Cessation of embolic signals after antithrombotic prevention is related to reduced risk of recurrent arterioembolic transient ischaemic attack and stroke.

OBJECTIVES: To evaluate the reduction of embolic signals after the initiation of an antithrombotic secondary prevention in patients with recent arterioembolic stroke and to determine the predictive value of decreased microembolism on the risk of early stroke recurrence. METHODS: Eighty six consecutive patients (55 men, 31 women; mean age 60.6 years) with a non-disabling arterioembolic ischaemic event in the anterior circulation within the last 30 days and a medium grade or high grade stenosis (> or =50%) of the ipsilateral carotid or middle cerebral artery underwent 1 hour transcranial Doppler monitoring as part of the admission examinations. Antithrombotic secondary prevention was started after completion of admission. Patients in whom embolic signals were detected underwent a second monitoring within 4 days (mean time 1.8 days). All patients were followed up prospectively to evaluate the relation between presence and persistence of embolic signals and the risk of recurrent transient ischaemic attack (TIA) and stroke within the next 6 weeks. RESULTS: In 44 patients, embolic signals were detected at admission, a mean 5.4 days (range 0 to 21 days) after the initial event. Twenty five were positive for embolic signals also at the second monitoring, in 19 signals had ceased. Forty two patients without embolic signals at admission served as controls. During follow up, six ischaemic events (two stroke, three TIA, one amaurosis fugax) occurred in 25 patients with persisting embolic signals but none in 19 patients in whom signals had ceased by the second monitoring. One patient in the control group had a TIA. The incidence of a recurrent event was 0.45 per 30 patient-days if embolic signals persisted compared with 0.015 if signals could not be detected or had ceased. Persistence of embolic signals was an independent predictor of a recurrent TIA or stroke (adjusted odds ratio 37.0; 95% confidence interval (95% CI) 3.5 to 333; p<0.003). Cessation and decrease of embolic signals was associated with the administration of antiplatelet agents but not with anticoagulation with intravenous heparin (p<0.001). CONCLUSIONS: Rapid cessation of embolic signals detected in patients with recently symptomatic arterial stenosis decreases increased risk of an early ischaemic recurrence. Effect of antithrombotic agents on embolic signals might serve as a marker for their efficacy on preventing stroke recurrence.

Rapid decline of cerebral microemboli of arterial origin after intravenous acetylsalicylic acid.

BACKGROUND AND PURPOSE: The present study investigated the influence of the antiplatelet agent acetylsalicylic acid (ASA) on cerebral microembolism as detected by transcranial Doppler sonography (TCD). METHODS: Nine patients with recent transient ischemic attack or minor stroke of arterial origin were investigated. Eight had not received an antiplatelet or anticoagulant medication before TCD, and in 1 patient a preexisting ASA medication (100 mg/d) had not been changed since the onset of stroke symptoms. An initial 1-hour TCD monitoring was extended for an additional 2.5 hours after an intravenous bolus injection of 500 mg ASA and was repeated for 1 hour on the following day. RESULTS: Microembolic signals (MES) were detected in all patients only on the symptomatic side. After the ASA bolus injection, a significant drop of the MES rate was found in 7 patients, all without previous medication, starting 30 minutes after the application (mean per hour=25.1 [range, 6 to 66] versus mean per hour=6.4 [range, 0 to 14]). In 3 of these patients, platelet aggregation tests were performed that demonstrated normal aggregation before bolus injection and inhibited aggregability as early as 30 minutes after bolus injection. The rate of MES remained unchanged in 1 patient without antiplatelet medication. The ninth patient, who had suffered an ischemic event on ASA, showed only a transient decrease of MES frequency. CONCLUSIONS: In patients with recent stroke of arterial origin, intravenous ASA can rapidly reduce cerebral microemboli as detected by TCD. Microemboli might be a useful parameter to monitor early effects of antiplatelet therapy.

Diagnostic impact and prognostic relevance of early contrast-enhanced transcranial color-coded duplex sonography in acute stroke.

BACKGROUND AND PURPOSE: We sought to evaluate the diagnostic value of echo-enhanced transcranial color-coded duplex sonography (TCCD) and the clinical relevance of vascular pathology assessed by sonography for early clinical outcome in acute ischemic stroke. METHODS: We present 23 consecutive patients with an anterior circulation stroke in whom clinical examination, CT, and ultrasonography were performed within 5 hours after the onset of symptoms. Transcranial Doppler sonography (TCD) and unenhanced and contrast-enhanced TCCD (Levovist, 4 g, 300 mg/mL) were compared for their ability to detect middle cerebral artery (MCA) occlusion and flow velocity reduction suggesting hemodynamic impairment in the MCA distribution pathway. Sonographic examination times were registered. Baseline clinical characteristics and CT findings were assessed. Neurological deficit was quantified according to the National Institutes of Health Stroke Scale score, with an early clinical improvement defined as decrease of the score by 4 or more points or a complete resolution of the deficit on day 4. RESULTS: Contrast-enhanced TCCD enabled diagnosis of intracranial vascular pathology in 20 affected hemispheres, whereas unenhanced TCCD and TCD were conclusive in 7 and 14 hemispheres, respectively (P=0.0001). Contrast-enhanced TCCD was superior in evaluating distal carotid (carotid-T) occlusion and differentiating major vessel occlusions from patent arteries with flow velocity diminution. Mean examination time for enhanced TCCD ranged from 5 to 7 minutes, depending on the number of investigated vessels (without or with MCA branches). Logistic regression selected a patent MCA without reduced blood flow velocity as the only independent predictor for an early clinical improvement (P<0.01). CONCLUSIONS: Contrast-enhanced TCCD is a promising tool for early prognosis in anterior circulation stroke. It is considered superior to unenhanced TCCD and TCD.