JTCS Medtronic Endurant
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Burkhoff, D.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Burkhoff, D.
Related Collections
Right arrow Congestive Heart Failure

J Thorac Cardiovasc Surg 2003;125:S50-S52
© 2003 The American Association for Thoracic Surgery

Editorials

New heart failure therapy: The shape of things to come?

Daniel Burkhoff, MD, PhD

From the Department of Medicine, Divisions of Circulatory Physiology and Cardiology, Columbia University, New York, NY.

Received for publication March 20, 2001. Accepted for publication March 27, 2001. Address for reprints: Daniel Burkhoff, MD, PhD, Department of Medicine, Divisions of Circulatory Physiology and Cardiology, Columbia University, 812 Black Building, 650 W 168th St, New York, NY 10032.

The first 20% of the full text of this article appears below.

Laplace's law, which can be used to estimate myocardial wall stress ({sigma}) from intraventricular pressure (LVP), radius of curvature (R), and wall thickness (h), has long been recognized as a fundamental physical principle in understanding cardiac function in health and disease: {sigma} = LVP x R/h. On the basis of this law, the enlarged chamber radius of the chronically failing heart exposes myocytes to increased systolic wall stress. This leads to cellular and chamber hypertrophy, which, in an adaptive process, acts to renormalize wall stress.Go 1 As the chamber continues to dilate over time, the limits of hypertrophy appear to be reached so that wall stress ultimately increases. This increased afterload further impairs the ability of the already weakened myocytes to shorten, and cardiac performance deteriorates. Globally referred to as ventricular remodeling, this process is partially preventable and reversible as demonstrated in studies of angiotensin-converting enzyme inhibitors,Go 2 ß-blockers,Go 3 and during hemodynamic unloading by prolonged support with a left ventricular assist device.Go 4

Several surgical therapies, such as the Myocor ventricular shape change device (Myocor, Inc, Plymouth, Minn), described in this issue by McCarthy and colleagues,Go 5 are being developed for treating heart failure by physically remodeling the dilated heart. Stress reduction via Laplace's law is usually sited as the rationale for these . . . [Full Text of this Article]




This article has been cited by other articles:


Home page
 Eur J Cardiothorac SurgHome page
F. Torrent-Guasp, M. J. Kocica, A. F. Corno, M. Komeda, F. Carreras-Costa, A. Flotats, J. Cosin-Aguillar, and H. Wen
Towards new understanding of the heart structure and function
Eur J Cardiothorac Surg, February 1, 2005; 27(2): 191 - 201.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 2003 by The American Association for Thoracic Surgery.