Predictors of exercise capacity and the impact of angiographic coronary artery disease in heart transplant recipients.
BACKGROUND
Maximal exercise capacity is limited in patients after heart transplantation. The extent to which transplant coronary artery disease contributes to exercise intolerance in these patients has not been well defined.


METHODS
This prospective study examined exercise capacity among 174 heart transplant recipients who underwent 358 exercise tests 0.3 to 13 years after surgery. Data were collected as part of routine posttransplantation treatment that each year consist of clinical and hemodynamic measurements (including ejection fraction, cardiac index, pulmonary capillary wedge pressure, and the presence of coronary artery disease) and cardiopulmonary exercise test (including measures of peak VO2). The mean follow-up was 3.5 +/- 0.2 years after transplantation. Serial exercise test data were available in 102 patients


RESULTS
Peak VO2 was 19.4 +/- 0.4 mL/kg per minute, representing 70% +/- 1.3% of the age-predicted value. Exercise capacity increased significantly after transplantation and then remained stable throughout long-term follow-up. Only age, maximal systolic blood pressure, pulmonary vascular resistance, and body mass index were independent determinants of exercise capacity (R2 = 0.51), whereas specific transplant factors such as denervation, hemodynamic variables, donor characteristics, immunosuppressive drugs, biochemical parameters, and transplant coronary artery disease (TxCAD) did not contribute to the explanation of reduced exercise capacity. Although TxCAD was not related to exercise capacity in the multivariate analysis, exercise capacity declined by 17.1% (P <.05) among those in whom CAD developed during follow-up.


CONCLUSIONS
Exercise capacity is reduced among heart transplant recipients, and age is the strongest determinant of aerobic performance. Specific transplant-related factors, including TxCAD, do not contribute significantly to the explanation of exercise capacity. However, the occurrence of TxCAD may contribute to reduced exercise capacity during follow-up, since peak VO2 appears to decline only among those who have TxCAD.
Gullestad
Lars
L
Department of Cardiology, Division of Heart and Lung Diseases, Rikshospitalet, Oslo, Norway. lars.gullestad@broadpark.no
Myers
Jonathan
J
Edvardsen
Thor
T
Kjekshus
John
J
Geiran
Odd
O
Simonsen
Svein
S
D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D005080:Exercise Test; D017079:Exercise Tolerance / Q000502:physiology*; D005260:Female; D005500:Follow-Up Studies; D016027:Heart Transplantation / Q000009:adverse effects / Q000502:physiology*; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011659:Pulmonary Gas Exchange