Arterial status after intravenous TPA therapy for ischaemic stroke. A need for further interventions.
BACKGROUND
Intravenous tissue plasminogen activator (TPA) is an approved therapy for acute ischaemic stroke in the United States. We aimed to noninvasively monitor the therapy to determine arterial recanalisation and persisting vascular abnormalities.


METHODS
We prospectively studied consecutive patients with symptoms of ischaemic stroke who received intravenous TPA and were monitored by 2 MHz transcranial Doppler (TCD) to determine occlusion and recanalisation (TIMI grades equivalent). For outcome assessment we used the National Institutes of Health 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 carotid 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 found 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 TPA bolus, these patients continued to have significant neurological deficits at 24 hours (15.0+/-8.2 vs 6.3+/-7.3 NIHSS points, p<0.001 in non-parametric statistics). High-grade residual stenoses with microembolic signals were seen on TCD in the MCA and BA (n=3) suggesting continuing clot dissolution. In patients without complete recanalisation (n=36, or 60%), TCD identified lesions potentially amenable to further interventions.


CONCLUSIONS
Persisting arterial occlusion after intravenous TPA therapy leads to poor short-term outcome. Noninvasive monitoring of TPA therapy with TCD can identify these high-risk patients for combined interventions such as intra-arterial thrombolysis, mechanical clot disruption, stenting or anticoagulation.
Christou
I
I
Center for Noninvasive Brain Perfusion Studies, Stroke Treatment Team, University of Texas-Houston Medical School, Houston, Texas, USA. avalexandrov@worldnet.att.net
Burgin
W S
WS
Alexandrov
A V
AV
Grotta
J C
JC
D000368:Aged; D001157:Arterial Occlusive Diseases / Q000000981:diagnostic imaging* / Q000188:drug therapy*; D002545:Brain Ischemia / Q000000981:diagnostic imaging* / Q000188:drug therapy*; D002560:Cerebrovascular Circulation; D005343:Fibrinolytic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D007262:Infusions, Intravenous; D011446:Prospective Studies; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage / Q000627:therapeutic use*; D016896:Treatment Outcome; D017585:Ultrasonography, Doppler, Transcranial
D005343:Fibrinolytic Agents; D010959:Tissue Plasminogen Activator