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J Thorac Cardiovasc Surg 1998;116:344-349
© 1998 Mosby, Inc.
Cardiopulmonary Support and Physiology |
From the Divisions of Circulatory Physiologya and Cardiothoracic Surgery,c Columbia Presbyterian Medical Center, New York, N.Y., and the Department of Biochemistry/Biophysics, University of Pennsylvania,b Philadelphia, Pa.
Received for publication Jan. 27, 1998; Revisions requested March 16, 1998; Revisions received April 15, 1998; Accepted for publication April 22, 1998.
Address for reprints:
Donna M. Mancini, MD, Division of Circulatory Physiology, Department of Medicine, Columbia Presbyterian Medical Center, 622 West 168th St., New York, NY 10032.
Objectives: Mitochondrial abnormalities have been described in cardiac tissue of patients with heart failure. These changes may result from chronic hypoxia. Our goal was to determine whether mitochondrial functional capacity can be improved in patients with heart failure by means of long-term left ventricular assist device therapy, which improves myocardial oxygen supply by decreasing myocardial work.
Methods: Mitochondria were isolated from myocardial tissue obtained from 13 patients with heart failure without a left ventricular assist device (HF group) and seven patients with heart failure treated with a left ventricular assist device (LVAD-HF group). Mitochondrial respiratory rates (State 2, State 3, and State 4) were measured by means of polarographic techniques with reduced nicotinamide adenine dinucleotide–dependent (pyruvate/malate, 
-ketoglutarate, glutamate) and –independent (succinate) substrates. The respiratory control index of Chance (State 3/State 4) and Lardy (State 3/State 2) and phosphorus to oxygen ratios were determined.
Results: The respiratory control index of Chance was higher in LVAD-HF than in HF when using NADH-dependent substrates pyruvate/malate and -ketoglutarate (pyruvate/malate HF: 4.9 ± 1.0; LVAD-HF: 6.5 ± 1.5; -ketoglutarate HF: 8.5 ± 2.4; LVAD-HF: 11.8 ± 2.9; both p = 0.04). Similarly, the respiratory control index of Lardy was greater in the LVAD-HF than the HF group when -ketoglutarate and glutamate were used as substrates (-ketoglutarate HF: 7.8 ± 1.7; LVAD-HF: 9.9 ± 1.5; glutamate HF: 7.6 ± 2.2; LVAD-HF: 10.7 ± 2.1; both p = 0.04). The phosphorus to oxygen ratio was comparable for both groups using all substrates. No change in mitochondrial respiration was observed after left ventricular assist device therapy with the NADH-independent substrate, succinate.
Conclusion: Cardiomyocyte mitochondrial function is improved by long-term therapy with a left ventricular assist device. This improvement suggests that cardiomyocyte metabolic dysfunction in heart failure may be reversed with left ventricular assist device support.
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