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Askiel Bruno

Publications and source records attributed to Askiel Bruno.

12 recordsLinked to original sources

Using change in the National Institutes of Health Stroke Scale to measure treatment effect in acute stroke trials.

BACKGROUND AND PURPOSE: Outcome measures in acute stroke trials are being refined. Changes in neurological deficits might be useful outcome measures because they can measure the entire spectrum of deficits. METHODS: We analyzed data from the acute stroke treatment trial Trial of Org 10172 in Acute Stroke Treatment (TOAST). Using logistic regression analysis, we modeled the probability of the TOAST predefined very favorable outcome (VFO; both Glasgow Outcome Scale 1 and modified Barthel Index 19 to 20) at 3 months. Within-subject changes (baseline-3 months) on the National Institutes of Health Stroke Scale (NIHSS) was the main predictor of interest. RESULTS: The baseline median NIHSS for the entire TOAST cohort was 7, and it improved by 4 points (interquartile range 3 to 6) among 603 patient with VFO and by 2 points (interquartile range -1 to 5) among 638 patients without a VFO (P<0.001). The odds for VFO increased by 2.29 (95% CI, 2.06 to 2.54; P<0.001) for each 1-point improvement on the NIHSS. In receiver operating characteristic analysis, final NIHSS < or =2 was a good predictor of VFO, but no single NIHSS change cut point was a good predictor of VFO. CONCLUSIONS: NIHSS change appears to be a useful outcome measure for acute stroke trials and is not fully comparable to dichotomized functional outcomes.

Acute Disease↗

A supervised method for calculating perfusion/diffusion mismatch volume in acute ischemic stroke.

Diffusion and perfusion (MR) imaging modalities identify overlapping but not identical areas of tissue as lesion following a stroke. It is thought that the 'mismatch' between modalities may represent tissue that could be recovered with proper (thrombolytic) treatment. We have designed a tool for semi-automated segmentation of the images and calculation of the mismatch volume. We present results from software phantoms and clinical data. Phantom results show our mismatch volume calculations are unbiased at realistic noise levels. Clinical data show that raters using our tool are consistent, fast (15min per subject) and indistinguishable from an expert using manual segmentation.

Adult↗

Cerebrovascular and cardiovascular complications of alcohol and sympathomimetic drug abuse.

Alcohol and stimulant abuse represents a major cause of cerebrovascular and cardiovascular disease in young adults. Although mild-to-moderate alcohol consumption has been linked to a decreased risk for stroke and CVD, excessive use is associated with an increased risk for intracranial hemorrhage and cardiomyopathy. Cocaine represents the single largest,cause of medical complications related to illegal drug use. Cocaine has been associated with cerebral infarction, intracranial hemorrhage, myocardial infarction, cardiomyopathy, and cardiac arrhythmias. Abuse of amphetamines is associated with complications similar to those of cocaine. The complications associated with stimulant abuse are thought to be primarily mediated through excess catecholamines, resulting in acute arterial hypertension, vasospasm, thrombosis, and accelerated atherosclerosis. Because many complications of alcohol and stimulant abuse are preventable and reversible, it is important to screen for these in patients with cerebrovascular and cardiovascular disease.

Alcoholism↗

Serial urinary 11-dehydrothromboxane B2, aspirin dose, and vascular events in blacks after recent cerebral infarction.

BACKGROUND AND PURPOSE: Incomplete platelet inhibition by aspirin (aspirin resistance) may be a reason for stroke recurrence in some patients. 11-dehydrothromboxane B2 (11-DTB2) is a stable thromboxane A2 metabolite that reflects in vivo platelet activation. This pilot study was intended to evaluate the reproducibility of urinary 11-DTB2 over time and to look for evidence of aspirin resistance. METHODS: All subjects were screened for the African American Antiplatelet Stroke Prevention Study (AAASPS) 7 to 90 days after noncardioembolic cerebral infarction. Of 83 subjects with at least 1 urine sample, 52 were enrolled in AAASPS (randomized to blinded treatment with aspirin 650 mg/d or ticlopidine 500 mg/d), and 31 were enrolled in an open-label antiplatelet therapy cohort. Subjects were followed up for 2 years, with 11-DTB2 measurements scheduled at baseline and 6, 12, and 24 months. Vascular events were cerebral infarction, myocardial infarction, or vascular death. RESULTS: Despite considerable individual up or down fluctuations, the median 11-DTB2 change did not significantly differ from zero in any of the subgroups. However, in 6 subjects with a 4-fold decrease in aspirin dose from 1300 to 325 or 81 mg/d, the 11-DTB2 level increased from 611 to 1881 pg/mg creatinine (P=0.06). Vascular events occurred in 7 of 61 aspirin-treated subjects, and 11-DTB2 levels did not correlate with the events. CONCLUSIONS: Fluctuations in urinary 11-DTB2 after cerebral infarction in blacks do not correlate with changes in aspirin doses, except perhaps when the dose changes by a factor of 4 or more. A larger study is needed to look further for aspirin resistance.

Anti-Inflammatory Agents, Non-Steroidal↗

How important is hyperglycemia during acute brain infarction?

BACKGROUND: Although well supported by animal studies, it remains unproven whether lowering hyperglycemia during acute cerebral infarction will improve outcomes. Further support for this therapeutic approach comes from clinical studies in acute myocardial infarction and in ventilated postsurgical patients, where lowering hyperglycemia improved outcomes. REVIEW SUMMARY: Animal studies support the hypothesis that hyperglycemia during acute brain ischemia augments the brain injury, but only in models with reperfusion. The available human studies to date are all observational and they usually find an association between hyperglycemia during acute cerebral infarction and worse outcome. Also, there is evidence that hyperglycemia during acute cerebral infarction is detrimental only with reperfusion. This association appears to be linear in the glucose ranges tested (normal to high). In addition, there is an association between admission hyperglycemia and hemorrhagic conversion of an acute cerebral infarct when thrombolytics are used. CONCLUSION: Sufficient evidence has accumulated to proceed to clinical efficacy trials to see if tight glycemic control compared with persistent hyperglycemia during acute cerebral infarction will improve outcomes. If such therapy proves beneficial, the increased cost, effort, and risk associated with tight glycemic control during acute cerebral infarction could be justified. Randomized clinical trials to test this hypothesis are currently in progress.

Acute Disease↗

Factors influencing outcome and treatment effect in PROACT II.

BACKGROUND AND PURPOSE: The PROACT II study demonstrated a significant benefit from treatment with intra-arterial pro-urokinase (r-proUK) in patients with middle cerebral artery occlusion treated within 6 hours of stroke onset. The purpose of the current study was to examine baseline factors to determine predictors of good outcome and response to treatment. METHODS: We selected from the baseline clinical, radiologic, and angiographic data variables that considered possibly related to outcome. A univariate analysis was performed to examine the association between these baseline factors and good outcome, defined as a modified Rankin scale score <or=2. A multivariate model then selected the most important variables independently influencing prognosis. A risk score for each patient was constructed on the basis of the patient's individual values for each independent variable. Patients were stratified into risk quartiles based on their risk scores, and an odds ratio for each risk quartile was calculated. The treatment effects of each quartile were compared. RESULTS: In the univariate analysis, screening National Institutes of Health stroke scale (NIHSS) score and age were strongly associated with good outcome. The multivariate model selected age, NIHSS score, and CT hypodensity as the most important prognostic variables. Dividing patients into quartiles based on risk scores achieved a uniform gradient of probability of good outcomes. A trend toward benefit of r-proUK treatment was seen in all risk quartiles, and no differential treatment effect was observed across risk groups. CONCLUSIONS: There was no evidence of differential effect of r-proUK across subgroups of patients stratified by risk.

Adult↗

Cerebrovascular complications of alcohol and sympathomimetic drug abuse.

Alcohol abuse has been linked to intracranial hemorrhage, both intracerebral and subarachnoid. Some studies have found a dose-response relationship, so that increasing levels of abuse are associated with greater risk of hemorrhage. However, alcohol abuse has not been clearly linked to cerebral infarction, and some studies find that mild-to-moderate drinking appears to be associated with a decreased risk of cerebral infarction. Intravenous administration of drugs of abuse predisposes to endocarditis, which may lead to embolic stroke. Associations have been reported between various sympathomimetic drugs and cerebral infarction. A possible mechanism for cerebral infarction is focal arterial vasoconstriction and occasionally cerebral vasculitis. Associations have also been reported between various sympathomimetic drugs and intracranial hemorrhage. A likely mechanism for intracranial hemorrhage is acute arterial hypertension. With the exception of endocarditis, management of stroke related to drug abuse is largely supportive, with emphasis on supportive care to prevent stroke complications, physical and occupational therapy, and aggressive addiction rehabilitation.

Alcohol Drinking↗

Aspirin and urinary 11-dehydrothromboxane B(2) in African American stroke patients.

BACKGROUND AND PURPOSE: The aim of the study was to evaluate the relationship between daily aspirin use and urinary excretion of a stable thromboxane metabolite, 11-dehydrothromboxane B(2) (11-DTB2), in African American stroke patients. METHODS: Subjects were a subgroup of those screened for the African American Antiplatelet Stroke Prevention Study. Subjects were within 4 months of noncardioembolic ischemic stroke and were not being treated with anticoagulants. Antithrombotic therapy at the time of urine collection varied according to the practice patterns of various attending physicians who treated the patients during their acute strokes. 11-DTB2 was measured by enzyme immunoassay in random urine samples 1 to 4 months after the stroke. RESULTS: Eighty-seven of 92 patients enrolled were able to give a urine sample at the time of enrollment. There were 51 men and 36 women aged 36 to 87 (mean 62) years. On the basis of antithrombotic treatment before the sample collection, we divided patients into 4 groups: (1) 16 patients treated with no aspirin (no antithrombotic drugs [n=4] or ticlopidine [n=12]), (2) 21 patients treated with 81 to 325 mg aspirin per day (81 mg/d [n=2], 325 mg/d [n=19]), (3) 20 patients treated with 650 mg aspirin per day, and (4) 30 patients treated with 975 to 1300 mg aspirin per day (975 mg/d [n=2] and 1300 mg/d [n=28]). In patients taking daily aspirin at any dose, the median urinary 11-DTB2 was 783 pg/mg creatinine compared with 1386 pg/mg creatinine in patients not taking daily aspirin (P=0.01 by Wilcoxon rank sum test). In multivariate regression analysis, aspirin use remained significantly associated with lower urinary 11-DTB2 (P=0.008). There was no dose-response effect between the 3 aspirin dose groups and urinary 11-DTB2 (P=0.70). CONCLUSIONS: In African American stroke patients, aspirin use is associated with significantly lower urinary 11-DTB2 independent of other vascular factors, and there does not appear to be a dose-response effect for aspirin doses of 325 to 1300 mg daily. The clinical significance of these finding remains to be determined.

Adult↗

Outcome of extracranial cervicocephalic arterial dissections: a follow-up study.

Cervicocephalic arterial dissections (CCAD) are an increasingly recognized cause of ischemic stroke in young adults. Various treatments have been suggested but no controlled trial has ever been performed. Medical treatment has included anticoagulant or platelet antiaggregant therapy. Surgical correction has been proposed for selected patients who have failed medical therapy. Percutaneous balloon angioplasty and stenting have been increasingly used in some patients, although long-term results are unknown. The objective of the study was to review our recent experience with the management and outcome of extracranial CCAD. We identified 27 patients with extracranial CCAD who were evaluated, treated and/or followed by our Stroke Service from September 1995 to August 2001. Clinical presentation, diagnostic evaluation, management, and outcome were reviewed. There were 15 men (56%) and 12 women (44%) with mean ages of 38 and 43 years respectively. Diagnosis was made by cerebral angiography in 15 (56%) patients and by MRI/MRA only in 12 (44%) patients. Twenty-two patients had spontaneous and five had traumatic extracranial CCAD. Most common associated disorders were arterial hypertension (37%) and migraine (26%). One patient presented only with a painful post-ganglionic Horner syndrome, another patient with neck pain and post-ganglionic Horner syndrome, another patient solely with protracted unilateral headaches, three with transient ischemic attacks (TIA), and 21 with ischemic strokes. The internal carotid artery (ICA) was the most frequently involved vessel (63%), followed by the vertebral artery (30%, and multivessel involvement in two patients (7%). Eighteen patients received anticoagulant therapy and nine platelet anti-aggregants. Follow-up extended from 2 to 115 months, with a mean of 58 months. At the end of follow-up, 23 (85%) patients had either no disability or only minor sequelae (modified Rankin score: 0 to 1), and four (15%) patients had moderate limitations (modified Rankin score: 2 to 3). Two patients had a recurrent ischemic stroke, one unrelated to recurrent CCAD, and the other following percutaneous balloon angioplasty/stenting for treatment of a persistent vertebral artery pseudoaneurysm. Most CCAD involved the extracranial ICA. The clinical presentation is variable, most patients having an ischemic stroke or TIAs. The short- and long-term outcome are usually favorable with either anticoagulant or platelet antiaggregant therapy. A medical initial approach to the management of extracranial CCAD is recommended for most patients.

Adult↗