• J. Am. Coll. Cardiol. · Aug 1996

    The sensation of dyspnea during exercise is not determined by the work of breathing in patients with heart failure.

    • D M Mancini, J La Manca, L Donchez, D Henson, and S Levine.
    • Division of Cardiology, Columbia Presbyterian Medical Center, New York 10032, USA.
    • J. Am. Coll. Cardiol. 1996 Aug 1; 28 (2): 391-5.

    ObjectivesThe 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.BackgroundPatients 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.MethodsNine 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.ResultsThe 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).ConclusionsAlthough 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.

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