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Clinical Investigations: DYSPNEA |

Relationship Between Impaired Pulmonary Diffusion and Cardiopulmonary Exercise Capacity After Heart Transplantation*

Ralf Ewert, MD; Roland Wensel, MD; Leonhard Bruch, MD; Sven Mutze, MD; Ulrike Bauer, MD; Mathias Plauth, MD; Franz-Xaver Kleber, MD
Author and Funding Information

*From the Deutsches Herzzentrum Berlin (Drs. Ewert, Wensel, and Bauer), Klinik für Innere Medizin (Drs. Bruch and Kleber), and Institut für Radiologie (Dr. Mutze), Unfallkrankenhaus Berlin, and IV. Medizinische Klinik (Dr. Plauth), Klinikum Charité, Humboldt Universität zu Berlin, Germany.

Correspondence to: Ralf Ewert, MD, Deutsches Herzzentrum Berlin, Augustenburger Platz 1, 13 353 Berlin, Germany; e-mail: rewert@dhzb.de



Chest. 2000;117(4):968-975. doi:10.1378/chest.117.4.968
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Study objectives: Diffusion impairment and reduced performance in cardiopulmonary exercise testing (CPX) have been found in patients after heart transplantation. The pathogenesis of these abnormalities is unclear. In particular, the contribution of pulmonary interstitial changes has not yet been verified.

Design: We analyzed pulmonary function tests, high-resolution CT (HRCT), echocardiography, left heart catheterization, and CPX in transplanted patients.

Patients: Forty long-term survivors were studied at a median of 47 months (range, 12 to 89 months) after heart transplantation.

Results: Diffusion was impaired in 40% (transfer factor for carbon monoxide) or 82.5% (carbon monoxide transfer coefficient) of the patients. Diffusion impairment was caused by a decreased diffusing capacity of the alveolar capillary membrane in 89% and/or by a decreased blood volume of the alveolar capillaries in 46% of cases. In five patients (12.5%), CT revealed interstitial lung changes. These patients did not have different values of diffusion capacity. Maximal oxygen uptake and ventilatory efficiency during exercise (minute ventilation/carbon dioxide output slope) were impaired in 92% and 46% of the cases, respectively.

Conclusions: Our data show that the diffusion abnormalities are caused by an impaired diffusion status of the alveolar capillary membrane. Interstitial changes detectable in HRCT were found not to be involved in this process. The reduced performance in CPX in our long-term survivors is caused by pulmonary perfusion abnormalities and low tidal volume, which is due to the deconditioning of respiratory muscle, rather than by interstitial changes or diffusion abnormalities.


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