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9541. Atrium-selective sodium channel block as a strategy for suppression of atrial fibrillation: differences in sodium channel inactivation between atria and ventricles and the role of ranolazine.
作者: Alexander Burashnikov.;José M Di Diego.;Andrew C Zygmunt.;Luiz Belardinelli.;Charles Antzelevitch.
来源: Circulation. 2007年116卷13期1449-57页
The development of selective atrial antiarrhythmic agents is a current strategy for suppression of atrial fibrillation (AF).
9543. Persistent use of evidence-based pharmacotherapy in heart failure is associated with improved outcomes.
作者: Gunnar H Gislason.;Jeppe N Rasmussen.;Steen Z Abildstrom.;Tina Ken Schramm.;Morten Lock Hansen.;Pernille Buch.;Rikke Sørensen.;Fredrik Folke.;Niels Gadsbøll.;Søren Rasmussen.;Lars Køber.;Mette Madsen.;Christian Torp-Pedersen.
来源: Circulation. 2007年116卷7期737-44页
Undertreatment with recommended pharmacotherapy is a common problem in heart failure and may influence prognosis. We studied initiation and persistence of evidence-based pharmacotherapy in 107,092 patients discharged after first hospitalization for heart failure in Denmark from 1995 to 2004.
9544. Stromal cell derived factor-1 alpha confers protection against myocardial ischemia/reperfusion injury: role of the cardiac stromal cell derived factor-1 alpha CXCR4 axis.
作者: Xiaofeng Hu.;Shujing Dai.;Wen-Jian Wu.;Wei Tan.;Xiaoping Zhu.;Jingyao Mu.;Yiru Guo.;Roberto Bolli.;Gregg Rokosh.
来源: Circulation. 2007年116卷6期654-63页
Stromal cell-derived factor-1alpha (SDF-1alpha) binding to its cognate receptor, CXCR4, regulates a variety of cellular functions such as stem cell homing, trafficking, and differentiation. However, the role of the SDF-1alpha-CXCR4 axis in modulating myocardial ischemia/reperfusion injury is unknown.
9545. Preoperative thresholds for pulmonary valve replacement in patients with corrected tetralogy of Fallot using cardiovascular magnetic resonance.
作者: Thomas Oosterhof.;Alexander van Straten.;Hubert W Vliegen.;Folkert J Meijboom.;Arie P J van Dijk.;Anje M Spijkerboer.;Berto J Bouma.;Aeilko H Zwinderman.;Mark G Hazekamp.;Albert de Roos.;Barbara J M Mulder.
来源: Circulation. 2007年116卷5期545-51页
To facilitate the optimal timing of pulmonary valve replacement, we analyzed preoperative thresholds of right ventricular (RV) volumes above which no decrease or normalization of RV size takes place after surgery.
9546. Endothelial nitric oxide synthase plays an obligatory role in the late phase of ischemic preconditioning by activating the protein kinase C epsilon p44/42 mitogen-activated protein kinase pSer-signal transducers and activators of transcription1/3 pathway.
作者: Yu-Ting Xuan.;Yiru Guo.;Yanqing Zhu.;Ou-Li Wang.;Gregg Rokosh.;Roberto Bolli.
来源: Circulation. 2007年116卷5期535-44页
The role of endothelial nitric oxide synthase (eNOS) in ischemic preconditioning (PC) and cardioprotection is poorly understood. We addressed this issue using a genetic, rather than pharmacological, approach.
9547. SCN4B-encoded sodium channel beta4 subunit in congenital long-QT syndrome.
作者: Argelia Medeiros-Domingo.;Toshihiko Kaku.;David J Tester.;Pedro Iturralde-Torres.;Ajit Itty.;Bin Ye.;Carmen Valdivia.;Kazuo Ueda.;Samuel Canizales-Quinteros.;Maria Teresa Tusié-Luna.;Jonathan C Makielski.;Michael J Ackerman.
来源: Circulation. 2007年116卷2期134-42页
Congenital long-QT syndrome (LQTS) is potentially lethal secondary to malignant ventricular arrhythmias and is caused predominantly by mutations in genes that encode cardiac ion channels. Nearly 25% of patients remain without a genetic diagnosis, and genes that encode cardiac channel regulatory proteins represent attractive candidates. Voltage-gated sodium channels have a pore-forming alpha-subunit associated with 1 or more auxiliary beta-subunits. Four different beta-subunits have been described. All are detectable in cardiac tissue, but none have yet been linked to any heritable arrhythmia syndrome.
9548. Nonsense mutations in hERG cause a decrease in mutant mRNA transcripts by nonsense-mediated mRNA decay in human long-QT syndrome.
作者: Qiuming Gong.;Li Zhang.;G Michael Vincent.;Benjamin D Horne.;Zhengfeng Zhou.
来源: Circulation. 2007年116卷1期17-24页
Long-QT syndrome type 2 (LQT2) is caused by mutations in the human ether-a-go-go-related gene (hERG). More than 30% of the LQT2 mutations result in premature termination codons. Degradation of premature termination codon-containing mRNA transcripts by nonsense-mediated mRNA decay is increasingly recognized as a mechanism for reducing mRNA levels in a variety of human diseases. However, the role of nonsense-mediated mRNA decay in LQT2 mutations has not been explored.
9549. Inhibition of apoptosis-regulated signaling kinase-1 and prevention of congestive heart failure by estrogen.
作者: Minoru Satoh.;Christian M Matter.;Hisakazu Ogita.;Kyosuke Takeshita.;Chao-Yung Wang.;Gerald W Dorn.;James K Liao.
来源: Circulation. 2007年115卷25期3197-204页
Epidemiological studies have shown gender differences in the incidence of congestive heart failure (CHF); however, the role of estrogen in CHF is not known. We hypothesize that estrogen prevents cardiomyocyte apoptosis and the development of CHF.
9550. Association of fetuin-A with mitral annular calcification and aortic stenosis among persons with coronary heart disease: data from the Heart and Soul Study.
作者: Joachim H Ix.;Glenn M Chertow.;Michael G Shlipak.;Vincent M Brandenburg.;Markus Ketteler.;Mary A Whooley.
来源: Circulation. 2007年115卷19期2533-9页
Fetuin-A is a multifunctional hepatic secretory protein that inhibits dystrophic vascular and valvular calcification. Lower serum fetuin-A concentrations are associated with valvular calcification in persons with end-stage renal disease. Whether fetuin-A is associated with valvular calcification in other patient populations is unknown.
9551. Clinical aspects of type-1 long-QT syndrome by location, coding type, and biophysical function of mutations involving the KCNQ1 gene.
作者: Arthur J Moss.;Wataru Shimizu.;Arthur A M Wilde.;Jeffrey A Towbin.;Wojciech Zareba.;Jennifer L Robinson.;Ming Qi.;G Michael Vincent.;Michael J Ackerman.;Elizabeth S Kaufman.;Nynke Hofman.;Rahul Seth.;Shiro Kamakura.;Yoshihiro Miyamoto.;Ilan Goldenberg.;Mark L Andrews.;Scott McNitt.
来源: Circulation. 2007年115卷19期2481-9页
Type-1 long-QT syndrome (LQTS) is caused by loss-of-function mutations in the KCNQ1-encoded I(Ks) cardiac potassium channel. We evaluated the effect of location, coding type, and biophysical function of KCNQ1 mutations on the clinical phenotype of this disorder.
9552. Heritability of platelet responsiveness to aspirin in activation pathways directly and indirectly related to cyclooxygenase-1.
作者: Nauder Faraday.;Lisa R Yanek.;Rasika Mathias.;J Enrique Herrera-Galeano.;Dhananjay Vaidya.;Taryn F Moy.;M Daniele Fallin.;Alexander F Wilson.;Paul F Bray.;Lewis C Becker.;Diane M Becker.
来源: Circulation. 2007年115卷19期2490-6页
The inability of aspirin (acetylsalicylic acid [ASA]) to adequately suppress platelet function is associated with future risk of myocardial infarction, stroke, and cardiovascular death. Genetic variation is a proposed but unproved mechanism for insufficient ASA responsiveness.
9553. Diagnostic thresholds for ambulatory blood pressure monitoring based on 10-year cardiovascular risk.
作者: Masahiro Kikuya.;Tine W Hansen.;Lutgarde Thijs.;Kristina Björklund-Bodegård.;Tatiana Kuznetsova.;Takayoshi Ohkubo.;Tom Richart.;Christian Torp-Pedersen.;Lars Lind.;Hans Ibsen.;Yutaka Imai.;Jan A Staessen.; .
来源: Circulation. 2007年115卷16期2145-52页
Current diagnostic thresholds for ambulatory blood pressure (ABP) mainly rely on statistical parameters derived from reference populations. We determined an outcome-driven reference frame for ABP measurement.
9554. Instability in the diagnosis of metabolic syndrome in adolescents.
作者: Elizabeth Goodman.;Stephen R Daniels.;James B Meigs.;Lawrence M Dolan.
来源: Circulation. 2007年115卷17期2316-22页
Factor analyses suggest that the structure underlying metabolic syndrome is similar in adolescents and adults. However, adolescence is a period of intense physiological change, and therefore stability of the underlying metabolic structure and clinical categorization based on metabolic risk is uncertain.
9555. Mutation of the circadian clock gene Per2 alters vascular endothelial function.
作者: Hema Viswambharan.;João M Carvas.;Vladan Antic.;Ana Marecic.;Corinne Jud.;Christian E Zaugg.;Xiu-Fen Ming.;Jean-Pierre Montani.;Urs Albrecht.;Zhihong Yang.
来源: Circulation. 2007年115卷16期2188-95页
The circadian clock regulates biological processes including cardiovascular function and metabolism. In the present study, we investigated the role of the circadian clock gene Period2 (Per2) in endothelial function in a mouse model.
9556. Cardiac structure and ventricular-vascular function in persons with heart failure and preserved ejection fraction from Olmsted County, Minnesota.
作者: Carolyn S P Lam.;Véronique L Roger.;Richard J Rodeheffer.;Francesca Bursi.;Barry A Borlaug.;Steve R Ommen.;David A Kass.;Margaret M Redfield.
来源: Circulation. 2007年115卷15期1982-90页
Mechanisms purported to contribute to the pathophysiology of heart failure with normal ejection fraction (HFnlEF) include diastolic dysfunction, vascular and left ventricular systolic stiffening, and volume expansion. We characterized left ventricular volume, effective arterial elastance, left ventricular end-systolic elastance, and left ventricular diastolic elastance and relaxation noninvasively in consecutive HFnlEF patients and appropriate controls in the community.
9557. Secondary prevention of stroke and transient ischemic attack: is more platelet inhibition the answer?
Recurrent cerebrovascular events constitute an estimated 200,000 of the 700,000 strokes reported annually in the United States, which makes secondary stroke prevention an important goal in the management of disease among patients who have experienced stroke or transient ischemic attack.
9558. Infarct tissue heterogeneity by magnetic resonance imaging identifies enhanced cardiac arrhythmia susceptibility in patients with left ventricular dysfunction.
作者: André Schmidt.;Clerio F Azevedo.;Alan Cheng.;Sandeep N Gupta.;David A Bluemke.;Thomas K Foo.;Gary Gerstenblith.;Robert G Weiss.;Eduardo Marbán.;Gordon F Tomaselli.;João A C Lima.;Katherine C Wu.
来源: Circulation. 2007年115卷15期2006-14页
The extent of the peri-infarct zone by magnetic resonance imaging (MRI) has been related to all-cause mortality in patients with coronary artery disease. This relationship may result from arrhythmogenesis in the infarct border. However, the relationship between tissue heterogeneity in the infarct periphery and arrhythmic substrate has not been investigated. In the present study, we quantify myocardial infarct heterogeneity by contrast-enhanced MRI and relate it to an electrophysiological marker of arrhythmic substrate in patients with left ventricular (LV) systolic dysfunction undergoing prophylactic implantable cardioverter defibrillator placement.
9559. Mechanistic role of I(f) revealed by induction of ventricular automaticity by somatic gene transfer of gating-engineered pacemaker (HCN) channels.
作者: Tian Xue.;Chung-Wah Siu.;Deborah K Lieu.;Chu-Pak Lau.;Hung-Fat Tse.;Ronald A Li.
来源: Circulation. 2007年115卷14期1839-50页
Although I(f), encoded by the hyperpolarization-activated cyclic-nucleotide-modulated (HCN) channel gene family, is known to be functionally important in pacing, its mechanistic action is largely inferential and indeed somewhat controversial. To dissect in detail the role of I(f), we investigated the functional consequences of overexpressing in adult guinea pig left ventricular cardiomyocytes (LVCMs) various HCN1 constructs that have been engineered to exhibit different gating properties.
9560. Relationship between central sympathetic drive and magnetic resonance imaging-determined left ventricular mass in essential hypertension.
作者: Joanna Burns.;Mohan U Sivananthan.;Stephen G Ball.;Alan F Mackintosh.;David A S G Mary.;John P Greenwood.
来源: Circulation. 2007年115卷15期1999-2005页
Sympathetic activation has been implicated in the development of left ventricular hypertrophy (LVH). However, the relationship between sympathetic activation and LV mass (LVM) has not been clearly defined across a range of arterial pressure measurements. The present study was planned to determine that relationship, using cardiac magnetic resonance imaging to accurately quantify LVM, in hypertensive patients with and without LVH and in normal subjects.
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