The mean age of the treated patients was 64.1 ± 16.4 years; seven were men. The clinical characteristics of the patients are presented in Table 1. Initial NIHSS scores ranged from 10 to 26. The interval from onset of symptoms to treatment ranged from 2 to 9 hours. Occlusion sites were located in the cervical ICA (n=4), intracranial ICA (n=4), middle cerebral artery(MCA) (n=6), and vertebrobasilar artery (n=2).
Figure 1 demonstrates the effect of incremental doses of reteplase on perfusion represented by the modified TIMI scale. The mean perfusion grade before treatment (0.1 ± 0.5) improved with increasing doses of reteplase to 2.7 ± 1.1 with4 U and 3.1 ± 0.8 with 8 U. All patients except three received8 U of reteplase; complete recanalization was achieved in two patients before reaching maximum dose, and angiographically visible extravasation of contrast medium in one patient necessitated termination of the procedure. After completion of the infusion, six patients experienced complete restoration of blood flow (modified TIMI 4), eight patients experienced near-complete restoration of flow (modified TIMI 3), one patient experienced partial restoration of flow (modified TIMI2), and one patient experienced a minimal response (modified TIMI 1). In Figure 2, an example of angiographic response to increasing doses of reteplase is shown. With increasing doses of reteplase, the mean thrombus grade decreased from a pretreatment score of 3.9 ± 0.3 to 1.6 ± 1.8 with 4 U and 0.66 1.4 with 8 U (Fig. 3). Neurological improvement at 24 hours(defined as a decline in NIHSS score of $4) was observed in seven patients. Two patients experienced further improvement in NIHSS score at 7 to 10 days. Adjunctive angioplasty of the occluded artery was performed in seven patients. Four patients underwent angioplasty after 8 U of reteplase was administered. Three other patients underwent angioplasty after administration of 4, 5, and ± U of reteplase, respectively. Intraparenchymal hemorrhages were observed in four patients. Two patients experienced localized hematomas with mass effect but no midline shift, and two others experienced localized hematomas with mass effect and midline shift (Fig.4). Neurological worsening (one-point increase in NIHSS score) at 24 hours was observed in one of these patients. The overall mortality during hospitalization was 56% (9 of 16patients). The causes of death included massive ischemic stroke (n=7), withdrawal of care at the family’s request after the development of aspiration pneumonia and renal failure (n5 1), and a combination of intracerebral hemorrhage and massive ischemic stroke (n=1). Only one death was attributable to complications of intra-arterial thrombolysis (Patient5; Table 1).
DISCUSSION