bluuebunny/crossref_metadata_2025_split huggingface dataset:
Early recurrent ischemic stroke. A case-control study.
Authors: Goldstein L B , Perry A 
Published: June 2011

Data concerning potentially treatable risk factors for early recurrent stroke are limited. Therefore, we carried out a retrospective case-control study to identify factors predisposing to early reinfarction.
We identified all patients admitted to Duke University Hospital or the Durham Veterans Administration Medical Center during 1 year having two documented ischemic strokes within 90 days (n = 12 of 273). Twelve randomly selected patients matched for age, sex, and race but having only a single stroke served as controls. There were no significant differences between the groups with respect to a variety of factors including the presence of hypertension, diabetes, a history of transient ischemic attack, a history of stroke, cerebral site of the index stroke, and subtype of the index stroke. A potential cardioembolic source was more frequently identified in the patients with early recurrent stroke (seven of the 12 case-control pairs were discordant for a potential cardioembolic source; McNemar's chi 2 test, p less than or equal to 0.02).
Of the variables examined, the presence of a potential cardioembolic source was the single statistically significant factor associated with reinfarction within the first 90 days after ischemic stroke. The limitations and possible therapeutic implications of these results are discussed.
Progression of carotid atherosclerosis in Japanese patients with coronary artery disease.
Authors: Tanaka H , Nishino M , Ishida M , Fukunaga R , Sueyoshi K 
Published: June 2011

Along with the recent changes in lifestyle in Japan, the incidence of coronary artery disease has increased while the incidence of stroke appears to be decreasing. We investigated the relation between the progression of carotid atherosclerosis and the severity of coronary artery disease in the Japanese population.
The 2-year change in extracranial carotid atherosclerosis in 50 Japanese patients who underwent coronary angiography was evaluated using carotid echotomography. To quantify the extent of carotid atherosclerosis, the maximal thickness measurements of all plaques were summed for an individual plaque score, except for new plaques found on reexamination. Carotid disease progression was evaluated by the sum of plaque score change and the thickness of the new plaque found on reexamination.
The plaque score changed by -3.2 to 10.1 mm (mean +/- SD, 1.06 +/- 2.42 mm). The extent of coronary atherosclerosis (p less than 0.02) and serum total cholesterol level (p less than 0.01) were different between the progressing (n = 17) and the nonprogressing (n = 30) groups of carotid atherosclerosis when the progressing group included the patients with a delta plaque score of greater than or equal to 1.0 mm. Neither age, serum triglyceride level, serum high-density lipoprotein cholesterol level, pack-years of smoking, percentage of smokers, percentage of hypertensive patients, nor percentage of diabetic patients was different between the two groups. Carotid disease progression was significantly higher in patients with three-vessel coronary disease than in patients without significant coronary artery disease (p less than 0.005). There was a significant positive linear correlation between carotid disease progression and Gensini's coronary artery disease score (R = 0.411, p less than 0.005).
Our data showed that severe coronary artery disease and a high serum total cholesterol level were strong predictors for carotid disease progression in Japanese patients with high rates of coronary artery disease.
Aortogenic embolic stroke: a transesophageal echocardiographic approach.
Authors: Toyoda K , Yasaka M , Nagata S , Yamaguchi T 
Published: June 2011

We studied the frequency and grade of atherosclerotic changes in the thoracic aorta and their significance as embologenic lesions in patients with stroke.
Using transesophageal echocardiography, we evaluated complicated lesions in the thoracic aortas of 62 patients who met our clinical criteria for embolic stroke. A complicated lesion was defined as a raised lesion with an irregular surface or acoustic shadow based on a comparative study of echocardiographic and histopathologic findings. The results were compared with plain radiographic findings and in some cases with computed tomographic or aortographic findings.
Twenty-six patients (42%) showed complicated aortic arch lesions on echocardiogram. Transesophageal echocardiography brought us more abundant information than other techniques. Aortic knob calcification by plain radiography correlated well with the presence of echocardiographically complicated lesions, suggesting its utility for rough screening of atherosclerotic changes. Fifty-two patients had other potential embolic sources in the heart or cervical arteries. Among the remaining 10 patients without extra-aortic embolic sources, three showed complicated lesions and were diagnosed as having aortogenic embolic stroke.
Aortic atherosclerosis should be recognized as an embolic source of stroke and the advantage of transesophageal echocardiography recognized in its evaluation.
Transcranial Doppler correlation with cerebral angiography in sickle cell disease.
Authors: Adams R J , Nichols F T , Figueroa R , McKie V , Lott T 
Published: June 2011

Cerebral infarction in sickle cell disease is associated with arterial narrowing or occlusions of intracranial arteries. Primary stroke prevention would be feasible if a noninvasive screening test could be developed to detect intracranial disease in patients before symptoms develop.
To determine the sensitivity and specificity of transcranial Doppler in detecting significant (greater than or equal to 50% lumen diameter reduction) intracranial arterial lesions, we compared transcranial Doppler and cerebral angiography in a primarily young, symptomatic group of 33 patients (18 males and 15 females) with sickle cell disease.
From a total of 34 examinations, transcranial Doppler detected significant abnormalities in 26 of 29 (sensitivity 90%, specificity 100%). Five were normal by both techniques. The transorbital examination detected abnormalities in two patients whose studies were otherwise unremarkable.
Transcranial Doppler is sensitive and specific for the detection of arterial vasculopathy of sickle cell disease. Screening should include a transorbital examination of the distal internal carotid artery as well as examination using the transtemporal approach.
Platelet-activating factor acetylhydrolase in plasma lipoproteins from patients with ischemic stroke.
Authors: Satoh K , Yoshida H , Imaizumi T , Takamatsu S , Mizuno S 
Published: June 2011

Platelet-activating factor is a potent bioactive phospholipid and may play an important role in occlusive vascular diseases. To assess the inactivation of this autacoid in plasma, we measured platelet-activating factor acetylhydrolase activity in plasma low density and high density lipoproteins from patients with ischemic stroke.
Low density and high density lipoproteins were separated by ultracentrifugation from plasma of 33 patients with cerebral thrombosis and 31 age-matched healthy control subjects, and platelet-activating factor acetylhydrolase activity in each fraction was assayed.
The average values of platelet-activating factor acetylhydrolase activity in low density lipoprotein from patients and control subjects were 41 +/- 18 and 29 +/- 17 nmol/ml per minute, respectively, and the difference was statistically significant (p less than 0.01 U test). There was no difference in activity in high density lipoprotein between the two groups (16 +/- 11 versus 14 +/- 9 nmol/ml per minute, respectively).
The increased plasma platelet-activating factor acetylhydrolase activity in stroke patients is primarily attributable to the increased binding to low density lipoprotein, and this increase may be an adaptation to the augmented generation of platelet-activating factor in ischemic stroke.
Stroke risk from alcohol consumption using different control groups.
Authors: Ben-Shlomo Y , Markowe H , Shipley M , Marmot M G 
Published: June 2011

Our aim in this study was to investigate the relation between chronic alcohol consumption and stroke.
A case-control study was carried out using two hospital-based control groups and the results of a community-based survey of alcohol consumption. Hospital-based control subjects were chosen either from "general" medical admissions or a subset of "select" admissions that excluded possible alcohol-related admissions. Cases were selected from hospital inpatients.
The relative risk for stroke associated with alcohol consumption greater than 300 grams per week for general control subjects was 0.73 (95% confidence interval [CI], 0.54-3.49) compared with 1.30 (95% CI, 0.42-4.05) for select control subjects. The odds ratio was further increased to 1.93 (95% CI, 0.87-4.28) using data from the community-based survey. None of these estimates were statistically significant.
These results illustrate how the risk associated with alcohol consumption varies depending on the choice of control groups and may explain the contradictory results from previous case-control studies. Because of different biases associated with control selection, we believe that the results of this study are consistent with those of other studies that demonstrate a modest increased risk for stroke associated with alcohol consumption.
Combined magnetic resonance imaging and proton magnetic resonance spectroscopy of patients with acute stroke.
Authors: Felber S R , Aichner F T , Sauter R , Gerstenbrand F 
Published: June 2011

The prospect for a therapeutic window for treatment of ischemic stroke encourages the noninvasive investigation of metabolic changes in acute ischemia. Recently, localized proton spectroscopy became available at 1.5-T magnetic resonance systems. In this study we evaluated the usefulness of combined magnetic resonance imaging and spectroscopy on the diagnosis of acute and chronic infarctions.
Combined magnetic resonance imaging and spectroscopy investigations were carried out with a 1.5-T system in 16 volunteers, eight patients with chronic infarction (greater than 8 months), and 10 patients with acute ischemic stroke (less than 8 hours). We used a stimulated echo sequence to acquire localized spectra from image-guided volumes of interest (16-27 ml).
There were no significant interindividual differences of choline, creatine, phosphocreatine, and N-acetyl aspartate resonances in the spectra from volunteers. In chronic infarctions, N-acetyl aspartate was decreased in relation to choline. Acute ischemic infarctions were characterized by decreased N-acetyl aspartate resonances and elevation of lactate.
The study demonstrates the feasibility of proton spectroscopy in stroke patients. Metabolic alterations in ischemic tissue can be monitored and can distinguish acute from chronic lesions.
Impairment of endothelium-dependent relaxation in human basilar artery after subarachnoid hemorrhage.
Authors: Hatake K , Wakabayashi I , Kakishita E , Hishida S 
Published: June 2011

The goal of this study was to determine the alterations in vascular reactivity of human basilar artery after subarachnoid hemorrhage.
Human basilar arteries were obtained from subjects who died within 1 day after subarachnoid hemorrhage and control subjects who died from causes other than brain involvement. Basilar artery strips were suspended for isometric tension recording in Krebs-Ringer solution. Morphometric study was also carried out on paraffin-embedded sections stained with van Gieson's elastica stain of preselected sites from the basilar arteries. The intimal and medial area and the intimal index ([intimal area/area circumscribed by internal elastic lamina] x 100) were evaluated.
Contractile responses to KCl, norepinephrine, and 5-hydroxytryptamine did not differ between subarachnoid hemorrhage and control groups. The endothelium-dependent relaxation responses to thrombin, bradykinin, and calcium ionophore A23187 were less for the subarachnoid hemorrhage group than for the control group. However, the endothelium-independent response to sodium nitroprusside of the subarachnoid hemorrhage group did not differ from that of the control group. Morphometric measurements were comparable between the two groups.
These results suggest that the decreased relaxation responses to thrombin and bradykinin occur at the level of endothelial cells and not smooth muscle cells and that decreased relaxation may be involved in delayed vasospasm after subarachnoid hemorrhage. Although the decreased relaxation was observed within 1 day after subarachnoid hemorrhage, a period in which delayed spasm does not occur, this time difference may be dependent on the severity of bleeding after rupture of an aneurysm.
Reduction of infarct volume and mortality by thrombolysis in a rat embolic stroke model.
Authors: Overgaard K , Sereghy T , Boysen G , Pedersen H , Diemer N H 
Published: June 2011

Thrombolytic therapy with recombinant tissue plasminogen activator was tested in a rat embolic stroke model.
The rat carotid territory was embolized with arterial-like microthrombi formed under pressure. Hemispheric cerebral blood flow before and after embolization was measured by the intraarterial Xenon-133 injection method. Fifteen minutes after embolization, 24 rats were treated with 3 mg/kg or 10 mg/kg tissue plasminogen activator, and 27 were treated with saline. Carotid angiography displayed the rate of occlusion of the cerebral arterial supply before and after treatment. Brains were fixed and evaluated neuropathologically and infarct volume was measured.
Cerebral blood flow was reduced 70-86% after embolization. The comparison of pretreatment and posttreatment angiography showed significant (p = 0.0005) reperfusion in the treated rats. Thrombolytic therapy significantly reduced the infarct volume from 55.1% to 24.4% of embolized hemisphere volume (p = 0.007) and increased the survival rate from 0.48 to 0.96 (p = 0.0004). Fifty-three percent of the embolized rats recanalized completely after thrombolytic treatment and developed almost no infarction (median volume 2.8%), and all survived. No hemorrhagic complications were observed.
Early thrombolytic therapy induced recanalization and reduced mortality and infarct volume after embolic stroke in this model.
Silent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group.
Authors: Herderscheê D , Hijdra A , Algra A , Koudstaal P J , Kappelle L J , van Gijn J 
Published: June 2011

We studied silent stroke (i.e., infarcts on computed tomographic scan not related to later symptoms) in patients after transient ischemic attack or minor ischemic stroke.
Ours is a cross-sectional study of 2,329 patients who were randomized in a secondary prevention trial after transient ischemic attack or minor ischemic stroke and had no residual deficit after the qualifying event.
Silent stroke was observed in 13% of the 2,329 patients. Lacunes formed 79%, cortical lesions 14%, and border zone lesions 7% of all silent strokes. Silent lacunes were most often located in the basal ganglia and symptomatic lacunes most often in the corona radiata. Age, hypertension, and current cigarette smoking were related to the presence of silent stroke. Silent stroke was equally common in different types of transient ischemic attack, including transient monocular blindness. Residual symptoms of any kind were more common in patients with silent stroke than in those without.
Because only the sites of silent stroke infarcts differed slightly from those of symptomatic infarcts and the frequency of vascular risk factors was similar to that of symptomatic infarcts, silent stroke may have the same bearing on future risk as known prior stroke.
Restriction fragment length polymorphism of the apoprotein A-I-C-III gene cluster in control and stroke-prone white and black subjects: racial differences.
Authors: Kasturi R , Yatsu F M , Alam R , Rogers S 
Published: June 2011

The presence of known restriction fragment length polymorphisms in the apoprotein A-I-C-III gene cluster, which encodes their respective apoproteins, was investigated using the restriction enzymes Sac I and Pst I to determine the potential role of genetic variations for stroke risk in an American population.
Ninety-eight subjects (70 white, 28 black subjects), both normal controls with no carotid stenosis and those with carotid stenosis believed at risk for stroke, defined as showing stenosis focally or diffusely at that site, composed the study population.
Sac I polymorphic S2 allele frequency was higher in stroke-risk groups, whereas Pst I polymorphic P2 allele frequency was similar in control and stroke-risk groups. Significantly higher levels of serum cholesterol, triglycerides, and low density lipoprotein (p less than 0.05) and significantly lower levels of high density lipoprotein (p less than 0.05) were observed in stroke-risk groups with diffuse stenosis. Results of our study with the two racial groups show the following: the frequency of Sac I polymorphism was significantly higher in American black compared with American white subjects (chi 2 = 3.92, p less than 0.05). Among serum lipids, triglycerides were significantly higher in white compared with black subjects (p less than 0.05). In white subjects, carotid artery stenosis was associated with significantly elevated total cholesterol and low density lipoprotein (p less than 0.01) but not with Sac I polymorphism. In black subjects the converse was observed, namely, the Sac I polymorphic S2 allele seemed to be associated with carotid bifurcation stenosis but did not reach statistical significance because of the small number of subjects. In addition, Sac I polymorphism did not correlate with any lipid profile. Pst I polymorphism was not associated with any lipid profile or carotid artery stenosis abnormalities.
Our results indicate that carotid artery stenosis identifies white subjects with increased plasma total cholesterol and low density lipoprotein, an atherogenic profile, but not with Sac I polymorphism. These findings suggest that carotid bifurcation stenosis in white subjects is associated with an atherogenic lipid profile but not with apoprotein A-I-C-III restriction fragment length polymorphisms. In black subjects, Sac I polymorphism seems to identify those individuals with significant carotid stenosis, a necessary precursor to atherothrombotic brain infarction, but not those with elevated total cholesterol, elevated low density lipoprotein, and/or reduced high density lipoprotein. These results suggest that Sac I polymorphism may identify black subjects at increased risk for atherothrombotic brain infarctions.
Magnetoencephalography of focal cerebral ischemia in rats.
Authors: Chen Q , Chopp M , Chen H , Tepley N 
Published: June 2011

The purpose of this study was to use magnetoencephalography to record magnetic field changes in the brain during middle cerebral artery occlusion.
A direct-current electrocorticogram (two channels) and a direct-current magnetoencephalogram (seven channels) were simultaneously recorded from five rats subjected to middle cerebral artery occlusion for 1-2 hours.
Direct-current electrocorticographic and direct-current magnetoencephalographic signal deflections were observed after the onset of middle cerebral artery occlusion and occurred repeatedly throughout the ischemic period, with a mean +/- SD time interval of 12 +/- 5 minutes. A one-to-one correspondence of the electrocorticographic and magnetoencephalographic signal deflections was demonstrated.
Direct-current magnetoencephalography can provide a new noninvasive technique for studying depolarization and/or spreading depression in focal cerebral ischemia.
Level of function predicts first stroke in the elderly.
Authors: Colantonio A , Kasl S V , Ostfeld A M 
Published: June 2011

Our aim in this study was to assess physical function as a predictor of stroke incidence in a probability sample of noninstitutionalized elderly subjects with no previous history of stroke.
The data were obtained from a prospective longitudinal study of 2,812 individuals aged 65 years of age and older living in New Haven, Connecticut. Incidence of stroke was monitored from the baseline interview in 1982 until December 1988 (n = 167). Physical function was measured by the Katz scale of activities of daily living and a three-item scale measuring gross mobility function (Rosow scale). Both measures of impairment of function were independently associated with stroke incidence controlling for age, sex, diabetes, hypertension, and angina (p less than 0.001).
Our findings suggest that in elderly persons, physical disability is a newly identified risk factor for stroke.
The preponderance of posterior circulatory events is independent of the route of cardiac catheterization.
Authors: Keilson G R , Schwartz W J , Recht L D 
Published: June 2011

Central nervous system complications of cardiac catheterization are most often attributed to embolic events that occur at the time of catheter manipulation. Nevertheless, the reason that over 50% of these events are localized to the posterior circulation remains unexplained. One potential explanation offered for this preponderance is the use of the brachial artery approach. In this report, we examined the relation between the route of catheterization and central nervous system complications.
We retrospectively analyzed all central nervous system complications that occurred after cardiac catheterization through a femoral route at our institution over a 3 1/2-year period. Thirteen patients were identified as having central nervous system complications. Using defined criteria, posterior circulatory events still accounted for at least 54% of central nervous system complications.
The preponderance of posterior circulatory events is apparently independent of the route of catheterization. Furthermore, given the array of neurological symptoms and their often complete resolution, we feel it is unlikely that embolism is the sole pathophysiological mechanism involved in these events.
Moderate hyperglycemia worsens acute blood-brain barrier injury after forebrain ischemia in rats.
Authors: Dietrich W D , Alonso O , Busto R 
Published: June 2011

Clinical and experimental data indicate that hyperglycemia can aggravate the consequences of stroke and cerebral ischemia. The purpose of this study was to examine the effects of moderate hyperglycemia on the response of the blood-brain barrier to normothermic (37 degrees C) and hypothermic (30 degrees C) global forebrain ischemia.
Sixteen rats underwent 20 minutes of four-vessel occlusion followed by 30 minutes of postischemic recirculation. We used the protein tracer horseradish peroxidase as an indicator of increased vascular permeability, and rats were perfusion-fixed for microscopic analysis. To produce moderate hyperglycemia, we gave an intraperitoneal injection of 50% dextrose 15 minutes before the ischemic insult.
After normothermic brain ischemia, normoglycemic rats (plasma glucose level, 115 +/- 3 mg/dl) demonstrated extravasated horseradish peroxidase mainly restricted to the cerebral cortex. In contrast, more severe and widespread protein extravasation was documented throughout the neuraxis of hyperglycemic (plasma glucose level, 342 +/- 27) rats. Sites of protein leakage included the cerebral cortex, striatum, hippocampus, thalamus, and cerebellum. Foci of protein extravasation were associated with pial and large penetrating vessels. Intraischemic hypothermia significantly attenuated the blood-brain barrier consequences of hyperglycemic brain ischemia.
Under normothermic ischemic conditions, hyperglycemia significantly worsens the degree of acute blood-brain barrier breakdown compared with normoglycemia. Postischemic blood-brain barrier disruption may play an important role in the pathogenesis of increased brain damage associated with systemic hyperglycemia.