Askiel Bruno

Acute blood glucose level and outcome from ischemic stroke

Objective: To study the relation between acute blood glucose level and outcome from ischemic stroke. Background: Hyperglycemia may augment acute ischemic brain injury and increase the risk of hemorrhagic transformation of the infarct. Methods: The authors analyzed the relation between admission blood glucose level (within 24 hours from ischemic stroke onset) and clinical outcome in 1,259 patients enrolled in the Trial of ORG 10172 in Acute Stroke Treatment (TOAST)—a placebo-controlled, randomized, double-blind trial to test the efficacy of a low-molecular weight heparinoid in acute ischemic stroke. Very favorable outcome was defined as a Glasgow Outcome Scale score of 1 and a modified Barthel index of 19 or 20. Neurologic improvement at 3 months was defined as a decrease by ≥4 points on the NIH Stroke Scale compared with baseline or a final score of 0. Hemorrhagic transformation of infarct was assessed within 10 days after onset of stroke with repeat cerebral CT. Stroke subtype as lacunar or nonlacunar (atherothromboembolic, cardioembolic, and other or undetermined etiology) was classified by one investigator after completion of stroke evaluation according to study protocol. Results: In all strokes combined (p = 0.03) and in nonlacunar strokes (p = 0.02), higher admission blood glucose levels were associated with worse outcome at 3 months according to multivariate logistic regression analysis adjusted for stroke severity, diabetes mellitus, and other vascular risks. In lacunar strokes, the relationship between acute blood glucose level and outcome was related to treatment. In the placebo group, higher admission blood glucose levels were associated with better outcome at 3 months. However, in the active drug group, as the glucose level increased from 50 to 150 mg/dL, the probability of a very favorable outcome decreased sharply and remained relatively unchanged as the glucose level increased further (p = 0.002, for overall effect of glucose on outcome). Acute blood glucose level was not associated with symptomatic hemorrhagic transformation of infarcts or with neurologic improvement at 3 months. Conclusions: During acute ischemic stroke hyperglycemia may worsen the clinical outcome in nonlacunar stroke, but not in lacunar stroke, and is not associated with an increased risk of hemorrhagic transformation of the infarct.

Effects of admission hyperglycemia on mortality and costs in acute ischemic stroke

BackgroundHyperglycemia at the time of acute ischemic stroke has been linked to worse outcome in both human and animal studies. ObjectiveTo describe the prevalence and severity of hyperglycemia on hospital admission among acute ischemic stroke patients, to examine the independent relationship of admission hyperglycemia to all-cause mortality, and to document the inpatient management of hyperglycemia. MethodsPatients hospitalized with acute ischemic stroke at one hospital from July 1993 to June 1998 (n = 656) were identified. Demographic data, diagnoses, and blood glucose (BG) values were retrieved from the electronic medical record system. Admission stroke severity, fingerstick BG results, and new diabetes diagnoses were obtained by chart review. Hyperglycemia was defined as admitting random serum BG ≥ 130 mg/dL. Hazard ratios (HR) for 30-day, 1-year, and 6-year mortality were calculated using multivariable Cox regression models. ResultsHyperglycemia at admission to hospital was present in 40% of patients with acute stroke. Patients with hyperglycemia were more often women and more likely to have prior diagnoses of diabetes and heart failure. Almost all of these patients remained hyperglycemic during their hospital stay (mean BG = 206 mg/dL), and 43% received no inpatient hypoglycemic drugs. Hyperglycemic patients had longer hospital stay (7 vs 6 days, p = 0.015) and higher inpatient hospital charges (

Stroke Patients’ Knowledge of Stroke Influence on Time to Presentation

6,611 vs

Protocol Violations in Community-Based rTPA Stroke Treatment Are Associated With Symptomatic Intracerebral Hemorrhage

5,262, p < 0.001). Hyperglycemia independently increased the risk for death at 30 days (HR 1.87, p ≤ 0.01), 1 year (HR 1.75, p ≤ 0.01), and 6 years after stroke (HR 1.41, p ≤ 0.01). ConclusionsAdmitting hyperglycemia was common among patients with acute ischemic stroke and was associated with increased short- and long-term mortality and with increased inpatient charges. Inpatient blood glucose management was suboptimal in this hospital. A trial of intensive treatment of hyperglycemia should be considered.

Neurologic manifestations of atrial myxoma. A 12-year experience and review.

BACKGROUND AND PURPOSEnNew treatments for acute stroke will likely have to be given soon after stroke onset. Little is known about stroke patients general knowledge about stroke, their interpretation of stroke symptoms, and how these factors influence the timing of their decision to seek medical attention.nnnMETHODSnWe interviewed consecutive stroke patients within 72 hours of stroke onset to define factors influencing time of arrival to the emergency department. Data recorded included demographic information, method of transportation, type of stroke symptoms, the patients interpretation of the symptoms, previous stroke, and knowledge of stroke warning signs. Stroke severity was measured with the Barthel Index. Early arrival was defined as within 3 hours of awareness of symptoms.nnnRESULTSnSixty-seven patients were interviewed; 96% had an ischemic stroke and 4% a cerebral hemorrhage. Although 38% of patients professed to know the warning signs of stroke, only 25% correctly interpreted their symptoms. Patients with prior stroke were more likely to correctly interpret their symptoms (45% versus 16%; P = .03) but were not more likely to present early (19% versus 39%; P = .35). Eighty-six percent of patients presenting more than 3 hours after stroke onset thought that their symptoms were not serious. The 24% (n = 16) of early arrivals were more likely to arrive by ambulance (81% versus 38%; P = .003) and had more severe stroke (Barthel Index score of 49 versus 72; P = .01) than late arrivals. Arrival by ambulance was independently associated with early arrival (odds ratio, 5.55; 95% confidence interval, 1.37 to 22.6).nnnCONCLUSIONSnApproximately one quarter of stroke patients correctly interpret their symptoms as representing a stroke. This knowledge is not associated with early presentation to the emergency department. Ambulance transport is independently associated with early arrival at the emergency department. Even when patients know that they are having a stroke, most present late because they perceive their symptoms as not serious. Widespread public education of stroke-prone individuals may increase the proportion of patients eligible for new acute stroke treatments.

Stroke associated with ephedrine use

Background— Recombinant tissue plasminogen activator (rTPA) is an established treatment for acute ischemic stroke. The rate and type of protocol violations in rTPA use and their effect on patient outcomes in this setting are not well understood. Objective— The objective of this study was to examine associations between protocol violations and outcomes in community-based rTPA use. Methods— We reviewed medical records of stroke patients treated with rTPA in 10 acute-care hospitals in Indianapolis from July 1996 to February 1998 and assessed complications and outcome. Retrospective National Institute of Health Stroke Scale (on admission and discharge), Canadian Neurological Scale, and length of hospital stay were calculated. Appropriate use of rTPA was determined by the National Institute of Neurological Disorders and Stroke (NINDS) protocol. Results— Fifty patients (mean age, 66 years; 76% white; 56% men) were treated by general neurologists (70%), stroke neurologists (24%), or emergency physicians (6%). Mean times to hospital arrival, brain CT, and start of rTPA infusion were 44, 86, and 141 minutes, respectively. In-hospital mortality rate was 10% (4 intracerebral hemorrhage [ICH], 1 cardiogenic shock). Complications were more frequent among patients with protocol violations (n=8) compared with those without all hemorrhages (75% versus 10%, P <0.001), symptomatic ICH (38% versus 5%, P <0.02), and ICH attributable to rTPA, occurring within 36 hours (38% versus 2.4%, P <0.01), respectively. Conclusions— NINDS protocol violations are relatively common and are associated with symptomatic cerebral and systemic hemorrhages. When the NINDS protocol is strictly followed, hemorrhage rates in community-based rTPA use are similar to those in the NINDS trial.

Cerebral infarction due to moyamoya disease in young adults.

We present the results of a 12-year retrospective analysis of 11 patients, eight women and three men, aged 16-76 years, with pathologically documented atrial myxomas. Nine of the 11 patients were found to have a left atrial myxoma; right atrial myxomas were identified in two. Five of the 11 patients (45%) had abnormalities on neurologic examination, and five of five had computed tomographic evidence of nonhemorrhagic cerebral infarction. Neurologic symptoms were the initial presentation in four patients. Six patients reported a history of cardiac disease; eight of the 11 had abnormalities on cardiac auscultation. Echocardiography in 10 patients was diagnostic in all but one. Gated magnetic resonance imaging of the heart in two patients demonstrated myxoma position and movement. Follow-up examinations (varying from 1 month to 7 years after tumor resection) in nine of 11 patients demonstrated no recurrent neurologic symptoms. Cerebral infarction is a common complication of atrial myxomas and may be the presenting feature. Recurrent cerebral emboli before surgery is not uncommon. Cardiac auscultation may be normal, and electrocardiographic changes are often nonspecific. Delayed neurologic events following surgery are rare.

Vascular Outcome in Men with Asymptomatic Retinal Cholesterol Emboli: A Cohort Study

Several sympathomimetic agents have been associated with ischemic and hemorrhagic stroke. Ephedrine, a sympathomimetic drug that has a high potential for abuse and can be readily obtained without a prescription in unrestricted quantities, has rarely been associated with stroke. We report ephedrine-related stroke in three patients. One patient developed a thalamic infarct after ingesting known quantities of ephedrine as street-purchased “speed” for weight loss. Two patients had fatal intracranial hemorrhages after ingesting unknown quantities of ephedrine; one of them had a history of drug abuse, and one lacked a history of ephedrine use or drug abuse. Ephedrine appears to predispose to both ischemic and hemorrhagic stroke. The mechanisms responsible for the different cerebrovascular complications remain to be proven. Restriction of ephedrine availability should be considered.

Factors Influencing Outcome and Treatment Effect in PROACT II

Moyamoya disease was diagnosed as the cause of cerebral infarction in eight young adults (seven women, one man), aged 17-40 (mean 33) years. All had angiographic abnormalities characteristic of moyamoya disease. Single-photon emission tomography showed bilateral carotid circulation hypoperfusion and posterior circulation hyperemia in all seven patients with regional cerebral blood flow studies. All seven women had used oral contraceptives before cerebral infarction. Four patients were treated medically; one died of a second cerebral infarction 9 months after diagnosis. Four patients underwent superficial temporal-to-middle cerebral artery anastomosis; they did well. Moyamoya disease should be included in the differential diagnosis of cerebral infarction as well as intracranial hemorrhage in young adults, particularly women. A possible relation between moyamoya disease and oral contraceptive use deserves investigation.

Incidence of spontaneous intracerebral hemorrhage among Hispanics and non-Hispanic whites in New Mexico

Cholesterol embolism from ulcerated atherosclerotic plaques has been long recognized and well documented [1-8]. It can affect any organ, and systemic cholesterol embolism can be fatal. Ophthalmoscopy offers a unique opportunity to noninvasively visualize cholesterol emboli in retinal arterioles. These emboli are bright orange, yellow, or copper-colored fragments and are usually seen at arteriolar bifurcations. Owing to their brightness, they are often conspicuous on dilated ocular examination and are periodically identified in eye clinics. Because of their thin, flat shape, the cholesterol crystals do not occlude the involved vessel and are often asymptomatic. Vascular occlusion results either from vessel fibrosis after repeated embolizations or from a thrombus attached to a cholesterol crystal. Retinal cholesterol emboli have been linked to ulcerated atherosclerotic plaques at the carotid artery bulb [1-3], but these emboli can originate from ulcerated atherosclerotic plaques in any artery leading to the retina, including the common carotid artery, the brachiocephalic artery, or the ascending aorta. Ulcerated atherosclerotic plaques do not necessarily produce hemodynamically significant stenosis. The prevalence of extracranial carotid artery stenosis greater than 50% ipsilateral to asymptomatic retinal cholesterol emboli ranges from 0% to 17% [9-11]. Symptomatic ocular ischemia is usually evaluated and treated regardless of the presence of retinal emboli, but the clinical significance of asymptomatic retinal cholesterol emboli has not been the subject of controlled studies. Retinal cholesterol emboli have been associated with increased mortality [12, 13], but previous studies used a cohort of both asymptomatic and symptomatic patients who were grouped together and compared with general population controls, and patients and controls were not matched for some important vascular risk factors. We compare the vascular outcome of a group of 70 patients with asymptomatic retinal cholesterol emboli with that of a matched control group. Methods All participants had a dilated ocular examination in the Albuquerque Veterans Affairs Medical Center Eye Clinic between January 1989 and February 1991. Approximately 4500 patients annually had a dilated ocular examination in that clinic during this study. Patients Persons who were examined in the eye clinic for any reason and in whom an asymptomatic retinal cholesterol embolus was found during examination were considered for this study. A retinal cholesterol embolus was diagnosed if a bright orange, yellow, or copper-colored fragment was seen in a retinal arteriole. The study optometrists drew a diagram of the embolus location and took photographs of the fundus. An embolus was considered asymptomatic if the patient had no history of sudden monocular visual loss and no corresponding scotoma or retinal infarction on examination. Seventy consecutive men with asymptomatic retinal cholesterol emboli were entered into the study; none had had an arteriogram, cardiac surgery, or other vascular surgery within 12 months before entry. The study neurologist interviewed and examined all patients and referred each of them for a total serum cholesterol level test, a carotid Duplex ultrasound test, and an electrocardiographic study. Controls We selected the controls retrospectively and randomly in 1993. Beginning with all patients who visited the eye clinic and who had a dilated ocular examination during the study period, a computer generated at random a list of potential participants [11]. Controls were selected from this list if they had no retinal emboli and no evidence of ocular ischemia on examination. The first 40 controls were selected without matching for vascular risk factors. This group was then compared with the 70 patients for age, hypertension, diabetes mellitus, ischemic heart disease, and smoking. The risk factors that differed substantially between the two groups were either sought or avoided in selecting the next group of 10 controls, so that the patient and control groups would be as closely matched as possible. This procedure was repeated twice more to obtain 70 controls that were well matched to the patients. Because all of the patients were men, we selected only men to be controls. When a possible control lacked the qualifying vascular risk factors, we considered the next person who had had a dilated ocular examination in the eye clinic. Approximately 15% of those screened were selected. We used no other selection criteria and the investigators selecting the controls were unaware of any outcome events. Vascular Risk Factors The study neurologist interviewed patients and reviewed medical records to identify history of hypertension, diabetes mellitus, and ischemic heart disease. We defined a patient as having hypertension if he was being treated for it or if his blood pressure was greater than 160 mm Hg systolic or 90 mm Hg diastolic on two consecutive clinic visits. We defined a patient as having diabetes mellitus if he was being treated for it or if his fasting blood glucose level was greater than 6.66 mmol/L (120 mg/dL). We accepted a serum cholesterol level if it was measured during the study period or within 1 year before study entry. We diagnosed ischemic heart disease if it was shown by an objective cardiac test (electrocardiography, echocardiography, stress test, or arteriography) or if the patient had had coronary bypass surgery. We defined current smoking as tobacco smoking within 2 years of study entry. Follow-up The study neurologist informed the patients about transient ischemic attack and stroke symptoms and asked to be telephoned if they suspected that a cerebrovascular event had occurred. He also explained the importance of limiting vascular risk factors, recommended 325 mg of aspirin daily to reduce the likelihood of ischemic events, and examined the patients at 6- to 9-month intervals. The patients primary physicians provided treatment for hypertension, diabetes mellitus, hypercholesterolemia, and ischemic heart disease, and assistance with cessation of smoking. We defined stroke as a sudden focal brain dysfunction lasting longer than 24 hours. Computed tomographic scans distinguished between cerebral infarction and hemorrhage. We identified the cause of cerebral infarction as carotid artery disease if there was greater than 50% carotid stenosis ipsilateral to carotid territory ischemia; as cardioembolic if there was a high risk for cardiac emboli; as small-vessel disease if the symptoms and neuroimaging test results were consistent with a small (<1.5 cm diameter), deep infarction; as other if another cause was found; or as undetermined. High-risk factors for cardiac emboli were atrial fibrillation, valvular heart disease, intracardiac thrombus, myocardial infarction in the preceding 3 months, or severe myocardial hypokinesia. When a patient developed a stroke, we did computed tomographic scans of the head, blood tests for hypercoagulability, a carotid Duplex test if the event was in a carotid artery territory, and echocardiography if heart disease was present. Additional tests were done on the basis of the results of these standard tests. The follow-up period for the controls was the same as that for the patients, from selection (January 1989 to February 1991) either to a telephone interview by the study neurologist between October and December 1993 or to death. The study neurologist also reviewed the medical records of the controls. When interview or review of the medical record suggested that a stroke may have occurred, the study neurologist reviewed the pertinent tests. The controls primary physicians provided treatment for hypertension, diabetes mellitus, hypercholesterolemia, and ischemic heart disease, and assistance with cessation of smoking. Review of medical records was done to confirm myocardial infarction, death, and cause of death. We classified death as vascular if atherosclerosis was the main cause. When a participant had more than one cerebral or myocardial infarction, we tabulated the first of each type of vascular event for analysis. Statistical Analysis We used a two-sided Fisher exact test to compare the baseline characteristics of patients and controls for categorical data and a two-sided t-test to compare the two groups for continuous data. Cox proportional-hazards analysis [14] measured adjusted relative risk, 95% CIs, and P values for outcome events associated with asymptomatic retinal cholesterol embolism. We considered controlling the analysis for stroke history, smoking history, and current smoking because these variables were the least adequately matched between patients and controls. With these three variables included in Cox proportional-hazards analysis, the adjusted relative risk associated with current smoking was minimal for all outcome events (range, 0.7 to 1.3); therefore, we controlled the analysis only for stroke history and smoking history. Annual rates of outcome events were given by the ratio of the number of particular events to person-years of observation for that event. Results Vascular risk factors of patients and controls at the time of study entry are shown in Table 1. Median ages of patients and controls were 69 and 68 years, respectively. Vascular outcomes for patients and controls are shown in Table 2. Mean duration of follow-up for all participants was 3.4 years (those alive at the end of the study were followed from 2.6 to 4.9 years). We lost 1 patient to follow-up after 2.6 years of observation. Fifty patients (71%) and 37 controls (53%) reported taking between 80 and 650 mg aspirin daily during follow-up. Five patients (7%) and 5 controls (7%) received warfarin during follow-up. Table 1. Vascular Risks among 70 Patients with Asymptomatic Retinal Cholesterol Emboli and 70 Controls at Study Entry Table 2. Vascular Outcome Events in 70 Patients with Asymptomatic Retinal Cholesterol Emboli and in 70 Contr