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Ann Thorac Surg 2002;73:1216-1221
© 2002 The Society of Thoracic Surgeons

Original article: cardiovascular

Disease-specific remodeling of cardiac mitochondria after a left ventricular assist device

Paul M. Heerdt, MD, PhD*a,b,e, Michael Schlame, MDa,d, Roswitha Jehle, MDa,d, Alessandro Barbone, MDf, Daniel Burkhoff, MD, PhDf, Thomas J.J. Blanck, MD, PhDa,c,d

a Department of Anesthesiology, Weill Medical College at Cornell University and the Hospital for Special Surgery, New York, New York, USA
b Department of Pharmacology, Weill Medical College at Cornell University and the Hospital for Special Surgery, New York, New York, USA
c Department of Physiology and Biophysics, Weill Medical College at Cornell University and the Hospital for Special Surgery New York, New York, USA
d Department of Anesthesiology, Memorial Sloan-Kettering Cancer Center, New York, New York, USA
e Department of Critical Care Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York, USA
f Department of Medicine, Columbia University New York, New York, USA

Accepted for publication November 19, 2001.

* Address reprint requests to Dr Heerdt, 525 East 68th St, Lasdon 2, Box 50, New York, NY 10021 USA
e-mail: pmheerd{at}mail.med.cornell.edu

Background. Failing hearts can exhibit elements of structural and molecular "reverse remodeling" after support with a left ventricular assist device (LVAD). The present study examined LVAD-induced remodeling of cardiac mitochondria.

Methods. Left ventricular tissue from 20 failing and 21 LVAD-supported hearts, catagorized as ischemic (ICM) or dilated (DCM) cardiomyopathy and four nonfailing hearts were studied. Myocyte mitochondrial ultrastructure was assessed by high-performance liquid chromatography determination of cardiolipin, a specific lipid component of the inner membrane, and its three major molecular species: L4, L3O, and L2O2.

Results. Both failing and LVAD-supported hearts exhibited a reduction in cardiolipin content that was independent of the type of cardiomyopathy. However, in failing/ICM hearts, there was a 25% increase in the L4/L3O ratio and a 70% increase in the L4/L2O2 ratio, indicating a change in cardiolipin composition. These alterations were normalized by LVAD support. In sharp contrast, molecular species ratios in DCM hearts were the same as those in nonfailing hearts regardless of whether LVAD support had been used or not.

Conclusions. These data demonstrate LVAD-induced reverse remodeling of myocyte cardiolipin composition in ICM but not DCM hearts.




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