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Biomedical subjects

Robert W Hobson

Publications and source records attributed to Robert W Hobson.

At least 19 recordsLinked to original sources
PubMed2007

Treatment of carotid artery disease: stenting or surgery.

Carotid endarterectomy (CEA) is the only form of cerebral revascularization for which Level 1 evidence of effectiveness has been reported. Recent studies demonstrate the feasibility of carotid artery stenting (CAS) as an alternative to CEA. Its popularity is due to the perceived advantages of a less invasive treatment for carotid occlusive disease. Two randomized trials have reported no difference in the composite stroke, death, and myocardial infarction rate between CAS and CEA. However, these trials were not powered to identify superiority between the two procedures. A trial sponsored by the National Institutes of Health is currently underway to make that determination. The lead-in phase of this trial noted low complication rates with CAS. These results have encouraged the US Food and Drug Administration to approve the use of CAS in patients with neurologic symptoms (ie, ipsilateral stroke, transient ischemic attacks, and amaurosis fugax) in association with severe medical co-morbidities. Patients with carotid restenosis after previous CEA, anatomically inaccessible lesions above C2, and radiation-induced stenoses may also benefit from preferential treatment with CAS. The National Institutes of Health have now expanded the Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST) to include asymptomatic patients, and resulting data will help to clarify the role of CAS in this subset as well.

Carotid Artery Diseases↗
PubMed2006

Endothelial nitric oxide synthase regulates microvascular hyperpermeability in vivo.

Nitric oxide (NO) is an important regulator of blood flow, but its role in permeability is still challenged. We tested in vivo the hypotheses that: (a) endothelial nitric oxide synthase (eNOS) is not essential for regulation of baseline permeability; (b) eNOS is essential for hyperpermeability responses in inflammation; and (c) molecular inhibition of eNOS with caveolin-1 scaffolding domain (AP-Cav) reduces eNOS-regulated hyperpermeability. We used eNOS-deficient (eNOS-/-) mice and their wild-type control as experimental animals, platelet-activating factor (PAF) at 10(-7) m as the test pro-inflammatory agent, and integrated optical intensity (IOI) as an index of microvascular permeability. PAF increased permeability in wild-type cremaster muscle from a baseline of 2.4 +/- 2.2 to a peak net value of 84.4 +/- 2.7 units, while the corresponding values in cremaster muscle of eNOS-/- mice were 1.0 +/- 0.3 and 15.6 +/- 7.7 units (P < 0.05). Similarly, PAF increased IOI in the mesentery of wild-type mice but much less in the mesentery of eNOS-/- mice. PAF increased IOI to comparable values in the mesenteries of wild-type mice and those lacking the gene for inducible NOS (iNOS). Administration of AP-Cav blocked the microvascular hyperpermeability responses to 10(-7) m PAF. We conclude that: (1) baseline permeability does not depend on eNOS; (2) eNOS and NO are integral elements of the signalling pathway for the hyperpermeability response to PAF; (3) iNOS does not affect either baseline permeability or hyperpermeability responses to PAF; and (4) caveolin-1 inhibits eNOS regulation of microvascular permeability in vivo. Our results establish eNOS as an important regulator of microvascular permeability in inflammation.

Animals↗
PubMed2006

Noninvasive identification of the unstable carotid plaque.

Intraplaque hemorrhage, enlarging lipid cores, and their proximity to the flow lumen are important determinants of carotid plaque rupture and neurological complications. We developed an image-analysis method for B-mode ultrasound, pixel distribution analysis (PDA), for preprocedural identification of these high-risk features in carotid plaques. This technique may improve selection of patients for carotid endarterectomy and carotid artery stenting. Forty-two patients with high-grade carotid stenosis in 45 arteries, 18 symptomatic and 27 asymptomatic, underwent preoperative ultrasound. Intraplaque hemorrhage, lipid, fibromuscular tissue, calcium, lipid core area, and distance from the flow lumen were quantified using pixel intensities of tissues in control subjects. These findings were contrasted between symptomatic and asymptomatic plaques and correlated with histology. Inter- and intraobserver variabilities were determined for this technique. Pixel intensities of control tissues were discrete and significantly different from each other (median: blood 0, lipid 27, muscle 45.5, fibrous tissue 204, and calcium 245). There was more intraplaque hemorrhage (p<0.001) and lipid (p=0.002) but less calcium (p<0.001) within symptomatic plaques. Lipid cores were larger (p=0.005) and their distance from the flow lumen was lower (p=0.01) in symptomatic plaques. Intraplaque hemorrhage, lipid, fibromuscular tissue, calcium, lipid core size, and distance from flow lumen measured by PDA correlated with histology. No significant inter- or intraobserver variabilities were observed in these measurements. PDA accurately identified more intraplaque hemorrhage and lipid, less calcium, and larger lipid cores located closer to the flow lumen in symptomatic patients with carotid stenosis. These data indicate that PDA may be used to identify high-risk carotid atherosclerotic plaques and thereby improve the selection of patients requiring treatment.

Aged↗
PubMed2006

Carotid stenting: should it replace endarterectomy in higher-risk patients?

Carotid artery stenting (CAS) has emerged as a useful and potentially less-invasive alternative to carotid endarterectomy (CEA) for treatment of extracranial carotid stenoses. It has been suggested that specific patient subgroups, including those with significant medical comorbidities, recurrent stenosis, anatomically inaccessible lesions, and a hostile neck, might benefit from CAS. The purpose of this report is to evaluate whether or not CAS should replace CEA in the treatment of the high-risk patient. Results from a recently published randomized clinical trial and several individual center and multicenter case analyses will be used in this review.

Blood Vessel Prosthesis Implantation↗
PubMed2005

Hyperglycemia alters PI3k and Akt signaling and leads to endothelial cell proliferative dysfunction.

Diabetes mellitus is a major risk factor for the development of vascular complications. We hypothesized that hyperglycemia decreases endothelial cell (EC) proliferation and survival via phosphatidylinositol 3-kinase (PI3k) and Akt signaling pathways. We cultured human umbilical vein ECs (HUVEC) in 5, 20, or 40 mM d-glucose. Cells grown in 5, 20, and 40 mM mannitol served as a control for osmotic effects. We measured EC proliferation for up to 15 days. We assessed apoptosis by annexin V and propidium iodide staining and flow cytometry, analyzed cell lysates obtained on culture day 8 for total and phosphorylated PI3k and Akt by Western blot analysis, and measured Akt kinase activity using a GSK fusion protein. HUVEC proliferation was also tested in the presence of pharmacological inhibitors of PI3k-Akt (wortmannin and LY294002) and after transfection with a constitutively active Akt mutant. ECs in media containing 5 mM d-glucose (control) exhibited log-phase growth on days 7-10. d-Glucose at 20 and 40 mM significantly decreased proliferation versus control (P < 0.05 for both), whereas mannitol did not impair EC proliferation. Apoptosis increased significantly in HUVEC exposed to 40 mM d-glucose. d-Glucose at 40 mM significantly decreased tyrosine-phosphorylated PI3k, threonine 308-phosphorylated-Akt, and Akt activity relative to control 5 mM d-glucose. Pharmacological inhibition of PI3k-Akt resulted in a dose-dependent decrease in EC proliferation. Transfection with a constitutively active Akt mutant protected ECs by enhancing proliferation when grown in 20 and 40 mM d-glucose. We conclude that d-glucose regulates Akt signaling through threonine phosphorylation of Akt and that hyperglycemia-impaired PI3k-Akt signaling may promote EC proliferative dysfunction in diabetes.

Cell Division↗
PubMed2005

Endovascular treatment of patients with carotid stenosis.

Carotid artery stenting is a less invasive technique for carotid revascularization as compared with endarterectomy. However, clinical efficacy for carotid endarterectomy has been established through rigorous randomized clinical trials. Clinical trials and registries on carotid stenting to date have not been powered to compare differential efficacy with endarterectomy in symptomatic patients. Consequently, caution is recommended in use of carotid stenting, pending reports from larger randomized clinical trials.

Carotid Artery, Common↗
PubMed2005

Mitogen-activated protein kinases regulate platelet-activating factor-induced hyperpermeability.

OBJECTIVE: The authors tested the hypothesis that p42/44- (ERK-1/2) and/or p38-mitogen-activated protein kinases (MAPK) are in vivo regulatory elements in the platelet-activating factor (PAF) activated signaling cascade that stimulates microvascular hyperpermeability. METHODS: FITC-dextran 70 was used as the macromolecular tracer for microvascular permeability in the mouse mesenteric fat tissue. Interstitial integrated optical intensity (IOI) was used as an index of permeability. RESULTS: An application of 10(-7) M PAF increased IOI from 23.1 +/- 3.6 to 70.8 +/- 7.4 (mean +/- SEM). Inhibition of ERK-1/2 with 3 microM and 30 microM AG126 reduced IOI to 32.3 +/- 2.5. Similarly, inhibition of p38-MAPK with 6 nM, 60 nM and 600 nM SB203580 lowered IOI to 29.1 +/- 2.4. CONCLUSIONS: The results demonstrate that ERK-1/2 and p38MAPK participate in the signaling cascade that regulates PAF-induced microvascular hyperpermeability in vivo.

Animals↗
PubMed2005

Carotid angioplasty with or without stent placement versus carotid endarterectomy for treatment of carotid stenosis: a meta-analysis.

OBJECTIVE: Carotid angioplasty with or without stent placement (CAS) has been proposed as an alternative method to carotid endarterectomy (CEA) for treatment of carotid stenosis. Small randomized trials have evaluated the comparative efficacy of both methods; however, definitive evidence is lacking. METHODS: A search was made for randomized clinical trials comparing CAS and CEA for treatment of carotid stenosis. A literature search of MEDLINE, PubMed, and Cochrane databases was supplemented by a review of bibliographies of relevant articles and personal files. A meta-analysis was performed using a random effects model because significant heterogeneity was observed. Outcomes compared included 1-month composite rates of stroke or death, all strokes, disabling strokes, myocardial infarction, cranial nerve injury, and major bleeding and 1-year rates of both minor and major ipsilateral strokes. RESULTS: We analyzed five randomized trials totaling 1154 patients (577 randomized to CEA and 577 randomized to CAS). The composite end point of 1-month stroke or death rate was not different between patients treated with CAS compared with those treated with CEA (relative risk [RR], 1.3; 95% confidence interval [CI], 0.6-2.8; P = 0.5). The 1-month stroke rate (831 patients analyzed: RR, 1.3; 95% CI, 0.4-3.6; P = 0.7) and disabling stroke rate (831 patients analyzed: RR, 0.9; 95% CI, 0.2-3.5; P = 0.9) was similar for CAS and CEA. The 1-month rates of myocardial infarction (814 patients analyzed: RR, 0.3; 95% CI, 0.1-0.9) and cranial nerve injury (918 patients analyzed: RR, 0.05; 95% CI, 0.01-0.3) were significantly lower for CAS. No significant differences were observed in 1-year rates of ipsilateral stroke (814 patients analyzed: RR, 0.8; 95% CI, 0.5-1.2; P = 0.2). CONCLUSION: The 30-day stroke and death rates associated with CAS and CEA were not significantly different. Lower rates of myocardial infarction and cranial nerve injury were observed with CAS compared with CEA.

Angioplasty↗
PubMed2004

Vascular endothelial growth factor stimulates differential signaling pathways in in vivo microcirculation.

Vascular endothelial growth factor (VEGF) induces mild vasodilation and strong increases in microvascular permeability. Using intravital microscopy and digital integrated optical intensity image analysis, we tested, in the hamster cheek pouch microcirculation, the hypothesis that differential signaling pathways in arterioles and venules represent an in vivo regulatory mechanism in the control of vascular diameter and permeability. The experimental design involved blocking specific signaling molecules and simultaneously assessing VEGF-induced changes in arteriolar diameter and microvascular transport of FITC-Dextran 150. Inhibition of Akt [indirectly via phosphatidylinositol 3-kinase with LY-294002 or wortmannin] or PKC (with bisindolylmaleimide) reduced VEGF-induced hyperpermeability. However, phosphatidylinositol 3-kinase/Akt inhibition enhanced the early phase and attenuated the late phase of VEGF-induced vasodilation, whereas blocking PKC had no effect. Inhibition of extracellular signal-regulated kinase (ERK)-1/2 (with PD-98059 or AG-126) also reduced VEGF-induced hyperpermeability but did not block VEGF-induced vasodilation. Blockade of endothelial nitric oxide synthase (with N(omega)-monomethyl-l-arginine) inhibited VEGF-induced changes in both permeability and diameter. Furthermore, immunofluorescence studies with human umbilical vein endothelial cells revealed that bisindolylmaleimide, PD-98059, and l-NMMA attenuate VEGF-induced reorganization of vascular endothelial cadherin. Our data demonstrate that 1) endothelial nitric oxide synthase is a common convergence pathway for VEGF-induced changes in arteriolar diameter and microvascular permeability; 2) PKC and ERK-1/2 do not play a major role in VEGF-induced vasodilation in the hamster cheek pouch microcirculation; and 3) Akt, PKC, and ERK-1/2 are elements of the signaling cascade that regulates VEGF-stimulated microvascular hyperpermeability. Our data provide evidence for differential signaling as a regulatory step in VEGF-stimulated microvascular dynamics.

Animals↗
PubMed2004

Observer variability of iliac artery measurements in endovascular repair of abdominal aortic aneurysms.

Accurate measurement of iliac arteries is essential for successful delivery of aortic endografts without iliac limb endoleak. Although intravascular ultrasound measurements may be reliable, they require an invasive procedure. Therefore, helical computed tomography (hCT) has become the most commonly used modality for obtaining preprocedure arterial diameter measurements. The accuracy of hCT remains ill-defined, however, because an anatomic gold standard with which to compare the measurements is not available. We therefore assessed inter- and intraobserver variability of hCT measurements. We also applied accepted cutoff measurements to determine the clinical impact of observer variability in predicting the need for adjunctive iliac access and iliac limb seal procedures. hCT scans were analyzed in 30 patients who had undergone successful placement of a bifurcated endograft (26 Ancure, 4 Aneurex). Mean age of patients was 75 years, the male/female ratio was 27:3. Three blinded observers measured transverse diameters (maximal aortic aneurysm [Amax], narrowest infrarenal aortic neck [Amin], maximal common iliac [Imax], and narrowest iliac artery [Imin]). Inter- and intraobserver variability was calculated as standard deviation of mean pair differences according to the method of Bland and Altman. The true incidence of adjunctive procedures to facilitate delivery of the device into the aorta and ensure iliac limb seal was compared with that predicted by the observers to obtain sensitivity, specificity, and positive (PPV) and negative predictive value (NPV) for the measurements. Interobserver variability of iliac measurements was higher than intraobserver variability (p < 0.05). Interobserver variability of Amax ranged from 4.37 to 10.73% of the mean Amax. Conversely, variability of Amin was 8.91-18.89%, that of Imax was 12.11-22.23%, and that of Imin was 10.51-18.73% (p < 0.05 vs. Amax). Therefore, interobserver variability influenced aortic neck and iliac diameter twice as much as it did aneurysm measurements. To successfully place 30 endografts we performed 8 adjunctive access procedures (4 angioplasties, 4 common iliac artery conduits) and 17 adjunctive procedures in 60 limbs to ensure limb seal (9 unilateral IIA coil embolizations, 8 stents). We used 8.5 (Ancure) and 8.0 (Aneurex) mm as lower limits of acceptability for uncomplicated access, and 13.4 (Ancure) and 16 (Aneurex) mm as the upper limits of acceptability for uncomplicated iliac limb seal. These limits were applied to measurements from the three observers to predict need for adjunctive access or iliac seal procedures in this cohort. Sensitivity, specificity, PPV, and NPV of these observer measurements for a need to perform additional access procedures were 0.67, 0.80, 0.55, and 0.87; the same values for a need to perform additional seal procedures were 0.71, 0.74, 0.52, and 0.86, respectively. Interobserver variability was approximately 20% of measured iliac diameter. This explains why helical CT measurements were noted to have low PPV in predicting the need for an adjunctive access or limb seal procedure. These data establish PPV and NPV for hCT and provide objective evidence for the need to improve iliac artery imaging. Until more accurate imaging becomes available, we recommend oversizing of iliac limbs by 10-20% in patients with wide landing zones and that surgeons be prepared to resolve unexpected iliac artery access or seal problems intraoperatively.

Aortic Aneurysm, Abdominal↗
PubMed2004

Carotid artery stenting: is there a need to revise ultrasound velocity criteria?

OBJECTIVES: Ultrasound (US) velocity criteria have not been well-established for patients undergoing carotid artery stenting (CAS). A potential source of error in using US after CAS is that reduced compliance in the stented artery may result in elevated velocity relative to the native artery. We measured arterial compliance in the stented artery, and developed customized velocity criteria for use early after CAS. METHODS: US was performed before and within 3 days after CAS, and after 1 month in a subset of 26 patients. Post-procedural peak systolic velocity (PSV) and end-diastolic velocity (EDV) of the internal carotid artery (ICA), PSV/EDV ratio, and internal carotid artery to common carotid artery ratio (ICA/CCA) were recorded. These were compared with degree of in-stent residual stenosis determined at carotid angiography performed at the completion of CAS. Peterson's elastic modulus (Ep) and compliance (Cp) of the ICA were determined in a subgroup of 20 patients at the distal end of the stent and in the same region in the native ICA before stenting. RESULTS: Ninety CAS procedures were analyzed. Mean (+/-SD) angiographic residual stenosis after CAS was 5.4 +/- 9.1%, whereas corresponding PSV by US was 120.4 +/- 32.4 cm/s; EDV, 41.4 +/- 18.6 cm/s; PSV/EDV ratio, 3.3 +/- 1.2; and ICA/CCA ratio, 1.6 +/- 0.5. PSV was unchanged at 1 month. Post-CAS PSV and ICA/CCA ratio correlated most with degree of stenosis (P <.0001 for both). Only six patients demonstrated in-stent residual stenosis 20% or greater, but the standard US threshold of PSV 130 cm/s or greater (validated for >20% ICA stenosis in our laboratory) categorized 38 of 90 patients as having stenosis 20% or greater. Receiver operator curve analysis demonstrated that a combined threshold of PSV 150 cm/s or greater and ICA/CCA ratio 2.16 or greater were optimal for detecting residual stenosis of 20% or greater, with sensitivity 100%, specificity 98%, positive predictive value 75%, and negative predictive value 100%. After placement of a stent, the ICA demonstrated significantly increased Ep (1.2 vs 4.4 x 10(3) mm Hg; P =.004) and decreased Cp (9.8 vs 3.2 %mm Hg x 10(-2); P =.0004). CONCLUSIONS: Currently accepted US velocity criteria validated in our laboratory for nonstented ICAs falsely classified several stented ICAs with normal diameter on carotid angiograms as having residual in-stent stenosis 20% or greater. We propose a new criterion that defines PSV less than 150 cm/s, with ICA/CCA ratio less than 2.16, as the best correlate to a normal lumen (0%-19% stenosis) in the recently stented ICA. This was associated with increased stiffness of the stented ICA (increased Ep, decreased Cp). These preliminary results suggest that placement of a stent in the carotid artery alters its biomechanical properties, which may cause an increase in US velocity measurements in the absence of a technical error or residual stenotic disease.

Aged↗
PubMed2004

Technical challenges in a program of carotid artery stenting.

OBJECTIVES: Successful carotid artery stenting (CAS) involves gaining access to the common carotid artery, characterizing and crossing the lesion, deploying an anti-embolic device and stent, and retrieving the anti-embolic device. These steps are critical determinants of the complexity of the procedure. The frequency with which technical challenges are encountered during CAS is ill-defined. The purpose of this investigation was to review the incidence and types of technical challenges encountered during CAS and determine their effect on outcome. METHODS: Data were prospectively collected for 194 consecutive CAS procedures (177 patients) and separated into group 1, standard CAS technique, and group 2, procedures with technical challenges requiring modifications to the technique. Technical challenges were defined as difficult femoral arterial access (aortoiliac occlusive disease), complex aortic arch anatomy (elongated or bovine arch, deep takeoff of the innominate artery, tandem stenoses (CCA, innominate artery), difficult internal carotid artery anatomy (tortuosity, high-grade stenosis), and circumferential internal carotid artery calcification. The incidence of technical challenges, types of technical modifications required, and effect on outcomes were determined. RESULTS: Fifty technically challenging situations (26%) were encountered in 194 CAS procedures (group 2), which required advanced technical skills. Standard methods were used in the other 144 procedures (group 1, 74%). No significant differences in 30-day stroke and death rates were noted between the groups (group 1, 3.1%; group 2, 2.0%; P = .564). CONCLUSIONS: Twenty-six percent of the procedures required a modification in the standard technique for successful CAS. Circumferential calcification and severe tortuosity continue to be relative contraindications to CAS. Recognition of these technical challenges and increasing facility with the methods to manage them will enable expanded use of CAS without increased morbidity and mortality.

Aged↗
PubMed2004

Credentialing of surgeons as interventionalists for carotid artery stenting: experience from the lead-in phase of CREST.

BACKGROUND: Credentialing of vascular surgeons to perform carotid artery stenting (CAS) continues to be a major issue confronting the specialty of Vascular Surgery. Cannulation of aortic arch branches, and placement of carotid antiembolic devices and stents constitute the major technical challenges to vascular surgeons becoming credentialed to perform CAS. The multicenter Carotid Revascularization Endarterectomy vs Stenting Trial (CREST), supported by the National Institute of Neurological Disorders and Stroke, National Institute of Health, reviews credentials of interventionalists, including surgeons, for the trial's "lead-in" phase of CAS to treat symptomatic (>50% stenosis) and asymptomatic (>70% stenosis). METHODS: Vascular surgeons requesting participation in CREST must have achieved basic interventional credentialing criteria as recommended by the Society of Vascular Surgery. Each interventionalist is asked to submit notes and narrative summaries from a series of 10 to 30 CAS procedures for review by a multi-specialty review committee before being approved to participate in CREST. Thereafter, during the lead-in phase of CREST, each approved interventionalist is asked to perform CAS procedures using the study devices in as many as 20 patients. In this interim report from the CREST lead-phase, the association of specialty of operator (vascular surgeon, neurosurgeon, other specialist) and periprocedural stroke and death rate was examined in patients undergoing CAS. In addition, current enrollment volume in the lead-in phase by specialty of the principal investigator was examined. RESULTS: Thirty-two of 134 (23.9%) CREST-credentialed interventionalists are vascular surgeons (n = 22; 16.4%) or neurosurgeons (n = 10; 7.5%). For events monitored through March 31, 2004, 789 patients had undergone CAS procedures performed by these 134 specialists. Thirty-day stroke and death rate was 4.6%, and myocardial infarction was observed in 1.1% of patients. Serious adverse events have not been clustered at individual institutions, and no significant differences have been observed between vascular surgeons or neurosurgeons and other credentialed specialists. CONCLUSIONS: Vascular surgeons with basic catheter and guide wire skills, particularly those who have incorporated diagnostic cerebral angiography into their practice, can be credentialed to perform CAS. Individuals or groups should devote a number of cases (n = 10-30 per surgeon) to CAS to accomplish this goal. Pending US Food and Drug Administration approval of devices and Center for Medicaid and Medicare Services reimbursement, institutional financial support for the performance of these procedures must be secured. The learning curve for CAS should not be considered so formidable as to discourage surgeons from adding these techniques of CAS to their procedural inventory.

Angioplasty, Balloon↗
PubMed2004

Carotid artery stenting is associated with increased complications in octogenarians: 30-day stroke and death rates in the CREST lead-in phase.

BACKGROUND: A heightened risk of stroke and death among octogenarians undergoing carotid artery stenting (CAS) has been reported. The multicenter Carotid Revascularization Endarterectomy vs. Stent Trial (CREST) supported by the National Institute of Neurological Disorders, National Institutes of Health, compares the efficacy of carotid endarterectomy (CEA) and CAS in an ongoing clinical trial. This effort also includes a "lead-in" phase of symptomatic (>50% stenosis) and asymptomatic (>70% stenosis) patients. The protocol calls for patients to receive aspirin and clopidogrel before and 30-days after CAS and to be examined by a study neurologist preprocedure, at 24-hours, and at 30-day. The occurrence of stroke and death was reviewed by an independent clinical events committee. METHODS: The association of age and periprocedural stroke and death was examined in 749 lead-in patients undergoing CAS (30.7% symptomatic, 69.3% asymptomatic). Patients were separated into four age categories: less than 60, 60 to 69, 70 to 79, and 80 years or older, and the proportion of patients with stroke and death during the 30-day periprocedural period was calculated for each category. RESULTS: An increasing proportion of patients suffered stroke and death with increasing age (P = .0006); 2 (1.7%) of 120 patients under age 60, 3 (1.3%) of 229 aged 60 to 69, 16 (5.3%) of 301 aged 70 to 79, and 12 (12.1%) of 99 patients aged 80 years and older. These increasingly high complication rates at older ages were not mediated by adjustment for symptomatic status, use of antiembolic devices, gender, percentage of carotid stenosis, or the presence of distal arterial tortuosity. CONCLUSIONS: Interim results from the lead-in phase of CREST show that the periprocedural risk of stroke and death after CAS increases with age in the course of a credentialing registry. This effect is not mediated by potential confounding factors. Randomized trial data are needed to compare the CAS versus CEA periprocedural risk of stroke and death by age. Pending results from randomized studies, care should be taken when CAS is performed in older patient populations.

Adult↗