Showing papers by "Arthur M. Feldman published in 2005"
TL;DR: This document summarizes current capabilities, research and operational priorities, and plans for further studies that were established at the 2015 USGS workshop on quantitative hazard assessments of earthquake-triggered landsliding and liquefaction.
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4,975 citations
TL;DR: The American College of Cardiology (ACC)/AHA Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed.
Abstract: The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed. This process gives priority to areas where major changes in text, particularly recommendations,
433 citations
TL;DR: Pump failure deaths are the predominant mode of death in patients with advanced HF and are modestly reduced by both CRT and CRT-D, while only CRT -D reduced SCD and thus produced a favorable effect on cardiac mortality.
218 citations
Thomas Jefferson University1, Johns Hopkins University2, University of Colorado Denver3, University of Southern California4, University of California, Los Angeles5, Johns Hopkins University School of Medicine6, Penn State Milton S. Hershey Medical Center7, Georgetown University8, United States Department of Veterans Affairs9, Boston Scientific Corporation10
TL;DR: For the COMPANION trial patients, the use of CRT-P andCRT-D was associated with a cost-effectiveness ratio below generally accepted benchmarks for therapeutic interventions of 50,000 dollars per QALY to 100,000 dollar per QalY.
190 citations
Journal Article•
176 citations
TL;DR: Alarming abnormalities in action potential propagation and Ca(2+) handling contribute to the initiation of atrial arrhythmias in this mouse model of heart failure.
Abstract: Transgenic mice overexpressing the inflammatory cytokine TNF-α in the heart develop a progressive heart failure syndrome characterized by biventricular dilatation, decreased ejection fraction, decr...
124 citations
TL;DR: It is demonstrated that the serine and tyrosine phosphorylation pathways are differentially activated during different pathophysiological processes (cardiomyopathy and I/R injury) and that NF-kappaB contributes to infarct development after I/ R.
Abstract: The role of NF-κB in cardiac physiology and pathophysiology has been difficult to delineate due to the inability to specifically block NF-κB signaling in the heart. Cardiac-specific transgenic mode...
90 citations
TL;DR: Blockade of NF-κB activation did not ameliorate myocardial inflammation but improved cardiac function and survival in male TNF-α TG mice.
Abstract: Objective : NF-κB, a key transcription factor that regulates inflammatory processes, has been shown to be activated in the failing human heart with enhanced expression of proinflammatory cytokines. In the present study, we assessed the hypothesis that cardiotoxic effects of proinflammatory cytokines are mediated by the activation of NF-κB.
Methods : Transgenic mice with cardiac-specific overexpression of TNF-α were used as a model of cytokine-induced cardiomyopathy. To block the activation of NF-κB, transgenic mice (TG/p50+/+) were crossed with knockout mice in which the p50 subunit of NF-κB was disrupted (WT/p50−/−).
Results : The electrophoretic mobility shift assay demonstrated that NF-κB was activated in the myocardium of TG/p50+/+ mice, while it was completely abolished in TG/p50−/− mice. Male TG mice died of congestive heart failure earlier than females, where the disruption of the p50 subunit significantly improved the survival. Compared with TG/p50+/+ mice, TG/p50−/− mice showed a significant reduction of ventricular dilatation and hypertrophy with preserved fractional shortening. Although the myocardial expression of proinflammatory cytokines or infiltration of inflammatory cells was not affected, increased expression and activity of MMP-9 were significantly suppressed in TG/p50−/− mice.
Conclusion : Blockade of NF-κB activation did not ameliorate myocardial inflammation but improved cardiac function and survival in male TNF-α TG mice. An inhibition of NF-κB may be a new therapeutic strategy for cardiac remodeling and heart failure, especially when proinflammatory cytokines are activated.
89 citations
TL;DR: This document summarizes the evidence reviewed at a 1-day round table to review the impact of ICD therapy in the primary prevention of sudden cardiac death and the effect of CRT in patients with congestive heart failure and the discussions of that evidence.
73 citations
TL;DR: In cardiomyopathy of recent onset, increased expression of Fas and TNFR1 was associated with minimal recovery of LV function and represents a potential target for therapeutic intervention.
48 citations
TL;DR: Selective ablation of the MMP-2 gene reduces survival and exacerbates cardiac failure in association with the increased level of myocardial inflammation.
Abstract: Tumor necrosis factor-α (TNF-α) plays a pathophysiological role in the development and progression of heart failure. Matrix metalloproteinase (MMP)-2 is involved in extracellular matrix remodeling....
TL;DR: Efficacy measures include standard exercise tolerance tests on a treadmill (modified Naughton protocol), with measurements of peak oxygen uptake and exercise duration time; quality of life questionnaires; NYHA classification; and neurohormonal markers of HF.
TL;DR: These studies are Phase III, multicenter, randomized, double-blinded, placebo-controlled trials designed to test the general hypothesis that chronic oral administration of low doses of enoximone can produce beneficial effects in subjects with advanced or ultra-advanced chronic heart failure.
TL;DR: A transgenic mouse model of congestive heart failure consequent to cardiac-specific overexpression of tumor necrosis factor-α (T NF-α) (TNF1.6) displays marked sex-related phenotypic differenc...
Abstract: A transgenic mouse model of congestive heart failure (CHF) consequent to cardiac-specific overexpression of tumor necrosis factor-α (TNF-α) (TNF1.6) displays marked sex-related phenotypic differenc...
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TL;DR: A roundtable discussion by cardiac specialists and pharmacologists was convened on August 18, 2003, to discuss and critique the results of the Carvedilol or Metoprolol European Trial (COMET), which were recently published in The Lancet.
Abstract: A roundtable discussion by cardiac specialists and pharmacologists was convened on August 18, 2003, to discuss and critique the results of the Carvedilol or Metoprolol European Trial (COMET), which were recently published in The Lancet.1 Michael R. Bristow, MD, PhD, Head of the Division of Cardiology at the University of Colorado Health Sciences Center in Denver, CO, moderated the discussion. Panelists included Kirkwood F. Adams, Jr., MD, Associate Professor of Medicine and Radiology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC; Jerry L. Bauman, PharmD, Professor of Pharmacy Practice and Medicine, University of Illinois at Chicago, Chicago, IL; Arthur M. Feldman, MD, PhD, Magee Professor of Medicine, Jefferson Medical College, Philadelphia, PA; Thomas D. Giles, MD, Professor of Medicine, Louisiana State University School of Medicine, New Orleans, LA; Sidney Goldstein, MD, Professor of Medicine, Case Western Reserve University, Detroit, MI; Douglas L. Mann, MD, Professor of Medicine, Winters Center for Heart Failure Research, Houston, TX; and Robert L. Talbert, PharmD, Professor of Pharmacy, University of Texas at Austin, Professor of Pharmacology and Medicine, University of Texas Health Science Center, San Antonio, TX.
TL;DR: The arrival of the digital age has provided the opportunity for information to be captured instantaneously and rapidly transmitted around the globe, but it also raises new challenges for ensuring that new information is distributed with appropriate oversight and within acceptable ethical boundaries.