Myocardial Gene Expression in Dilated Cardiomyopathy Treated with Beta-Blocking Agents
Open Access
- 2 May 2002
- journal article
- clinical trial
- Published by Massachusetts Medical Society in New England Journal of Medicine
- Vol. 346 (18), 1357-1365
- https://doi.org/10.1056/nejmoa012630
Abstract
Beta-blocker therapy may improve cardiac function in patients with idiopathic dilated cardiomyopathy. We tested the hypothesis that beta-blocker therapy produces favorable functional effects in dilated cardiomyopathy by altering the expression of myocardial genes that regulate contractility and pathologic hypertrophy.Keywords
This publication has 24 references indexed in Scilit:
- Blunted peripheral vasodilatory response is a hallmark of progressive deterioration in mild to moderate congestive heart failureJournal of Cardiac Failure, 2001
- What Type of β-Blocker Should Be Used to Treat Chronic Heart Failure?Circulation, 2000
- Differential Effects of β-Blockers in Patients With Heart FailureCell Metabolism, 2000
- β-Adrenergic Receptor Blockade in Chronic Heart FailureCell Metabolism, 2000
- Why does the myocardium fail? Insights from basic scienceThe Lancet, 1998
- Changes in gene expression in the intact human heart. Downregulation of alpha-myosin heavy chain in hypertrophied, failing ventricular myocardium.JCI Insight, 1997
- Medical Therapy Can Improve the Biological Properties of the Chronically Failing HeartCirculation, 1996
- Analysis of beta-adrenergic receptor mRNA levels in human ventricular biopsy specimens by quantitative polymerase chain reactions: Progressive reduction of beta1-adrenergic receptor mRNA in heart failureJournal of the American College of Cardiology, 1996
- Reversible alterations in myocardial gene expression in a young man with dilated cardiomyopathy and hypothyroidism.Proceedings of the National Academy of Sciences of the United States of America, 1992
- Selective gene expression in failing human heart. Quantification of steady-state levels of messenger RNA in endomyocardial biopsies using the polymerase chain reaction.Cell Metabolism, 1991