Pierre Fayad

Long-Term Results of Carotid Stenting versus Endarterectomy in High-Risk Patients

BACKGROUND We previously reported that, in a randomized trial, carotid stenting with the use of an emboli-protection device is not inferior to carotid endarterectomy for the treatment of carotid artery disease at 30 days and at 1 year. We now report the 3-year results. METHODS The trial evaluated carotid artery stenting with the use of an emboli-protection device as compared with endarterectomy in 334 patients at increased risk for complications from endarterectomy who had either a symptomatic carotid artery stenosis of at least 50% of the luminal diameter or an asymptomatic stenosis of at least 80%. The prespecified major secondary end point at 3 years was a composite of death, stroke, or myocardial infarction within 30 days after the procedure or death or ipsilateral stroke between 31 days and 1080 days (3 years). RESULTS At 3 years, data were available for 260 patients (77.8%), including 85.6% of patients in the stenting group and 70.1% of those in the endarterectomy group. The prespecified major secondary end point occurred in 41 patients in the stenting group (cumulative incidence, 24.6%; Kaplan-Meier estimate, 26.2%) and 45 patients in the endarterectomy group (cumulative incidence, 26.9%; Kaplan-Meier estimate, 30.3%) (absolute difference in cumulative incidence for the stenting group, -2.3%; 95% confidence interval, -11.8 to 7.0). There were 15 strokes in each of the two groups, of which 11 in the stenting group and 9 in the endarterectomy group were ipsilateral. CONCLUSIONS In our trial of patients with severe carotid artery stenosis and increased surgical risk, no significant difference could be shown in long-term outcomes between patients who underwent carotid artery stenting with an emboli-protection device and those who underwent endarterectomy. (ClinicalTrials.gov number, NCT00231270 [ClinicalTrials.gov].).

Embolotherapy of large pulmonary arteriovenous malformations: long-term results.

BACKGROUND The purpose of this study was to document the long-term results of transcatheter embolotherapy of large pulmonary arteriovenous malformations (PAVMs). METHODS From a data base of 221 consecutive patients with PAVMs treated by embolotherapy between 1978 and 1995, 45 patients with 52 PAVMs, supplied by feeding arteries 8 mm in diameter or larger, were selected for a retrospective investigation. RESULTS Of 45 patients with 52 large PAVMs, 38 patients (84%) with 44 PAVMs (85%) were cured by the first embolotherapy (mean follow-up, 4.7 years). Acute periprocedural complications included self-limited pleurisy (31%), angina secondary to air embolus (2%), and paradoxical embolization of a device during deployment (4%). None of these events led to short- or long-term sequelae. Seven patients (16%) had persistence of the PAVM attributable to either recanalization (n = 4) or interim accessory artery growth (n = 3). Two of these patients presented with ischemic stroke several years after the initial treatment. Persistent PAVMs (n = 8) were retreated successfully by a second procedure (n = 7), or a third procedure (n = 1) (mean follow-up, 5.9 and 5.3 years, respectively). CONCLUSIONS Embolotherapy of large PAVMs results in permanent occlusion in an overwhelming majority of patients. Continued patency due to recanalization or accessory artery growth is easily detected and treated.

Pulmonary arteriovenous malformations Cerebral ischemia and neurologic manifestations

Background: There is an increasingly recognized association between pulmonary arteriovenous malformations (PAVM) and cerebral ischemia, frequently attributed to paradoxical embolization. PAVM occur in 20 to 30% of the hereditary hemorrhagic telangiectasia (HHT) population. Objective: To evaluate the risk determinants for cerebral ischemia and neurologic manifestations in patients with PAVM. Methods: A retrospective cross-sectional study was performed on consecutive patients admitted between 1988 and 1992 for treatment of PAVM. The number of PAVM, feeding artery (FA) diameters, and aneurysmal sizes were determined by pulmonary angiography. Patients were categorized as having single or multiple PAVM with an FA diameter of ≥3 mm. History, examination, and cerebral imaging studies were used to determine the prevalence of neurologic manifestations. Patients were defined as having cerebral paradoxical embolization if there was radiologic evidence of cortical infarction. Results: There were 75 cases: 26 single PAVM and 49 multiple PAVM. Cortical infarction was present in 14% of patients with single PAVM. Patients with multiple PAVM had a greater prevalence of any infarction (OR 3.2; 95% CI, 1.2 to 9.44, p = 0.030), cortical infarctions (OR 2.3; 95% CI, 0.58 to 9.2, p = 0.230), subcortical infarctions (OR 2.1; 95% CI, 0.58 to 7.95, p = 0.249), abscesses (OR 2.3; 95% CI, 0.46 to 11.94; p = 0.295), and seizures (OR 6.4, 95% CI 0.77 to 53.2, p = 0.054). Patients with multiple PAVM had markedly greater odds of having any clinical or radiologic evidence of cerebral ischemic involvement (OR 4.5; 95% CI, 1.47 to 14; p = 0.008). Conclusion: There is a strong association between single PAVM and various neurologic manifestations. The prevalence is greater for patients with multiple PAVM, suggesting increased predisposition for paradoxical embolization with a greater number of malformations.

Proton magnetic resonance spectroscopy of cerebral lactate and other metabolites in stroke patients.

Background and Purpose Proton magnetic resonance spectroscopy can measure in vivo brain lactate and other metabolites noninvasively. We measured the biochemical changes accompanying stroke in 16 human subjects with cortical or deep cerebral infarcts within the first 3 weeks after symptom onset, and performed follow-up studies on six. Methods One-dimensional proton spectroscopic imaging encompassing the infarct region was performed with a 2.1-T whole-body magnet using the stimulated echo pulse sequence and an echo time of 270 msec. Results All but one of the cortical stroke patients had increased lactate within or near the infarct. Persistently elevated cerebral lactate was documented in five of six cases studied serially as long as 251 days after infarction. iV-acetylaspartate levels were decreased in most cortical strokes. Elevated lactate, accompanied by minimal reduction in iV-acetylaspartate, was recorded in two of four patients in the first week following a small subcortical infarct. Conclusions Long-term elevation of lactate commonly occurs after stroke. This lactate may arise from ongoing ischemia or infiltrating leukocytes, or it may be a residual of the lactate formed during the initial insult. The ability to observe stroke-elevated lactate pools at any time after lesion onset provides an approach to distinguishing among these possibilities in the future.

Spectroscopic imaging of stroke in humans: Histopathology correlates of spectral changes

Previous studies of human stroke by 1H nuclear magnetic resonance spectroscopy have shown elevation of lactate lasting 3 to 6 months. Complete metabolic turnover of the elevated lactate pool has been demonstrated 5 weeks after a stroke. Its cellular localization is among the first questions requiring clarification. Information pertinent to this question came to us from a patient with a 2-week-old stroke by 1H nuclear magnetic resonance spectroscopic imaging 1 week before his death led to neuropathologic examination of the brain. 1H spectra from voxels including the infarcts showed increased lactate and decreased N-acetylaspartate. Histopathology showed sheets of foamy macrophages in the infarct, but few neurons. Macrophage density ranged from 196 cells/mm2 near the surface of the infarct to 788 near its medial margin. Glial density was 500 to 800 cells/mm2. Lactate concentration in voxels including portions of the infarct was estimated at 7 to 14 mM. Voxels showing low N-acetylaspartate and high lactate on spectroscopic imaging were associated with histopathologic sections containing foamy macrophages. Brain macrophages—which begin to appear 3 days after infarction and gradually disappear over several months—could be a major source of elevated lactate signals that persist for months after stroke.

Factors associated with early presentation of acute stroke.

Background and Purpose Patients with stroke symptoms commonly delay many hours before seeking medical attention. We sought to explore the factors associated with early presentation of stroke patients to physicians. Methods We prospectively studied 100 consecutive acute stroke patients presenting to three large, urban medical centers. Using a standardized, structured interview and chart review, we assessed patient education about stroke, risk factors, clinical features of the stroke, source of stroke recognition, and timing of presentation. We did not study the distance from the site of stroke onset to the site of physician contact. Results Stroke onset time was known in 96 of the patients. Mean patient age was 71.3 years, 79% had at least one stroke risk factor, 26% had prior transient ischemic attack, 19% had prior stroke, 74% had some high school education, and 86% had regular physicians. Only 8% had been previously educated about stroke symptoms. Eighty one percent of strokes were ischemic. The mean time to physician contact was 13.4 ± 2.3 hours (median, 4.0 hours) and to neurologist contact was 21.2 ± 2.9 hours. A skewed distribution of presentation times accounts for the mean-median differences. A small number of patients presenting very late could have an effect on the correlations between presentation time and the variables studied. Early presentation time was associated with increased age, the sudden onset of a stable deficit, and recognition that the symptoms signified stroke. Only the sudden onset of a stable deficit correlated independently with early presentation time (P=.0048). There was no correlation between presentation time and prior transient ischemic attack or stroke, headache, vomiting, loss of consciousness or seizures at onset, or stroke subtype, but a type II error could not be excluded. Conclusions Despite their education level, regular health care, and risk factors, especially prior stroke and transient ischemic attack, these patients were not knowledgeable about stroke and delayed many hours before contacting physicians. The course of symptoms and recognition that they signified stroke were associated with earlier presentation. Patient education focused on groups at risk may hasten the presentation and treatment of acute stroke.

A comparative study of the cerebrovascular complications of cocaine: alkaloidal versus hydrochloride--a review.

Cocaine, especially in its alkaloidal or “crack” form, has been increasingly associated with cerebrovascular disease. Before the crack epidemic, cocaine hydrochloride (HCl) was also implicated as a cause of stroke. However, less is known about the differences in stroke subtypes, age at stroke onset, or presence of underlying structural cerebrovascular disease with different forms of cocaine use. We compared 26 patients (previously reported) from our four institutions plus 16 cases reported in the literature of stroke associated with alkaloidal cocaine to 63 (57 reported in the literature and six not previously reported from our four institutions) cases of stroke associated with cocaine HCl. Ischemic and hemorrhagic strokes are equally likely after alkaloidal cocaine use, whereas cocaine HCl is more likely (approximately 80% of the time) to cause hemorrhagic stroke, with approximately half the intracranial hemorrhages occurring from ruptured cerebral saccular aneurysms or vascular malformations. The presence of an underlying cerebral aneurysm was more common among patients with cocaine HCl-associated strokes than alkaloidal cocaine-associated strokes. Cerebral infarction was significantly more common among the alkaloidal cocaine users than in all the cocaine HCl users, and this was also true when alkaloidal cocaine users were compared with parenteral cocaine HCl (intravenous and intramuscular) users. Only hemorrhagic stroke has been reported with intravenous cocaine HCl use. We conclude that the pathogenesis of cocaine-related stroke is heterogeneous, and depends, in part, on the form of cocaine used.

Stereotactic computed tomographic-guided aspiration and thrombolysis of intracerebral hematoma : protocol and preliminary experience.

BACKGROUND AND PURPOSE We review preliminary experience with patients harboring intracerebral hematoma (ICH) treated by stereotactic computed tomographic (CT) guided thrombolysis and aspiration and assess procedure feasibility and safety. METHODS Twelve patients with supratentorial ICH >/=25 mL without suspected underlying structural etiology or coagulopathy and an initial Glasgow Coma Scale (GCS) score of >/=5 were treated. A catheter was directed stereotactically or manually into the ICH through a burr hole under CT guidance. Hematoma aspiration was followed by instillation of urokinase (5 000 to 10 000 IU). This was repeated every 6 to 8 hours at bedside, with interval CT imaging, until the ICH volume diminished to <25 mL, less than half of its initial volume, or after a maximum of 10 aspirations/instillations. RESULTS Mean age was 69 years (range 55 to 82 years). Median initial GCS was 12 (range 5 to 14). There were 7 ganglionic and 5 lobar ICH, and baseline hematoma size ranged 29 to 70 mL (mean 46 mL). Final ICH volume ranged from 14 to 51 mL (mean 21 mL), with ICH volume reduction by an average of 57% (range 38% to 70%). One patient (8. 3%) suffered hematoma expansion during the procedure. At 6 months after the procedure, 3 patients (25%) had achieved a good recovery (Glasgow Outcome Scale [GOS] score of 5), 5 patients (42%) were dependent (GOS 3), and 1 (8.3%) remained vegetative (GOS 2). Three patients (25%) died in hospital (1 from cardiac arrhythmia and 2 from respiratory failure). CONCLUSIONS CT-guided thrombolysis and aspiration appears safe and effective in the reduction of ICH volume. Further studies are needed to assess optimal thrombolytic dosage and must include controlled comparisons of mortality, disability outcome, time until convalescence, and cost of care in treated and untreated patients.

Clinical Correlates of Proton Magnetic Resonance Spectroscopy Findings After Acute Cerebral Infarction

BACKGROUND AND PURPOSE We sought to determine whether lactate and N-acetyl signals measured by proton magnetic resonance spectroscopy (MRS) in the first days after stroke correlate with clinical measures of disability and functional outcome. METHODS One-dimensional spectroscopic imaging was performed after stroke on 32 patients using a 2.1-T magnet. The Toronto Stroke Scale score at the time of the MRS study and the Barthel Index score at hospital discharge were determined from patient records. Lesion volume was estimated by a tracing algorithm from the scout magnetic resonance image obtained as part of the MRS study. The scaled lactate and N-acetyl signals from the voxel having the highest measured lactate were used to predict the clinical variables and lesion volume, as well as relative perfusion within the lesion, in those patients who underwent single-photon emission computed tomography (SPECT) blood flow imaging, using a multiple regression analysis. The correlation of lesion volume with the clinical variables was also evaluated. RESULTS Lesion lactate signal was correlated with the Toronto Stroke Scale score, Barthel Index score, lesion volume, and SPECT score, all at P < .01. The N-acetyl level correlated with the Barthel Index score and lesion volume at P < .05. Lesion volume was also strongly correlated with the clinical variables (P < .0001). CONCLUSIONS This is the first study to document the clinical predictive value of proton MRS measurements in patients after stroke. The association with functional outcome is stronger for lactate than for N-acetyl. Spectroscopic assessment of the metabolic status of cerebral tissues shortly after infarction may have significant clinical utility.

Coronary Risk Evaluation in Patients With Transient Ischemic Attack and Ischemic Stroke A Scientific Statement for Healthcare Professionals From the Stroke Council and the Council on Clinical Cardiology of the American Heart Association/American Stroke Association

Stroke and myocardial infarction (MI) share common risk factors and pathological mechanisms, and coronary artery disease (CHD) is an important cause of death in patients with cerebrovascular disease. This Scientific Statement addresses issues in management of the relatively healthy patient with brain ischemia (a transient ischemic attack [TIA] or an ischemic stroke) who does not have recognized CHD but often has risk factors in addition to having had a TIA or stroke that indicate an increased likelihood of disability or death from cardiac disease in the future. This Statement should not be confused with the official American College of Cardiology (ACC)/American Heart Association (AHA) practice guidelines. The reader is referred to the ACC/AHA guidelines for management of recognized and symptomatic CHD1 and the American College of Chest Physicians (ACCP)2 and American Stroke Association (ASA)3–5 guidelines for evaluation of cardiac causes of TIA and stroke, which are important related but separate issues. Several small studies have shown that patients with TIA and stroke have a high prevalence of asymptomatic CHD.6–8 Rokey et al6 performed exercise thallium (Tl) 201 scintigraphy and exercise radionuclide ventriculography on 50 consecutive patients with TIA or stroke. Sixteen patients had symptoms suggestive of cardiac ischemia; the other 34 patients were asymptomatic. The results of myocardial perfusion imaging were abnormal in 15 of 16 symptomatic patients (94%) and 14 of 34 asymptomatic patients (41%). Twenty-two patients who had abnormal myocardial perfusion imaging results underwent coronary angiography, which showed severe CHD (≥70% stenosis of the lumen of ≥1 coronary artery) in 18 patients (10 of 13 symptomatic patients and 8 of 9 asymptomatic patients). Twelve of the 18 patients with severe CHD had multivessel disease. In a study by Di Pasquale et al,7 83 consecutive patients with TIA or minor stroke and no …