Author + information
- Received September 15, 1995
- Revision received January 18, 1996
- Accepted March 12, 1996
- Published online August 1, 1996.
- Donna M. Mancini, MDa,*,
- John La Manca, PhDa,
- Lisa Donchez, RNa,
- David Henson, MD* and
- Sanford Levine, MD*
- ↵*Address for correspondence: Dr. Donna M. Mancini, Division of Cardiology, Columbia Presbyterian Medical Center, 622 West 168th Street, New York, New York 10032.
Objectives. The present study sought to investigate whether the work of breathing was reduced after heart transplantation. Accordingly, the tension time index of the diaphragm was measured in patients with heart failure and in transplant recipients.
Background. Patients with heart failure are frequently limited by exertional dyspnea that may be due to the increased work of breathing. After heart transplantation, exertional dyspnea is markedly diminished. Whether work of breathing is reduced in posttransplant recipients is unknown.
Methods. Nine patients with heart failure, six normal subjects and six heart transplant recipients were studied. Transdiaphragmatic pressure was measured throughout exercise. Accessory respiratory muscle oxygenation was assessed using near-infrared spectroscopy. Peak oxygen consumption, time in inspiration, time per breath and maximal inspiratory and expiratory pressures were measured in all subjects.
Results. The tension time index remained markedly abnormal after heart transplantation both at rest ([mean ± SD] normal group 0.01 ± 0.006, heart failure group 0.026 ± 0.018, transplant group 0.058 ± 0.015, p < 0.004) and at peak exercise (normal group 0.03 ± 0.02, heart failure group 0.10 ± 0.03, transplant group 0.10 ± 0.04, p < 0.0001). Accessory respiratory muscle deoxygenation was present only in patients with heart failure (near-infrared absorbency changes [arbitrary units]: normal group −3 ± 6, heart failure group 28 ± 5, transplant group −3.5 ± 4.4, p < 0.0001).
Conclusions. Although heart transplantation alleviates dyspnea in patients with heart failure, the work of breathing as assessed by the tension time index of the diaphragm is not decreased. Amelioration of exertional dyspnea is achieved by other mechanisms, such as improved respiratory muscle perfusion.
This study was supported by a Southeastern Pennsylvania American Heart Association Grant-in-Aid, Philadelphia, Pennsylvania.
- Received September 15, 1995.
- Revision received January 18, 1996.
- Accepted March 12, 1996.
- American College of Cardiology