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European Journal of Heart Failure 2007 9(4):325-328; doi:10.1016/j.ejheart.2006.09.008
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© 2007 European Society of Cardiology

Reversal of ventricular remodeling: Important to establish and difficult to define

Paul J. Hauptmana,* and Hani N. Sabbahb

a Division of Cardiology FDT-15, Saint Louis University Hospital 3635 Vista Avenue, St. Louis MO 63110, United States
b Division of Cardiovascular Medicine, Henry Ford Health System Detroit MI, United States

* Corresponding author. Tel.: +1 314 577 8896; fax: +1 314 268 5138. E-mail address: hauptmpj@slu.edu

Key Words: Remodeling • Heart Failure

Received June 29, 2006;
The first 150 words of the full text of this article appear below.

"I do applaud your noble goals. Now let's see if you achieve them" Guenevere to the Knights in "Camelot",1

Lyrics by Alan Jay Lerner

Since the term "remodeling" was used more than 20 years ago [1], a multitude of studies in both animal models of experimentally-induced heart failure and humans with heart failure have described extensive pathophysiologic changes that occur following myocardial injury at both the "global" and "cellular" levels. These changes occur regardless of the type of injury such as ischemia, pressure overload, volume overload or other factors that lead to intrinsic abnormalities in the contractile machinery [2-6]. The abnormalities that occur in left ventricular (LV) size and shape, cardiac interstitium, electrophysiological milieu, and myocyte biology indicate that phenotypically and genotypically, by autocrine, paracrine and endocrine mechanisms, the heart dramatically undergoes a major maladaptive transition as heart failure ensues and progresses relentlessly toward the intractable phenotype that . . . [Full Text of this Article]


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