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Ann Thorac Surg 2001;71:S185-S187
© 2001 The Society of Thoracic Surgeons

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Soap box symposium

Passive ventricular constraint for the treatment of congestive heart failure

^a Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, New York, USA

Address reprint requests to Dr Oz, Milstein 7-435, 177 Fort Washington Ave, New York, NY 10032
e-mail: mco2@columbia.edu

Presented at the Fifth International Conference on Circulatory Support Devices for Severe Cardiac Failure, New York, NY, Sept 15–17, 2000.

The underlying etiology of congestive heart failure may entail structural, biochemical, or physiological abnormalities. Regardless of the initiating insult, the heart compensates with a number of acute adaptive mechanisms to maintain adequate cardiac output [1]. Such adaptive mechanisms include cardiac dilation and activation of neurohormonal adjustments to maintain arterial pressure and perfusion of vital organs [2]. The chronic effect of these compensatory changes results in structural and functional changes to the heart, known as "remodeling" [3], that become a hallmark in the progression of heart failure.

Several factors can stimulate the remodeling process, including neurohormonal activation and mechanical stress. The compensatory ventricular dilation increases biomechanical wall stress and creates stretch of the cardiac myocytes [4]. Such stretch induces maladaptive changes in gene expression and stimulation of autocrine/paracrine neurohormonal activity, with adverse effects on the extracellular matrix and promotion of myocyte apoptosis [1, 5, 6]. Once begun, the remodeling process is auto-inductive, leading to further remodeling and progression of ventricular dysfunction and, baring intervention, inexorably to end-stage heart failure.

One surgical means of intervention is represented by the Acorn Cardiac Support Device (CSD), a mesh-like implantable device that is surgically positioned around the heart and adjusted to provide circumferential diastolic support. The CSD is intended to reduce wall stress and myocyte stretch during end-diastole and periodic hemodynamic overload conditions. By reducing or limiting the stress and stretch on the myocardium, a key component of the remodeling process may be halted or reversed.

Device and implantation/implant procedures

The CSD is made from a mesh-like polyester . . . [Full Text of this Article]

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