Arterial status after intravenous TPA therapy for ischaemic stroke. A needfor further interventions

Citation
I. Christou et al., Arterial status after intravenous TPA therapy for ischaemic stroke. A needfor further interventions, INT ANGIOL, 20(3), 2001, pp. 208-213
Citations number
19
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
INTERNATIONAL ANGIOLOGY
ISSN journal
03929590 → ACNP
Volume
20
Issue
3
Year of publication
2001
Pages
208 - 213
Database
ISI
SICI code
0392-9590(200109)20:3<208:ASAITT>2.0.ZU;2-R
Abstract
Background. Intravenous tissue plasminogen activator (TPA) is an approved t herapy for acute ischaemic stroke in the United States. We aimed to noninva sively monitor the therapy to determine arterial recanalisation and persist ing vascular abnormalities. Methods. We prospectively studied consecutive patients with symptoms of isc haemic stroke who received intravenous TPA and were monitored by 2 MHz tran scranial Doppler (TCD) to determine occlusion and recanalisation (TIMI grad es equivalent). For outcome assessment we used the National Institutes of H ealth Stroke Scale (NIHSS) score. Results. Sixty patients were studied (age 71 +/- 15 years, pre-TPA NIHSS 18 +/- 6.1, TPA bolus at 141 +/- 68 min after stroke onset). The internal car otid artery (ICA) was occluded in 25%, middle cerebral artery (MCA) in 80%; combined (ICA+MCA) occlusion was found in 19%; and basilar artery (BA) was occluded in 7%. Also, 2% had normal TCD and 8% of patients had no temporal windows. Complete recanalisation on TCD of all insonated arteries was foun d in 19 patients (32%) at 44 +/- 22 min after a TPA bolus. However, 67% of MCA, 25% of BA, and all ICA occlusions did not completely recanalise (TIMI grades 0-2). If flow impairment persisted for more than two hours after a T PA bolus, these patients continued to have significant neurological deficit s at 24 hours (15.0 +/- 8.2 vs 6.3 +/- 7.3 NIHSS points, p < 0.001 in non-p arametric statistics). High-grade residual stenoses with microembolic signa ls were seen on TCD in the MCA and BA (n = 3) suggesting continuing clot di ssolution. In patients without complete recanalisation (n = 36, or 60%), TC D identified lesions potentially amenable to further interventions. Conclusions. Persisting arterial occlusion after intravenous TPA therapy le ads to poor short-term outcome. Noninvasive monitoring of TPA therapy with TCD can identify these high-risk patients for combined interventions such a s intra-arterial thrombolysis, mechanical clot disruption, stenting or anti coagulation.