (Fig. 1). On the other hand, values of FPA in CSF were initially elevated and then reached to a peak on 15th to 21st day after stroke (p<0.01). However values of Bβ 15-42 in CSF remained at control level (Fig. 2).
Suggestions of these results are as follows. Coagulation activity was accelerated following the onset of stroke with a short time lag. This delay of coagulation activity was considered to be due to the stroke progression, that is, continuous activation of thromdin in the ischemic regions. And it caused the elevation of FPA that released into the subarachnoid space crossing the broken blood-brain barrier. While fibrinolytic activity in plasma was continuously elevated, that in CSF was not influenced by stroke. The reason of this difference was not proven in our series.