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J Thorac Cardiovasc Surg 2001;121:902-908
© 2001 The American Association for Thoracic Surgery


Surgery for Acquired Cardiovascular Disease

Time course of reverse remodeling of the left ventricle during support with a left ventricular assist device

John D. Madigan, BAb, Alessandro Barbone, MDb, Asim F. Choudhri, BSb, David L. S. Morales, MDb, Bolin Cai, MDa, Mehmet C. Oz, MDb, Daniel Burkhoff, MD, PhDa

From the Departments of Medicinea and Surgery,b Columbia University, New York, NY.

Received for publication March 15, 2000. Revisions requested April 12, 2000; revisions received Oct 26, 2000. Accepted for publication Oct 31, 2000. Address for reprints: John D. Madigan, c/o Daniel Burkhoff, Columbia University, Department of Medicine, Black Building 812, 650 West 168th St, New York, NY 10032 (E-mail: jdm50{at}columbia.edu).

Background: Support with a left ventricular assist device leads to normalization of left ventricular chamber geometry, regression of myocyte hypertrophy, alterations in left ventricular collagen content, and normalized expression of genes involved with excitation-contraction coupling in patients with heart failure. The objective of this study was to investigate the time course of these processes.
Methods: Passive left ventricular pressure-volume relationships were obtained from explanted hearts of 19 patients with heart failure undergoing transplantation without left ventricular assist device support, 25 patients with heart failure supported before transplantation (duration of support ranging between 8 and 155 days), and 5 normal human hearts not suitable for transplantation. Left ventricular size was indexed by the volume at which left ventricular pressure reached 30 mm Hg. Left ventricular tissue samples were probed for sarcoplasmic endoreticular calcium adenosine triphosphatase 2a expression and processed for analysis of myocyte diameter and relative myocardial collagen content.
Results: The volume at which left ventricular pressure reached 30 mm Hg was not significantly different between hearts without and with assist device support for less than 40 days. However, the volume at which left ventricular pressure reached 30 mm Hg in patients with assist devices supported for more than 40 days was significantly smaller than that of the hearts without assist devices but was larger than that of normal hearts. A similar pattern was observed for myocyte diameter. Sarcoplasmic endoreticular calcium adenosine triphosphatase 2a expression increased to normal levels by about 20 days of support with an assist device. Relative collagen content was significantly increased in hearts supported for more than 40 days.
Conclusion: Maximum structural reverse remodeling by left ventricular assist devices is complete by about 40 days. Molecular reverse remodeling of sarcoplasmic endoreticular calcium adenosine triphosphatase 2a expression is quicker, being complete by about 20 days.




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