BASIS FOR AEROBIC IMPAIRMENT IN PATIENTS AFTER HEART-TRANSPLANTATION

Citation
Lm. Bussieres et al., BASIS FOR AEROBIC IMPAIRMENT IN PATIENTS AFTER HEART-TRANSPLANTATION, The Journal of heart and lung transplantation, 14(6), 1995, pp. 1073-1080
Citations number
44
Categorie Soggetti
Cardiac & Cardiovascular System",Transplantation
ISSN journal
10532498
Volume
14
Issue
6
Year of publication
1995
Part
1
Pages
1073 - 1080
Database
ISI
SICI code
1053-2498(1995)14:6<1073:BFAIIP>2.0.ZU;2-D
Abstract
Background and Methods: To evaluate the physiologic basis for the subo ptimal peak oxygen uptake observed after heart transplantation, we cal culated the functional aerobic impairment ([(peak predicted oxygen upt ake - peak observed oxygen uptake)/peak predicted oxygen uptake] x 100 ) and related it to donor/recipient, operative, and maximal exercise v ariables. Fifty-seven heart transplant recipients (mean age 50 +/- 10 years: 1 to 9 years after transplantation) underwent maximal upright c ycle exercise testing. Concomitant exercise central hemodynamic measur ements were obtained in 36 patients (63%). Results: The mean peak oxyg en uptake was 21.7 +/- 6.5 ml/kg/min and functional aerobic impairment was 34% +/- 17%. Functional aerobic impairment correlated positively (p < 0.01) with peak systemic vascular resistance (r = 0.55) and negat ively with peak cardiac index (r = -0.62) and peak systemic arterioven ous oxygen difference (r = -0.66). A weak correlation was found betwee n functional aerobic impairment and the duration of cardiac disease (r = 0.35, p < 0.01) but not the origin of heart failure. No correlation was seen between functional aerobic impairment and donor age, total i schemic time, time since transplantation, recipient age, and resting a nd exercise right and left ventricular filling pressures. Conclusions: These results suggest that the decreased exercise capacity observed i n heart transplant recipients is in part due to increased peripheral v ascular resistance and decreased oxygen extraction possibly due to ske letal muscle atrophy. These factors may be the result of irreversible changes from long-standing heart disease, deconditioning, or the effec t of cyclosporine and prednisone.