Prevalence of vertebral artery origin stenosis and occlusion in outpatient extracranial ultrasonography

Most data on the prevalence of vertebral artery origin (VAo) disease is derived from hospital-based studies of patients with posterior circulation strokes and TIA. The prevalence of VAo disease in patients without posterior circulation symptoms or asymptomatic patients is poorly characterized. Our objective was to examine the prevalence of VAo stenosis and occlusion in consecutive patients, presenting for extracranial ultrasonography to an outpatient laboratory. We retrospectively identified 2490 consecutive extracranial duplex studies performed in an ambulatory neurovascular ultrasound laboratory. All studies were reviewed for the presence of >50% VAo stenosis, defined as a PSV > 114 cm/s, and VA occlusion. We also reviewed the prevalence of >50% carotid stenosis, defined as a PSV > 120 cm/s, in the same population, to draw comparisons with VAo stenosis prevalence. We identified right VAo stenosis in 52/1955 (2.7%) and occlusion in 74/1955 (3.9%) and left-sided VAo stenosis in 45/1973 (2.5%) and occlusion in 64/1973 (3.6%). The prevalence of having any (either right or left) VAo stenosis or occlusion was 8.2% and 1.4% had bilateral VAo stenosis or occlusion. Right carotid stenosis and occlusion was found in 236/2399 (9.8%) and 53/2399 (2.2%) and left carotid stenosis and occlusion in 236/2397 (9.8%) and 45/2397 (1.9%), respectively. Any carotid disease, either right or left, was present in 18.9% and 4.7% had bilateral carotid disease. Although less prevalent than cervical carotid disease, we found that approximately 8% of patients who presented to an ambulatory ultrasound laboratory had >50% VAo disease

Abstract 3422: Prevalence Of Vertebral Artery Origin Stenosis In Outpatients Referred For Extracranial Duplex

Introduction: Extracranial atherosclerotic stenosis of the vertebral artery occurs characteristically at the vertebral artery origin (VAo) and is an important cause of posterior circulation stroke. The proximal segment of the vertebral artery is technically difficult to insonate. Only a few studies have reported on the prevalence of VAo disease in patients with stroke and little is known about its prevalence in non-hospitalized populations. Our objective was to determine the prevalence of VAo stenosis in subjects referred for outpatient extracranial ultrasonography. Methods: All studies performed in an outpatient neurosonology laboratory, affiliated with an academic medical center were retrospectively reviewed for VAo stenosis. The proximal vertebral segments were insonated following a standard protocol. VAo stenosis was diagnosed if the peak systolic velocity (PSV) > 114cm/sec, according to previously validated criteria. We also considered the VAo to be occluded if no flow signal could be found in any of its pre-and intraforaminal segments. Studies were also analyzed for internal carotid artery origin (ICAo) stenosis >50% to allow comparison between prevalence of carotid and VAo stenosis. Results: A total of 2490 subjects were available for analysis. The right and left VAo could not be insonated in18% and 25% of patients. Right-sided VAo stenosis or occlusion was present in 52/1955 (2.7%) and 74/1955 (3.9%) respectively; left-sided VAo stenosis or occlusion was present in 45/1793 (2.5%) and 64/1973 (3.6%) respectively. Overall, in those with at least one VAo insonated, 204/ 2119 (8.2%) patients had VAo stenosis or occlusion. In 29/ 2119 (1.4%), bilateral VAo stenosis or occlusion was found. Mean flow velocities were significantly lower in patients without stenosis (right 54.2±18.9 vs.149.0±57.8cm/s; left 53.5±17.5 vs.143.9±31.4cm/s). The prevalence of having either right or left ICAo stenosis or occlusion was 453/ 2401 (18.9%) and bilateral ICAo stenosis or occlusion was 112/ 2401 (4.7%). In univariate analysis, but not multivariate analysis, hypertension and diabetes were risk factors for VAo stenosis. Conclusion: The prevalence of VAo stenosis and occlusion was 8.2% in a diverse population of patients presenting to an ambulatory ultrasound laboratory. We found the prevalence of ICAo stenosis to be higher than VAo stenosis in the same population. Our findings contribute to the understanding of the prevalence of proximal vertebral artery disease in non-hospitalized patients

Anticoagulation and Microembolus Detection in a Case of Internal Carotid Artery Dissection

ABSTRACT Background. Microembolic signals (MES) have been demonstrated by transcranial Doppler (TCD) in cases of internal carotid artery dissection. The influence of treatment on MES in arterial dissection is uncertain. The authors here present a case of internal carotid artery dissection in which we detected a reduction of MES after the initiation of intravenous heparin. Methods. A 37‐year‐old woman developed a right temporal headache 10 days prior to admission. This was followed by episodes of left arm numbness and weakness. Magnetic resonance imaging (MRI) showed a right frontal and deep subcortical ischemic infarct. Catheter angiography confirmed a right internal carotid artery dissection with intracranial extension. She was then monitored with TCD for MES before and after intravenous heparin was started. Results. The first TCD, performed 12 days after symptom onset, showed 39 MES during 60 minutes of insonation of the right middle cerebral artery. Treatment with intravenous heparin resulted in a decline in MES by 50% after 96 hours. This decline continued and no further MES were detected after 11 days of anticoagulation. Conclusion. The authors were able to demonstrate a decline of MES with heparin anticoagulation in a case of internal carotid artery dissection

MR imaging after hip and knee replacement

Diffusion-weighted (DW) imaging abnormalities often develop in patients after invasive procedures associated with cerebral microembolism. Cerebral microembolism has recently been shown during orthopedic surgery. We here examine the effects of intraoperative microembolism on acute magnetic resonance(MR) imaging in patients undergoing hip and knee replacement. We enrolled 24 patients, at least 65 years old, requiring elective knee or hip replacement surgery. MR with DW and axial fluid-attenuated inversion recovery (FLAIR) imaging was performed pre- and postoperatively. All patients were monitored intraoperatively for microemboli. The mean age of patients was 74 years. All patients had intraoperative microemboli. The mean number of emboli detected was 9.9 +/- 18 per surgery. MR imaging was obtained a mean of 3.5 days postoperatively. No DW imaging abnormalities were found after surgery. One patient had new findings on postoperative FLAIR imaging. Intraoperative microembolism occurred universally, but did not lead to acute DW imaging abnormalities following knee and hip replacement. Acute imaging abnormalities on FLAIR imaging are rare but may occasionally occur after joint surgery

High-Dose Atorvastatin Enhances Impaired Cerebral Vasomotor Reactivity

The influence of statin therapy on cerebral vasomotor function has not been fully characterized. We report the effects of high-dose atorvastatin therapy on cerebral vasomotor reactivity (VMR) in patients with controlled hypertension and dyslipidemia. We prospectively enrolled 36 patients with controlled hypertension and a low-density lipoprotein (LDL) cholesterol concentration >100 mg/dL. Atorvastatin 80 mg was given daily for 6 months and then discontinued. VMR was assessed by hypercapnic and hypocapnic transcranial Doppler challenge in both the right and left middle cerebral artery (MCA) at baseline, and after 3 and 6 months of therapy. Forty-five days after statin cessation, a repeat VMR was performed. VMR impairment was defined as ≤70%. Blood pressure, lipid levels, liver function, and creatine kinase level were monitored. Mean patient age was 60 years, 16 were men, and 13 had a previous history of subcortical infarction. Mean LDL cholesterol level before treatment was 154 ± 30 mg/dL. Atorvastatin lowered LDL by 53% at 3 months and by 46% at 6 months. Baseline VMR was 71% ± 21% in the right MCA and 70% ± 19% in the left MCA. No significant effect of atorvastatin on VMR was seen at 3 months and 6 months in the study population as a whole. In the subgroup of patients with baseline VMR impairment, atorvastatin therapy was associated with significantly improved VMR at both 3 and 6 months. This effect persisted for at least 45 days after discontinuation of therapy. Our findings indicate that high-dose atorvastatin therapy can significantly improve impaired cerebral VMR, and that the effects of atorvastatin on VMR persist for 1.5 months after discontinuation of therapy. We found no benefit of atorvastatin therapy in patients with preserved baseline vasoreactivity

Sickle Cell Disease and Stroke: Data from the Florida Stroke Registry (S35.002)

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