bluuebunny/crossref_metadata_2025_split huggingface dataset:
Takotsubo Cardiomyopathy Is Not Due to Plaque Rupture: An Intravascular Ultrasound Study
Authors: Haghi Dariusch , Roehm Stefanie , Hamm Karsten , Harder Niels , Suselbeck Tim , Borggrefe Martin , Papavassiliu Theano 
Published: May 2010

AbstractBackgroundPlaque rupture with subsequent transient thrombotic coronary occlusion by a fast‐dissolving clot is one of the proposed pathogenic mechanisms in Takotsubo cardiomyopathy (TC).HypothesisThe aim of this study was to seek evidence for the hypothesis of transient coronary thrombosis as the underlying mechanism of TC by means of intravascular ultrasound (IVUS).MethodsIn our database of 63 consecutive patients with TC we identified 10 patients (16%) who had undergone IVUS during their initial left heart catheterisation.ResultsA median length of 67 mm of the left anterior descending artery was analyzed (interquartile range [IQR]: 63.3–70.1 mm). Median lumen diameter, median vessel diameter, median plaque and media volume were 2.9 mm (IQR: 2.7–3.1 mm), 4.2 mm (IQR: 3.8–4.4 mm), and 90.9 mm3 (IQR: 70.4–101.4 mm3), respectively. Plaque rupture, positive remodeling, and presumed intracoronary thrombus were absent in all patients.ConclusionIn conclusion, plaque rupture does not account for the regional wall motion abnormalities observed in TC. The previously reported observation of plaque rupture in TC seems to constitute an incidental finding. We suggest that the theory of aborted myocardial infarction as the underlying cause of TC should be abandoned once and for all. Copyright © 2010 Wiley Periodicals, Inc.
Prophylactic Implantation of Cardioverter Defibrillators in Idiopathic Nonischemic Cardiomyopathy for the Primary Prevention of Death: A Narrative Review
Authors: Cevik Cihan , Nugent Kenneth , Perez‐Verdia Alejandro , Fish R. David 
Published: May 2010

AbstractImplantable cardioverter defibrillator (ICD) therapy reduces sudden cardiac death rates and reduces mortality in patients with ischemic heart disease and low ejection fractions. One‐third of the deaths in patients with nonischemic cardiomyopathy are sudden. However, the efficacy of ICDs in the primary prevention of death in these patients is less clear. The most common cause of mortality in patients treated with ICDs is heart failure progression. ICD shocks can cause direct myocardial injury, fibrosis, inflammation, and adverse psychological outcomes, and these changes may contribute to the ventricular dysfunction in patients who already have a significantly depressed ejection fraction. We have reviewed the published randomized controlled trials and meta‐analysis of prophylactic ICD therapy in the primary prevention of death in patients with nonischemic cardiomyopathy. The individual randomized controlled trials do not report a statistically significant reduction of mortality unless the ICD treatment is added to cardiac resynchronization therapy, but the meta‐analysis did show a significant mortality reduction and favored ICD therapy in these patients. Medical management of many study participants was suboptimal, at least based on current guidelines. The patients with non‐ischemic cardiomyopathy have good outcomes with medical therapy, and ICD therapy in this relatively low‐risk population needs better selection criteria. Copyright © 2010 Wiley Periodicals, Inc.
The Association of Statin Use and Statin Type and Cognitive Performance: Analysis of the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study
Authors: Glasser Stephen P. , Wadley Virginia , Judd Suzanne , Kana Bhumika , Prince Valerie , Jenny Nancy , Kissela Brett , Safford Monika , Prineas Ronald , Howard George 
Published: May 2010

AbstractBackgroundStatin use and type have been variably associated with impaired or improved cognitive performance.HypothesisTo assess the association of statin use and type (lipophilic vs hydrophilic) and cognitive impairment.MethodsCross‐sectional analysis of 24 595 participants (7191 statin users and 17 404 nonusers) age ≥ 45 years, from a population‐based national cohort study (Reasons for Geographic And Racial Differences in Stroke) enrolled between January 2003 and October 2008, with oversampling from the southeastern Stroke Belt and African Americans. Statin use and type were documented in participants' homes by a trained health professional. Cognitive performance was assessed with a prior validated instrument of global cognitive status (Six‐Item Screener). Cognitive impairment was defined as a score of < 4.ResultsOverall, an association of cognitive impairment and statin use was observed (8.6% of users vs 7.7% of nonusers had cognitive impairment, P = 0.014); but, after adjusting for variables known to be associated with cognition (age, gender, race, income, education level, and cardiovascular disease), the association was attenuated (odds ratio [OR]: 0.98, confidence interval [CI]: 0.87–1.10). No association was observed between statin type (lipophilic vs hydrophilic) and cognition (OR: 1.03, CI: 0.86–1.24), and there were no regional differences in cognitive impairment in statin users (8% in the Stroke Belt and 7.9% in other regions, P = 0.63).ConclusionsStatin use and type were marginally associated with cognitive impairment. After adjusting for known variables that affect cognition, no association was observed. No regional differences were observed. This large study found no evidence to support an association between statins and cognitive performance. Copyright © 2010 Wiley Periodicals, Inc.
Cost Burden of Cardiovascular Hospitalization and Mortality in ATHENA‐Like Patients With Atrial Fibrillation/Atrial Flutter in the United States
Authors: Naccarelli Gerald V. , Johnston Stephen S. , Lin Jay , Patel Parag P. , Schulman Kathy L. 
Published: May 2010

AbstractBackgroundThe ATHENA trial (A placebo‐controlled, double‐blind, parallel arm Trial to assess the efficacy of dronedarone 400 mg bid for the prevention of cardiovascular Hospitalization or death from any cause in patiENts with Atrial fibrillation/atrial flutter) demonstrated that dronedarone reduced the risk of cardiovascular (CV) hospitalization/death by 24% (P < 0.001) in patients with atrial fibrillation (AF) and atrial flutter (AFL).HypothesisIn order to estimate the cost savings associated with dronedarone use, we estimated the costs associated with CV hospitalizations and inpatient mortality in a large cohort of ATHENA‐like patients.MethodsIn this retrospective analysis, we evaluated the cost of CV hospitalization/mortality in real‐world ATHENA‐like patients without heart failure and with employer‐sponsored Medicare supplemental insurance in the United States. Patients similar to those in ATHENA (age ≥ 70 years with AF/AFL and ≥ 1 stroke risk factor, without heart failure) who were hospitalized between January 2, 2005, and January 1, 2007, were identified from the MarketScan databases from Thomson Reuters. Health care costs were evaluated during the 12 months following the index hospitalization.ResultsThe analysis included 10 200 ATHENA‐like patients. Hospitalization for CV causes occurred in 53.9% of patients, with a total of 6700 CV hospitalizations for fatal/nonfatal causes. The most common nonfatal causes of CV hospitalizations were AF/other supraventricular rhythm disorders (20.2% of all CV hospitalizations), congestive heart failure (CHF; 14.3%), and transient ischemic attack (TIA)/stroke (10.7%). Mean costs per CV hospitalization for nonfatal causes were $10908. Inpatient deaths from CV causes occurred in 264 (2.6%) patients; the most common causes of CV inpatient death were intracranial/gastrointestinal hemorrhage (24.2% of CV deaths), TIA/stroke (17.0%), and CHF (15.9%). Mean hospitalization costs per CV inpatient death were $18 565.ConclusionsHealth care costs associated with CV hospitalizations and inpatient deaths among ATHENA‐like patients in the US are high. Novel antiarrhythmic therapies such as dronedarone, with the potential to reduce CV hospitalizations/mortality in similar patients, could decrease health care costs if adopted in clinical practice. Copyright © 2010 Wiley Periodicals, Inc.
A Retrospective Review to Evaluate the Safety of Right Heart Catheterization via the Internal Jugular Vein in the Assessment of Pulmonary Hypertension
Authors: Ranu Harpreet , Smith Katherine , Nimako Kofi , Sheth Abhijat , Madden Brendan P. 
Published: May 2010

AbstractBackgroundRight heart catheterization (RHC) is important in the evaluation of pulmonary hypertension, but is not without risk.HypothesisWe wished to assess the safety, efficacy, and tolerability of RHC performed via the internal jugular vein (IJV) at our tertiary cardiothoracic center.MethodsA retrospective review of the medical records for all patients undergoing RHC via the IJV between January 1, 2007 and July 31, 2009 was performed. We do not routinely use ultrasound guidance or stop anticoagulation. Operators with a median experience of 450 procedures performed the RHCs.ResultsRight heart catheterization was performed on 349 patients with a median age of 66 years (range, 17–89), median mean pulmonary artery pressure of 30 mm Hg (range, 8–69), and a median internationalized normal ratio of 2.5. Of 349 patients, we were unable to obtain intravenous access in only 1 patient; 342 (98%) patients tolerated RHC with local anesthetic alone; and 6 patients required additional sedation with benzodiazepines. The median time for the procedure was 15 minutes. Complications occurred in 6 patients (1.7%) and included carotid puncture (n = 3), sinus bradycardia below 45 beats/min, which responded promptly to atropine and intravenous fluid (n = 2), and complete heart block without hemodynamic compromise (n = 1). There were no pneumothoraxes, pulmonary hemorrhage, or deaths related to the procedure.ConclusionRight heart catheterization via the IJV is quick, safe, and well tolerated. It is not associated with an increased risk of pneumothorax or other complications when performed by experienced operators. Copyright © 2010 Wiley Periodicals, Inc.
Progression of Coronary Artery Disease During Long‐Term Follow‐Up of the Swiss Interventional Study on Silent Ischemia Type II (SWISSI II)
Authors: Schoenenberger Andreas W. , Jamshidi Peiman , Kobza Richard , Zuber Michel , Stuck Andreas E. , Pfisterer Matthias , Erne Paul 
Published: May 2010

AbstractBackgroundThis study evaluates cardiovascular risk factors associated with progression of coronary artery disease (CAD) in patients with silent ischemia following myocardial infarction.HypothesisCoronary artery disease only progresses slowly with comprehensive risk factor intervention.MethodsA total of 104 of 201 patients (51.7%) of the Swiss Interventional Study on Silent Ischemia Type II (SWISSI II) with baseline and follow‐up coronary angiography were included. All patients received comprehensive cardiovascular risk factor intervention according to study protocol. Logistic regression was used to evaluate associations between baseline cardiovascular risk factors and CAD progression.ResultsThe mean duration of follow‐up was 10.3±2.4 years. At baseline, 77.9% of patients were smokers, 45.2% had hypertension, 73.1% had dyslipidemia, 7.7% had diabetes, and 48.1% had a family history of CAD. At last follow‐up, only 27 patients of the initial 81 smokers still smoked, only 2.1% of the patients had uncontrolled hypertension, 10.6% of the patients had uncontrolled dyslipidemia, and 2.1% of the patients had uncontrolled diabetes. Coronary artery disease progression was found in up to 81 (77.9%) patients. Baseline diabetes and younger age were associated with increased odds of CAD progression. The time interval between baseline and follow‐up angiography was also associated with CAD progression.ConclusionCoronary artery disease progression was highly prevalent in these patients despite comprehensive risk factor intervention. Further research is needed to optimize treatment of known risk factors and to identify other unknown and potentially modifiable risk factors. Copyright © 2010 Wiley Periodicals, Inc.
Where Is the Radiation History for the Cardiac Patient?
Authors: Richard Conti C. 
Published: May 2010

AbstractWhen evaluating a cardiac patient, the present illness, medical history, surgical history, family history, social history, and review of systems are dutifully recorded along with the physical exam, ECG, chest x‐ray, and routine blood tests and urinalysis. Copyright © 2010 Wiley Periodicals, Inc.
Synaptic and nonsynaptic localization of protocadherin‐γC5 in the rat brain
Authors: Li Yanfang , Serwanski David R. , Miralles Celia P. , Fiondella Christopher G. , Loturco Joseph J. , Rubio Maria E. , De Blas Angel L. 
Published: May 2010

AbstractIt has been proposed that γ‐protocadherins (Pcdh‐γs) are involved in the establishment of specific patterns of neuronal connectivity. Contrary to the other Pcdh‐γs, which are expressed in the embryo, Pcdh‐γC5 is expressed postnatally in the brain, coinciding with the peak of synaptogenesis. We have developed an antibody specific for Pcdh‐γC5 to study the expression and localization of Pcdh‐γC5 in brain. Pcdh‐γC5 is highly expressed in the olfactory bulb, corpus striatum, dentate gyrus, CA1 region of the hippocampus, layers I and II of the cerebral cortex, and molecular layer of the cerebellum. Pcdh‐γC5 is expressed in both neurons and astrocytes. In hippocampal neuronal cultures, and in the absence of astrocytes, a significant percentage of synapses, more GABAergic than glutamatergic, have associated Pcdh‐γC5 clusters. Some GABAergic axons show Pcdh‐γC5 in the majority of their synapses. Nevertheless, many Pcdh‐γC5 clusters are not associated with synapses. In the brain, significant numbers of Pcdh‐γC5 clusters are located at contact points between neurons and astrocytes. Electron microscopic immunocytochemistry of the rat brain shows that 1) Pcdh‐γC5 is present in some GABAergic and glutamatergic synapses both pre‐ and postsynaptically; 2) Pcdh‐γC5 is also extrasynaptically localized in membranes and in cytoplasmic organelles of neurons and astrocytes; and 3) Pcdh‐γC5 is also localized in perisynaptic astrocyte processes. The results support the notions that 1) Pcdh‐γC5 plays a role in synaptic specificity and/or synaptic maturation and 2) Pcdh‐γC5 is involved in neuron–neuron synaptic interactions and in neuron–astrocyte interactions, including perisynaptic neuron–astrocyte interactions. J. Comp. Neurol. 518:3439–3463, 2010. © 2010 Wiley‐Liss, Inc.
Localization of Kv1.3 channels in presynaptic terminals of brainstem auditory neurons
Authors: Gazula Valeswara‐Rao , Strumbos John G. , Mei Xiaofeng , Chen Haijun , Rahner Christoph , Kaczmarek Leonard K. 
Published: May 2010

AbstractElimination of the Kv1.3 voltage‐dependent potassium channel gene produces striking changes in the function of the olfactory bulb, raising the possibility that this channel also influences other sensory systems. We have examined the cellular and subcellular localization of Kv1.3 in the medial nucleus of the trapezoid body (MNTB) in the auditory brainstem, a nucleus in which neurons fire at high rates with high temporal precision. A clear gradient of Kv1.3 immunostaining along the lateral to medial tonotopic axis of the MNTB was detected. Highest levels were found in the lateral region of the MNTB, which corresponds to neurons that respond selectively to low‐frequency auditory stimuli. Previous studies have demonstrated that MNTB neurons and their afferent inputs from the cochlear nucleus express three other members of the Kv1 family, Kv1.1, Kv1.2, and Kv1.6. Nevertheless, confocal microscopy of MNTB sections coimmunostained for Kv1.3 with these subunits revealed that the distribution of Kv1.3 differed significantly from other Kv1 family subunits. In particular, no axonal staining of Kv1.3 was detected, and most prominent labeling was in structures surrounding the somata of the principal neurons, suggesting specific localization to the large calyx of Held presynaptic endings that envelop the principal cells. The presence of Kv1.3 in presynaptic terminals was confirmed by coimmunolocalization with the synaptic markers synaptophysin, syntaxin, and synaptotagmin and by immunogold electron microscopy. Kv1.3 immunogold particles in the terminals were arrayed along the plasma membrane and on internal vesicular structures. To confirm these patterns of staining, we carried out immunolabeling on sections from Kv1.3−/− mice. No immunoreactivity could be detected in Kv1.3−/− mice either at the light level or in immunogold experiments. The finding of a tonotopic gradient in presynaptic terminals suggests that Kv1.3 may regulate neurotransmitter release differentially in neurons that respond to different frequencies of sound. J. Comp. Neurol. 518:3205–3220, 2010. © 2010 Wiley‐Liss, Inc.
Unmyelinated auditory type I spiral ganglion neurons in congenic Ly5.1 mice
Authors: Jyothi Vinu , Li Manna , Kilpatrick Lauren A. , Smythe Nancy , LaRue Amanda C. , Zhou Daohong , Schulte Bradley A. , Schmiedt Richard A. , Lang Hainan 
Published: May 2010

AbstractWith the exception of humans, the somata of type I spiral ganglion neurons (SGNs) of most mammalian species are heavily myelinated. In an earlier study, we used Ly5.1 congenic mice as transplant recipients to investigate the role of hematopoietic stem cells in the adult mouse inner ear. An unanticipated finding was that a large percentage of the SGNs in this strain were unmyelinated. Further characterization of the auditory phenotype of young adult Ly5.1 mice in the present study revealed several unusual characteristics, including 1) large aggregates of unmyelinated SGNs in the apical and middle turns, 2) symmetrical junction‐like contacts between the unmyelinated neurons, 3) abnormal expression patterns for CNPase and connexin 29 in the SGN clusters, 4) reduced SGN density in the basal cochlea without a corresponding loss of sensory hair cells, 5) significantly delayed auditory brainstem response (ABR) wave I latencies at low and middle frequencies compared with control mice with similar ABR threshold, and 6) elevated ABR thresholds and deceased wave I amplitudes at high frequencies. Taken together, these data suggest a defect in Schwann cells that leads to incomplete myelinization of SGNs during cochlear development. The Ly5.1 mouse strain appears to be the only rodent model so far identified with a high degree of the “human‐like” feature of unmyelinated SGNs that aggregate into neural clusters. Thus, this strain may provide a suitable animal platform for modeling human auditory information processing such as synchronous neural activity and other auditory response properties. J. Comp. Neurol. 518:3254–3271, 2010. © 2010 Wiley‐Liss, Inc.
Molecular analysis of neocortical layer structure in the ferret
Authors: Rowell Joanna J. , Mallik Atul K. , Dugas‐Ford Jennifer , Ragsdale Clifton W. 
Published: May 2010

AbstractMolecular markers that distinguish specific layers of rodent neocortex are increasingly employed to study cortical development and the physiology of cortical circuits. The extent to which these markers represent general features of neocortical cell type identity across mammals, however, is unknown. To assess the conservation of layer markers more broadly, we isolated orthologs for 15 layer‐enriched genes in the ferret, a carnivore with a large, gyrencephalic brain, and analyzed their patterns of neocortical gene expression. Our major findings are: 1) Many but not all layer markers tested show similar patterns of layer‐specific gene expression between mouse and ferret cortex, supporting the view that layer‐specific cell type identity is conserved at a molecular level across mammalian superorders; 2) Our panel of deep layer markers (ER81/ETV1, SULF2, PCP4, FEZF2/ZNF312, CACNA1H, KCNN2/SK2, SYT6, FOXP2, CTGF) provides molecular evidence that the specific stratifications of layers 5 and 6 into 5a, 5b, 6a, and 6b are also conserved between rodents and carnivores; 3) Variations in layer‐specific gene expression are more pronounced across areas of ferret cortex than between homologous areas of mouse and ferret cortex; 4) This variation of area gene expression was clearest with the superficial layer markers studied (SERPINE2, MDGA1, CUX1, UNC5D, RORB/NR1F2, EAG2/KCNH5). Most dramatically, the layer 4 markers RORB and EAG2 disclosed a molecular sublamination to ferret visual cortex and demonstrated a molecular dissociation among the so‐called agranular areas of the neocortex. Our findings establish molecular markers as a powerful complement to cytoarchitecture for neocortical layer and cell‐type comparisons across mammals. J. Comp. Neurol. 518:3272–3289, 2010. © 2010 Wiley‐Liss, Inc.
Distribution of sex steroid hormone receptors in the brain of an African cichlid fish, Astatotilapia burtoni
Authors: Munchrath Lauren A. , Hofmann Hans A. 
Published: May 2010

AbstractSex steroid hormones released from the gonads play an important role in mediating social behavior across all vertebrates. Many effects of these gonadal hormones are mediated by nuclear steroid hormone receptors, which are crucial for integration in the brain of external (e.g., social) signals with internal physiological cues to produce an appropriate behavioral output. The African cichlid fish Astatotilapia burtoni presents an attractive model system for the study of how internal cues and external social signals are integrated in the brain as males display robust plasticity in the form of two distinct, yet reversible, behavioral and physiological phenotypes depending on the social environment. In order to better understand where sex steroid hormones act to regulate social behavior in this species, we have determined the distribution of the androgen receptor, estrogen receptor alpha, estrogen receptor beta, and progesterone receptor mRNA and protein throughout the telencephalon and diencephalon and some mesencephalic structures of A. burtoni. All steroid hormone receptors were found in key brain regions known to modulate social behavior in other vertebrates including the proposed teleost homologs of the mammalian amygdalar complex, hippocampus, striatum, preoptic area, anterior hypothalamus, ventromedial hypothalamus, and ventral tegmental area. Overall, there is high concordance of mRNA and protein labeling. Our results significantly extend our understanding of sex steroid pathways in the cichlid brain and support the important role of nuclear sex steroid hormone receptors in modulating social behaviors in teleosts and across vertebrates. J. Comp. Neurol. 518:3302–3326, 2010. © 2010 Wiley‐Liss, Inc.