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  • Author or Editor: Colin P. Derdeyn x
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Yasha Kadkhodayan, Colin P. Derdeyn, Dewitte T. Cross III and Christopher J. Moran

Object

The goal in this retrospective study was to examine the procedural complication rate for carotid angioplasty and stent placement performed without cerebral protection devices.

Methods

Between March 1996 and December 2003, 167 carotid angioplasty and/or stent placement procedures were performed without cerebral protection devices in 152 patients (57 women and 95 men whose mean age was 64 years, range 19–92 years). Seven of these patients underwent angioplasty alone. Eighty-nine patients presented with focal neurological symptoms. Indications for surgery included atherosclerosis, radiation-associated stenosis, dissection, pseudoaneurysm, and stretched endovascular coils from aneurysm treatment. In this study, the patients' medical records were reviewed for clinical characteristics, techniques used, and resulting intraprocedural and 30-day complication rates.

The intraprocedural stroke rate was four (2.4%) of 167; this included three hemispheric strokes and one retinal embolus. All events occurred in patients who had symptomatic stenosis. The procedural transient ischemic complication rate was six (3.6%) of 167, as was the procedural nonneurological complication rate. During the 30 days post-procedure, one patient had died and three had suffered permanent ischemic events (two cerebral and one ocular). The composite 30-day postprocedural stroke and death rate was eight (5%) of 160. The rate of asymptomatic angiographically confirmed abnormalities was 0.6% (one treated vessel that was occluded but asymptomatic). The 30-day rate of nonneurological complications was 2.5%. A strong association between intraprocedural thromboembolic events (eight cases) and prior ischemic symptoms was found (p = 0.01).

Conclusions

Carotid angioplasty and stent placement without cerebral protection devices is safe, particularly in patients without symptomatic stenosis.

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Robert L. Grubb Jr., William J. Powers, Colin P. Derdeyn, Harold P. Adams Jr. and William R. Clarke

The St. Louis Carotid Occlusion Study demonstrated that ipsilateral increased O2 extraction fraction (OEF) (Stage II hemodynamic failure) measured by positron emission tomography (PET) is a powerful independent risk factor for subsequent stroke in patients with symptomatic complete carotid artery (CA) occlusion. The ipsilateral ischemic stroke rate at 2 years has been shown to be 5.3% in 42 patients with normal OEF and 26.5% in 39 patients with increased OEF (p = 0.004). In patients in whom hemispheric symptoms developed within 120 days, the 2-year ipsilateral stroke rates were 12% in 27 patients with normal OEF and 50% in 18 patients with increased OEF. Previous PET studies have demonstrated that anastomosis of the superficial temporal artery (STA) to a middle cerebral artery (MCA) cortical branch can restore OEF to normal.

The authors discuss the undertaking of a study that will test the hypothesis that STA–MCA anastomosis, when combined with the best medical therapy, can reduce ipsilateral ischemic stroke by 40% at 2 years in patients with symptomatic internal CA occlusion and Stage II hemodynamic failure occurring within 120 days after surgery. Only patients with increased OEF distal to a symptomatic occluded CA will be randomized to surgery or medical treatment. The primary endpoint will be all strokes and death occurring between randomization and the 30-day postoperative cut off (with an equivalent period in the nonsurgical group), as well as subsequent ipsilateral ischemic stroke developing within 2 years. It is estimated that 186 patients will be required in each group. Assuming that 40% of PET scans will demonstrate increased OEF, this will require enrolling 930 clinically eligible individuals.

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Thomas Jiang, Arie Perry, Ralph G. Dacey Jr., Gregory J. Zipfel and Colin P. Derdeyn

Atherosclerotic disease has been suspected as a cause of moyamoya disease in some patients but has not, to the authors' knowledge, been confirmed by pathological studies. The authors present the histopathological findings in a patient with moyamoya collateral formation associated with atherosclerotic occlusive disease of the distal internal carotid artery (ICA). Typical atheromatous changes were evident in the distal ICA and proximal middle cerebral artery. In addition, intimal thickening, fibrosis, and abnormal internal elastic lamina were present in these vessels. These findings are common in moyamoya but not in atherosclerotic disease. Proliferation and enlargement of the lenticulostriate arteries in the basal ganglia was also identified. Moyamoya phenomenon secondary to atherosclerotic disease has similar histopathological features to idiopathic moyamoya phenomenon, both in the affected large basal arteries and lenticulostriate collaterals. These findings support the hypothesis advanced by Peerless that moyamoya is a 2-step process involving an obliterative vasculopathy of the terminal ICA and a secondary proliferative response.

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Dennis J. Rivet, James K. Goddard III, Keith M. Rich and Colin P. Derdeyn

✓ Definitive endovascular treatment of dural arteriovenous fistulas (DAVFs) requires obliteration of the site of the fistula: either the diseased dural sinus or the pial vein. Access to this site is often limited by occlusion of the sinus proximal and distal to the segment containing the fistula. The authors describe a technique in which the mastoid emissary vein is used to gain access to a Borden–Shucart Type II DAVF in the transverse–sigmoid sinus. Recognition of this route of access, if present, may facilitate endovascular treatment of these lesions. Access to the transverse sinus via this approach can be straightforward and may be underused.

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Avi Mazumdar, Dennis J. Rivet, Colin P. Derdeyn, DeWitte T. Cross III and Christopher J. Moran

Object

This study was conducted to determine whether there is a change in intracranial arterial diameters after verapamil infusion for vasospasm and, if it is present, to determine whether the change occurs in proximal, intermediate, or distal vessels.

Methods

The authors measured arterial diameters in all patients treated with intraarterial verapamil at their institutions between August 2003 and September 2004. In all, 18 treatments were examined in 15 patients. Measurements were made before and after verapamil infusion in a blinded fashion with the aid of a magnification loupe at nine predetermined arterial sites on each angiogram. Baseline arterial measurements were made on each patient's initial angiogram and on the angiogram demonstrating spasm prior to endovascular therapy as well in 14 of the patients. Charts were retrospectively reviewed to determine whether the patients benefited from intraarterial vera-pamil.

From the time of the initial angiogram to the time of vasospasm, there was a 21.6% decrease (p = 0.092) in proximal artery diameter, a 47.1% decrease (p < 0.05) in intermediate artery diameter, and a 12.4% decrease (p < 0.05) in distal artery diameter. There were no significant changes in the diameters of proximal, intermediate, or distal vessels after verapamil infusion (mean dose 7.4 mg, range 2.5–10 mg). After infusion of intraarterial verapamil, the proximal vessels showed a 1.1% decrease in diameter, the intermediate vessels showed a 9.4% increase, and the distal vessels showed a 3.3% decrease.

Conclusions

Administration of intraarterial verapamil does not cause a significant increase in the diameter of vasospastic vessels at the administered doses.

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Roberto C. Heros

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Ananth K. Vellimana, Andria L. Ford, Jin-Moo Lee, Colin P. Derdeyn and Gregory J. Zipfel

Symptomatic intracranial arterial disease is associated with a high rate of recurrent ischemic events. The management of this condition is controversial, with some advocating medical therapy as a sole means of treatment and others recommending endovascular therapy in addition to best medical management. In rare cases, surgical intervention is considered. A thorough review of the available literature was performed, and treatment recommendations based on these data are provided.

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DeWitte T. Cross III, David L. Tirschwell, Mary Ann Clark, Dan Tuden, Colin P. Derdeyn, Christopher J. Moran and Ralph G. Dacey Jr.

Object. The goal of this study was to determine whether a hospital's volume of subarachnoid hemorrhage (SAH) cases affects mortality rates in patients with SAH. For certain serious illnesses and surgical procedures, outcome has been associated with hospital case volume. Subarachnoid hemorrhage, usually resulting from a ruptured cerebral aneurysm, yields a high mortality rate. There has been no multistate study of a diverse set of hospitals to determine whether in-hospital mortality rates are influenced by hospital volume of SAH cases.

Methods. The authors conducted an analysis of a retrospective, administrative database of 16,399 hospitalizations for SAH (9290 admitted through emergency departments). These hospitalizations were from acute-care hospitals in 18 states representing 58% of the US population. Both univariate and multivariate analyses were used to assess the case volume—mortality rate relationship. The authors used patient age, sex, Medicaid status, hospital region, data source year, hospital case volume quartile, and a comorbidity index in multivariate generalized estimating equations to model the relationship between hospital volume and mortality rates after SAH.

Patients with SAH who were treated in hospitals in which low volumes of patients with SAH are admitted through the emergency department had 1.4 times the odds of dying in the hospital (95% confidence interval 1.2–1.6) as patients admitted to high-volume hospitals after controlling for patient age, sex, Medicaid status, hospital region, database year, and comorbid conditions.

Conclusions. Patients with a diagnosis of SAH on their discharge records who initially presented through the emergency department of a hospital with a high volume of SAH cases had significantly lower mortality rates. Concentrating care for this disease in high-volume SAH treatment centers may improve overall survival.

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Chad W. Washington, Colin P. Derdeyn, Ralph G. Dacey Jr., Rajat Dhar and Gregory J. Zipfel

Object

Studies using the Nationwide Inpatient Sample (NIS), a large ICD-9–based (International Classification of Diseases, Ninth Revision) administrative database, to analyze aneurysmal subarachnoid hemorrhage (SAH) have been limited by an inability to control for SAH severity and the use of unverified outcome measures. To address these limitations, the authors developed and validated a surrogate marker for SAH severity, the NIS-SAH Severity Score (NIS-SSS; akin to Hunt and Hess [HH] grade), and a dichotomous measure of SAH outcome, the NIS-SAH Outcome Measure (NIS-SOM; akin to modified Rankin Scale [mRS] score).

Methods

Three separate and distinct patient cohorts were used to define and then validate the NIS-SSS and NIS-SOM. A cohort (n = 148,958, the “model population”) derived from the 1998–2009 NIS was used for developing the NIS-SSS and NIS-SOM models. Diagnoses most likely reflective of SAH severity were entered into a regression model predicting poor outcome; model coefficients of significant factors were used to generate the NIS-SSS. Nationwide Inpatient Sample codes most likely to reflect a poor outcome (for example, discharge disposition, tracheostomy) were used to create the NIS-SOM.

Data from 716 patients with SAH (the “validation population”) treated at the authors' institution were used to validate the NIS-SSS and NIS-SOM against HH grade and mRS score, respectively.

Lastly, 147,395 patients (the “assessment population”) from the 1998–2009 NIS, independent of the model population, were used to assess performance of the NIS-SSS in predicting outcome. The ability of the NIS-SSS to predict outcome was compared with other common measures of disease severity (All Patient Refined Diagnosis Related Group [APR-DRG], All Payer Severity-adjusted DRG [APS-DRG], and DRG).

Results

The NIS-SSS significantly correlated with HH grade, and there was no statistical difference between the abilities of the NIS-SSS and HH grade to predict mRS-based outcomes. As compared with the APR-DRG, APSDRG, and DRG, the NIS-SSS was more accurate in predicting SAH outcome (area under the curve [AUC] = 0.69, 0.71, 0.71, and 0.79, respectively).

A strong correlation between NIS-SOM and mRS was found, with an agreement and kappa statistic of 85% and 0.63, respectively, when poor outcome was defined by an mRS score > 2 and 95% and 0.84 when poor outcome was defined by an mRS score > 3.

Conclusions

Data in this study indicate that in the analysis of NIS data sets, the NIS-SSS is a valid measure of SAH severity that outperforms previous measures of disease severity and that the NIS-SOM is a valid measure of SAH outcome. It is critically important that outcomes research in SAH using administrative data sets incorporate the NIS-SSS and NIS-SOM to adjust for neurology-specific disease severity.

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Roberto C. Heros