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J Thorac Cardiovasc Surg 2006;132:459-463
© 2006 The American Association for Thoracic Surgery
Editorial |
a Cardiovascular Research Foundation, Orangeburg, NY
b Department of Cardiothoracic, Surgery, Drexel University College of Medicine, Philadelphia, Pa.
Received for publication April 26, 2006; accepted for publication April 27, 2006. * Address for reprints: Daniel Burkhoff, MD, PhD, The Jack H Skirball Center for Cardiovascular Research, Cardiovascular Research Foundation, 8 Corporate Dr, Orangeburg, NY 10962 (Email: dburkhoff@crf.org).
| The first 300 words of the full text of this article appear below. |
One of the fundamental characteristics of chronic heart failure is the progressive chamber dilation and deterioration of pump function that is driven by the increased hemodynamic and neurohormonal stresses present in this condition.1
This process, referred to as ventricular remodeling, involves structural, cellular, extracellular, molecular, biochemical, and metabolic mechanisms. It is now widely appreciated that remodeling is not just a manifestation of disease, but is an important mechanism of disease. Considering just the structural aspects of remodeling, it follows from Laplace's law (pressure
wall tension/radius) that even with normal myocardial force-generating capacity, chamber pumping strength decreases as chamber radius increases. Thus, many therapies are now evaluated on their ability to restore normal heart size and induce reverse remodeling. At least some of the benefits of angiotensin-converting enzyme inhibitors,2
ß-blockers,3
cardiac resynchronization therapy,4
and passive ventricular constraint5
are attributed to their ability to inhibit or reverse remodel the heart. However, for a vast majority of patients, the degree of reverse remodeling achieved with these standard approaches is limited.
For almost 50 years, various techniques have been developed for surgically correcting the dilated left ventricle that accompanies systolic heart failure.6-9
Surgical resection or exclusion of a section of the dilated chamber reduces chamber radius and by Laplace's law has been postulated to increase ventricular pressure- and flow-generating capability. Indeed, prior studies in patients with ischemic10
or idiopathic11,12
cardiomyopathies have shown that such surgical ventricular restoration (SVR) reduces chamber size and increases ejection fraction (EF), seemingly providing physiologic evidence of improved pump function.
However, when applied to patients with idiopathic cardiomyopathy (with a form of SVR commonly referred to as the Batista operation), clinical outcomes were poor despite the fact that these apparently beneficial physiologic effects were achieved.11,12
Many surviving patients continued to experience symptoms and there was a high rate of transplantation
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