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Children with sickle cell anemia with normal transcranial Doppler ultrasounds and without silent infarcts have a low incidence of new strokes.
Jordan LC, Roberts Williams DO, Rodeghier MJ, Covert Greene BV, Ponisio MR, Casella JF, McKinstry RC, Noetzel MJ, Kirkham FJ, Meier ER, Fuh B, McNaull M, Sarnaik S, Majumdar S, McCavit TL, DeBaun MR
(2018) Am J Hematol 93: 760-768
MeSH Terms: Adolescent, Anemia, Sickle Cell, Cerebral Infarction, Child, Child, Preschool, Humans, Incidence, Ischemic Attack, Transient, Prospective Studies, Seizures, Stroke, Ultrasonography, Doppler, Transcranial
Show Abstract · Added March 24, 2020
In a prospective cohort study, we tested the hypothesis that children with sickle cell anemia (SCA) with normal transcranial Doppler ultrasound (TCD) velocities and without silent cerebral infarcts (SCIs) would have a lower incidence rate of new neurological events (strokes, seizures or transient ischemic attacks) compared to children with normal TCD measurements and SCIs, not receiving regular blood transfusions. Nonrandomized participants from the silent cerebral infarct transfusion (SIT) Trial who had screening magnetic resonance imaging (MRI) of the brain and normal TCD measurements were included. Follow-up ended at the time of first neurological event (stroke, seizure or transient ischemic attack), start of regular blood transfusion, or loss to follow-up, whichever came first. The primary endpoint was a new neurological event. Of 421 participants included, 68 had suspected SCIs. Mean follow-up was 3.6 years. Incidence rates of new neurological events in nontransfused participants with normal TCD values with SCIs and without SCIs were 1.71 and 0.47 neurological events per 100 patient-years, respectively, P = .065. The absence of SCI(s) at baseline was associated with a decreased risk of a new neurological event (hazard ratio 0.231, 95% CI 0.062-0.858; P = .029). Local pediatric neurologists examined 67 of 68 participants with suspected SCIs and identified 2 with overt strokes classified as SCIs by local hematologists; subsequently one had a seizure and the other an ischemic stroke. Children with SCA, without SCIs, and normal TCD measurements have a significantly lower rate of new neurological events when compared to those with SCIs and normal TCD measurements. Pediatric neurology assessment may assist risk stratification.
© 2018 Wiley Periodicals, Inc.
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MeSH Terms
CYP2C19 and CES1 polymorphisms and efficacy of clopidogrel and aspirin dual antiplatelet therapy in patients with symptomatic intracranial atherosclerotic disease.
Hoh BL, Gong Y, McDonough CW, Waters MF, Royster AJ, Sheehan TO, Burkley B, Langaee TY, Mocco J, Zuckerman SL, Mummareddy N, Stephens ML, Ingram C, Shaffer CM, Denny JC, Brilliant MH, Kitchner TE, Linneman JG, Roden DM, Johnson JA
(2016) J Neurosurg 124: 1746-51
MeSH Terms: Aged, Aspirin, Carboxylic Ester Hydrolases, Clopidogrel, Cytochrome P-450 CYP2C19, Female, Gene Frequency, Genotyping Techniques, Heterozygote, Humans, Intracranial Arteriosclerosis, Ischemic Attack, Transient, Kaplan-Meier Estimate, Male, Myocardial Infarction, Platelet Aggregation Inhibitors, Polymorphism, Single Nucleotide, Prospective Studies, Stroke, Ticlopidine
Show Abstract · Added March 14, 2018
OBJECT Symptomatic intracranial atherosclerotic disease (ICAD) has a high risk of recurrent stroke. Genetic polymorphisms in CYP2C19 and CES1 are associated with adverse outcomes in cardiovascular patients, but have not been studied in ICAD. The authors studied CYP2C19 and CES1 single-nucleotide polymorphisms (SNPs) in symptomatic ICAD patients. METHODS Genotype testing for CYP2C19*2, (*)3, (*)8, (*)17 and CES1 G143E was performed on 188 adult symptomatic ICAD patients from 3 medical centers who were medically managed with clopidogrel and aspirin. Testing was performed prospectively at 1 center, and retrospectively from a DNA sample biorepository at 2 centers. Multiple logistic regression and Cox regression analysis were performed to assess the association of these SNPs with the primary endpoint, which was a composite of transient ischemic attack (TIA), stroke, myocardial infarction, or death within 12 months. RESULTS The primary endpoint occurred in 14.9% of the 188 cases. In multiple logistic regression analysis, the presence of the CYP2C19 loss of function (LOF) alleles *2, *3, and *8 in the medically managed patients was associated with lower odds of primary endpoint compared with wild-type homozygotes (odds ratio [OR] 0.13, 95% CI 0.03-0.62, p = 0.0101). Cox regression analysis demonstrated the CYP2C19 LOF carriers had a lower risk for the primary endpoint, with hazard ratio (HR) of 0.27 (95% CI 0.08-0.95), p = 0.041. A sensitivity analysis of a secondary composite endpoint of TIA, stroke, or death demonstrated a significant trend in multiple logistic regression analysis of CYP2C19 variants, with lower odds of secondary endpoint in patients carrying at least 1 LOF allele (*2, *3, *8) than in wild-type homozygotes (OR 0.27, 95% CI 0.06-1.16, p = 0.078). Cox regression analysis demonstrated that the carriers of CYP2C19 LOF alleles had a lower risk forthe secondary composite endpoint (HR 0.22, 95% CI 0.05-1.04, p = 0.056). CONCLUSIONS This is the first study examining genetic variants and their effects in symptomatic ICAD. Variant alleles of CYP2C19 (*2, *3, *8) were associated with lower odds of the primary and secondary composite endpoints. However, the direction of the association was opposite of what is expected based on this SNP. This may reflect an incomplete understanding of this genetic variation and its effect in symptomatic ICAD and warrants further investigations.
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20 MeSH Terms
Neurological complications and outcomes in the Berlin Heart EXCOR® pediatric investigational device exemption trial.
Jordan LC, Ichord RN, Reinhartz O, Humpl T, Pruthi S, Tjossem C, Rosenthal DN
(2015) J Am Heart Assoc 4: e001429
MeSH Terms: Child, Child, Preschool, Extracorporeal Membrane Oxygenation, Female, Follow-Up Studies, Heart Failure, Heart Transplantation, Heart-Assist Devices, Humans, Infant, Ischemic Attack, Transient, Kaplan-Meier Estimate, Logistic Models, Male, Multivariate Analysis, Pediatrics, Prospective Studies, Prosthesis Design, Risk Assessment, Stroke, Survival Rate, Treatment Outcome, Waiting Lists
Show Abstract · Added March 24, 2020
BACKGROUND - The Berlin Heart EXCOR(®) ventricular assist device has been approved for use in the United States as a bridge to heart transplantation in children. We sought to characterize neurological events in children supported with the Berlin Heart EXCOR(®) device.
METHODS AND RESULTS - The multicenter prospective cohort consisted of all 204 children implanted with the Berlin Heart EXCOR(®) device at 47 centers in North America between May 2007 and December 2010. There were 73 neurological events in 59 patients, with 29% of the cohort experiencing ≥1 neurological event. Events included 52 strokes in 43 patients (21% of the cohort). The neurological event rate was 0.51 events per 100 patient-days. Many of the neurological events occurred early in the course of support, with 30 events recorded during the first 14 days of support. The mortality rate in participants with at least 1 neurological event was 42% (25 of 59), significantly higher than the 18% mortality rate (26 of 145) for those who did not have a neurological event (P=0.0006). Risk-factor analysis did not identify significant preimplantation predictors of neurological injury.
CONCLUSIONS - Of children treated with the Berlin Heart EXCOR(®) device as a bridge to transplant, 29% experienced at least 1 neurological event. The majority of neurological events were ischemic strokes, and many of those occurred early in the course of support. Neurological injury was the leading cause of death after implantation of the Berlin Heart EXCOR(®) device. Risk stratification for stroke or neurological injury is not possible based on baseline preimplantation characteristics.
CLINICAL TRIAL REGISTRATION URL - www.clinicaltrials.gov. Unique Identifier: NCT00583661.
© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
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Transient ischemic attack requiring hospitalization of children in the United States: kids' inpatient database 2003 to 2009.
Adil MM, Qureshi AI, Beslow LA, Jordan LC
(2014) Stroke 45: 887-8
MeSH Terms: Adolescent, Age Factors, Brain Ischemia, Child, Child, Preschool, Confidence Intervals, Databases, Factual, Female, Hospitalization, Humans, Infant, Ischemic Attack, Transient, Length of Stay, Male, Regression Analysis, Risk Factors, Stroke, United States
Show Abstract · Added March 24, 2020
BACKGROUND AND PURPOSE - Transient ischemic attacks (TIA) are not well described in children. We assessed the prevalence of risk factors for TIA requiring hospitalization in children in a large national database.
METHODS - Using the Healthcare Cost and Utilization Project Kids' Inpatient Database, children aged 1 to 18 years admitted for TIA in 2003, 2006, and 2009 were identified by International Classification of Diseases, Ninth Revision, Clinical Modification code 435. Descriptive analyses identified patient characteristics. Trend analysis determined the change in annual average hospitalization days from 2003 to 2009.
RESULTS - TIA was the primary diagnosis for 531 children. Important secondary diagnoses included sickle cell disease (20%), congenital heart disease (11%), migraine (12%), moyamoya disease (10%), and stroke (4%). Mean length of stay decreased from 3.0 days (95% confidence interval, 2.4-3.6) in 2003 to 2.3 days (95% confidence interval, 2.0-2.7) in 2009 (P=0.04). During the same period, 2590 children were admitted with ischemic stroke; 4.8 children with stroke were admitted for every child with TIA.
CONCLUSIONS - Recognized risk factors for TIA, including sickle cell disease, congenital heart disease, moyamoya, recent stroke, and migraine, were present in <60% of children. Pediatric admissions for ischemic stroke were ≈5-fold more common than for TIA. Further study is required to understand the risk of stroke after TIA in children to guide appropriate evaluation and treatment.
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Spectrum and prevalence of vasculopathy in pediatric neurofibromatosis type 1.
Kaas B, Huisman TA, Tekes A, Bergner A, Blakeley JO, Jordan LC
(2013) J Child Neurol 28: 561-9
MeSH Terms: Angiography, Aorta, Abdominal, Aortic Diseases, Arterial Occlusive Diseases, Cerebral Angiography, Child, Child, Preschool, Comorbidity, Cross-Sectional Studies, Disease Progression, Female, Humans, Hypertension, Image Enhancement, Ischemic Attack, Transient, Magnetic Resonance Angiography, Male, Moyamoya Disease, Neurofibromatosis 1, Optic Nerve Glioma, Stroke, Tomography, X-Ray Computed
Show Abstract · Added March 24, 2020
To describe the spectrum and associated clinical features of peripheral and cerebral vasculopathy in pediatric patients with neurofibromatosis type 1, children seen at a single center from 2000 to 2010 with appropriate imaging studies were identified. Scans were assessed for vascular disease by 2 pediatric neuroradiologists. Of 181 children, 80 had pertinent imaging studies: 77 had brain imaging, 6 had peripheral imaging, and 3 had both. Vasculopathy was identified in 14/80 children (18%, minimum prevalence of 14/181; 8%). Of those with vascular abnormalities, 2/14 had peripheral vasculopathy (1% minimum prevalence) and 12/14 had cerebrovascular abnormalities (7% minimum prevalence). No associations were found between vasculopathy and common clinical features of neurofibromatosis type 1, including optic pathway glioma, plexiform neurofibroma, skeletal abnormalities, attention-deficit hyperactivity disorder (ADHD), or suspected learning disability. Both peripheral and cerebral vasculopathy are important complications of pediatric neurofibromatosis type 1 and should be considered in the management of this complex disease.
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Multiple biomarkers and risk of clinical and subclinical vascular brain injury: the Framingham Offspring Study.
Pikula A, Beiser AS, DeCarli C, Himali JJ, Debette S, Au R, Selhub J, Toffler GH, Wang TJ, Meigs JB, Kelly-Hayes M, Kase CS, Wolf PA, Vasan RS, Seshadri S
(2012) Circulation 125: 2100-7
MeSH Terms: Aged, Albuminuria, Biomarkers, Blood Proteins, Brain, Brain Injuries, Cohort Studies, Creatinine, Endothelium, Vascular, Female, Hemostasis, Homocysteine, Hormones, Humans, Incidence, Inflammation, Ischemic Attack, Transient, Magnetic Resonance Imaging, Male, Middle Aged, Organ Size, Prospective Studies, Risk, Stroke, United States
Show Abstract · Added April 15, 2014
BACKGROUND - Several biomarkers have been individually associated with vascular brain injury, but no prior study has explored the simultaneous association of a biologically plausible panel of biomarkers with the incidence of stroke/transient ischemic attack and the prevalence of subclinical brain injury.
METHODS AND RESULTS - In 3127 stroke-free Framingham offspring (age, 59±10 years; 54% female), we related a panel of 8 biomarkers assessing inflammation (C-reactive protein), hemostasis (D-dimer and plasminogen activator inhibitor-1), neurohormonal activity (aldosterone-to-renin ratio, B-type natriuretic peptide, and N-terminal proatrial natriuretic peptides), and endothelial function (homocysteine and urinary albumin/creatinine ratio) measured at the sixth examination (1995-1998) to risk of incident stroke/transient ischemic attack. In a subset of 1901 participants with available brain magnetic resonance imaging (1999-2005), we further related these biomarkers to total cerebral brain volume, covert brain infarcts, and large white-matter hyperintensity volume. During a median follow-up of 9.2 years, 130 participants experienced incident stroke/transient ischemic attack. In multivariable analyses adjusted for stroke risk factors, the biomarker panel was associated with incident stroke/transient ischemic attack and with total cerebral brain volume (P<0.05 for both) but not with covert brain infarcts or white-matter hyperintensity volume (P>0.05). In backward elimination analyses, higher log-B-type natriuretic peptide (hazard ratio, 1.39 per 1-SD increment; P=0.002) and log-urinary albumin/creatinine ratio (hazard ratio, 1.31 per 1-SD increment; P=0.004) were associated with increased risk of stroke/transient ischemic attack and improved risk prediction compared with the Framingham Stroke Risk Profile alone; when the <5%, 5% to 15%, or >15% 10-year risk category was used, the net reclassification index was 0.109 (P=0.037). Higher C-reactive protein (β=-0.21 per 1-SD increment; P=0.008), D-dimer (β=-0.18 per 1-SD increment; P=0.041), total homocysteine (β=-0.21 per 1-SD increment; P=0.005), and urinary albumin/creatinine ratio (β=-0.15 per 1-SD increment; P=0.042) were associated with lower total cerebral brain volume.
CONCLUSION - In a middle-aged community sample, we identified multiple biomarkers that were associated with clinical and subclinical vascular brain injury and could improve risk stratification.
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25 MeSH Terms
Wagging the dog--moving closer to features defined by basic scientists, the protection of prodromal transient ischaemic attacks reveals itself.
McLaughlin BA, Kirshner H
(2008) Eur J Neurol 15: 755-6
MeSH Terms: Humans, Ischemic Attack, Transient, Ischemic Preconditioning, Stroke
Added January 26, 2015
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4 MeSH Terms
Prevalence of platelet nonresponsiveness to aspirin in patients treated for secondary stroke prophylaxis and in patients with recurrent ischemic events.
Gengo FM, Rainka M, Robson M, Gengo MF, Forrest A, Hourihane M, Bates V
(2008) J Clin Pharmacol 48: 335-43
MeSH Terms: Age Factors, Aged, Anti-Inflammatory Agents, Arachidonic Acid, Aspirin, Blood Platelets, Clopidogrel, Collagen, Coronary Artery Disease, Dipyridamole, Drug Therapy, Combination, Female, Humans, Ischemic Attack, Transient, Male, Odds Ratio, Platelet Aggregation, Recurrence, Stroke, Ticlopidine, Time Factors, Treatment Failure
Show Abstract · Added July 10, 2013
To determine the prevalence of platelet nonresponsiveness to aspirin treatment for secondary stroke prophylaxis, the authors studied consecutive patients during a 29-month period. Information regarding their ischemic events, risk factors, and medications was collected. Platelet aggregation in response to collagen and arachidonic acid was used to determine platelet responsiveness to aspirin. A total of 653 patients were evaluated. Of these, 129 patients (20%) were determined to be nonresponsive to aspirin based on continued platelet aggregation in response to collagen, arachidonic acid, or both. A total of 87 (13%) of the 653 patients were clinical aspirin failures (ie, presented with new focal cerebral ischemic symptoms while taking aspirin). Of the patients with new cerebral ischemic symptoms, 57 (66%) were determined to be platelet nonresponsive to aspirin. The odds ratio for platelet nonresponsiveness to aspirin in patients who suffered a recurrent ischemic event while taking aspirin was 14.25 (95% confidence interval: 8.5-23.7; P < .5). Continued platelet aggregation despite aspirin treatment occurred in 20% of ambulatory patients treated for secondary stroke prophylaxis. The prevalence of nonresponsiveness to aspirin was statistically higher in those patients who suffered recurrent cerebral ischemia while taking aspirin (P < .5) compared with patients who remained without new ischemic symptoms.
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22 MeSH Terms
Altered PPARgamma expression and activation after transient focal ischemia in rats.
Victor NA, Wanderi EW, Gamboa J, Zhao X, Aronowski J, Deininger K, Lust WD, Landreth GE, Sundararajan S
(2006) Eur J Neurosci 24: 1653-63
MeSH Terms: Animals, Benzamides, Enzyme Activation, Gene Expression Regulation, Immunohistochemistry, Ischemic Attack, Transient, Male, PPAR gamma, Protein Binding, Pyridines, RNA, Messenger, Rats, Rats, Wistar, Reverse Transcriptase Polymerase Chain Reaction, Rosiglitazone, Thiazolidinediones, Time Factors
Show Abstract · Added May 26, 2016
Stroke is a devastating disease with limited treatment options. Recently, we found that the peroxisome proliferator-activated receptor-gamma (PPARgamma) agonists troglitazone and pioglitazone reduce injury and inflammation in a rat model of transient cerebral ischemia. The mechanism of this protection is unclear, as these agents can act through PPAR-gamma activation or through PPAR-gamma-independent mechanisms. Therefore, we examined PPAR-gamma expression, DNA binding and transcriptional activity following stroke. In addition, we used a PPAR-gamma antagonist, T0070907, to determine the role of PPAR-gamma during ischemia. Using immunohistochemical techniques and real-time PCR, we found low levels of PPAR-gamma mRNA and PPAR-gamma immunoreactivity in nonischemic brain; however, PPAR-gamma expression dramatically increased in ischemic neurons, peaking 24 h following middle cerebral artery occlusion. Interestingly, we found that in both vehicle- and agonist-treated brains, DNA binding was reduced in the ischemic hemisphere relative to the contralateral hemisphere. Expression of a PPAR-gamma target gene, lipoprotein lipase, was also reduced in ischemic relative to nonischemic brain. Both DNA binding and lipoprotein lipase expression were increased by the addition of the PPAR-gamma agonist rosiglitazone. Finally, we found that rosiglitazone-mediated protection after stroke was reversed by the PPAR-gamma antagonist T0070907. Interestingly, infarction size was also increased by T0070907 in the absence of PPAR-gamma agonist, suggesting that endogenous PPAR-gamma ligands may mitigate the effects of cerebral ischemia.
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17 MeSH Terms
Killer proteases and little strokes--how the things that do not kill you make you stronger.
O'Duffy AE, Bordelon YM, McLaughlin B
(2007) J Cereb Blood Flow Metab 27: 655-68
MeSH Terms: Animals, Cell Survival, Diabetes Mellitus, Heat-Shock Proteins, Humans, Ischemic Attack, Transient, Ischemic Preconditioning, Neurons, Neurosurgical Procedures, Peptide Hydrolases, Proteasome Endopeptidase Complex, Stroke, Synaptic Transmission, Ubiquitin
Show Abstract · Added January 26, 2015
The phenomenon of ischemic preconditioning was initially observed over 20 years ago. The basic tenant is that if stimuli are applied at a subtoxic level, cells upregulate endogenous protective mechanisms to block injury induced by subsequent stress. Since this discovery, many conserved signaling mechanisms that contribute to activation of this potent protective program have been identified in the brain. A clinical correlate of this basic research finding can be found in patients with a history of transient ischemic attack (TIA), who have a decreased morbidity after stroke. In spite of multidisciplinary efforts to design safer, more effective stroke therapies, we have thus far failed to translate our understanding of endogenous protective pathways to treatments for neurodegeneration. This review is designed to provide clinicians and basic scientists with an overview of stress biology after TIA and preconditioning, discuss new therapeutic strategies to target the protein dysfunction that follows ischemic injury, and propose enhanced biochemical profiling to identify individuals at risk of stroke after TIA. We pay particular attention to the unanticipated consequences of overly aggressive intervention after TIA in which we have found that traditional cytotoxic agents such as free radicals and apoptosis associated proteases is essential for neuroprotection and communication in the stressed brain. These data emphasize the importance of understanding the complex interplay between chaperones, apoptotic proteases including caspases, and the proteolytic degradation machinery in adaptation to neurological injury.
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14 MeSH Terms