Pulmonary oxygen uptake and heart rate kinetics during the six-minute walk test in transplant recipients.

BACKGROUND: The effect of organ transplantation on arterial compliance, pulmonary oxygen uptake (VO2p) and heart rate kinetics during the 6-minute walk test (6-MWT) remains unknown. METHODS: Twenty-two thoracic (heart and/or lung) organ transplant recipients (TOTR, 51+/-12 years) and 30 abdominal (kidney, kidney-pancreas, or liver) organ transplant recipients (AOTR, 46+/-11 years) from the 2006 Canadian Transplant Games, and 37 healthy controls (HC) completed a 6-MWT. VO2p, heart rate kinetics, and arterial compliance were determined. RESULTS: The 6-MWT distance and highest VO2p were significantly lower in TOTR and AOTR versus HC. The highest 6-MWT heart rate was lower in TOTR (11%) and AOTR (13%) versus HC. VO2p kinetics were slower in TOTR (52+/-11 sec, P

Relation of etiology of heart failure (ischemic versus nonischemic) before transplantation to delayed pulmonary oxygen uptake kinetics after heart transplantation.

The effect that pretransplantation heart failure cause has on pulmonary oxygen uptake (VO2p) kinetics and peak aerobic power (VO2peak) in heart transplant recipients (HTRs) has not been studied. We examined VO2p kinetics and VO2peak in HTRs with previous ischemic heart failure (I-HTRs; n=16, mean age 64+/-6 years) or nonischemic heart failure (NI-HTRs; n=13, mean age 50+/-12 years). HTRs performed an incremental exercise (VO2peak) test and a constant work rate submaximal exercise (VO2p kinetics) test. A monoexponential model was used to determine the phase II VO2p time constant (tau). Phase II VO2p tau was slower in I-HTRs (49+/-10 seconds) than in NI-HTRs (34+/-10 seconds) (p<0.001). No significant difference was found between I-HTRs and NI-HTRs for VO2peak (19.0+/-6.4 vs 23.0+/-8.2 ml.kg-1.min-1, respectively), change in heart rate from rest to steady-state exercise (11+/-8 vs 9+/-9 beats.min-1, respectively), or peak exercise heart rate (140+/-22 vs 144+/-22 beats.min-1, respectively). In conclusion, the prolonged phase II VO2p tau in I-HTRs compared with NI-HTRs suggests that the magnitude of alteration in VO2p kinetics after heart transplantation may be dependent on previous heart failure cause.

Impaired pulmonary oxygen uptake kinetics and reduced peak aerobic power during small muscle mass exercise in heart transplant recipients.

We examined peak and reserve cardiovascular function and skeletal muscle oxygenation during unilateral knee extension (ULKE) exercise in five heart transplant recipients (HTR, mean +/- SE; age: 53 +/- 3 years; years posttransplant: 6 +/- 4) and five age- and body mass-matched healthy controls (CON). Pulmonary oxygen uptake (Vo(2)(p)), heart rate (HR), stroke volume (SV), cardiac output (Q), and skeletal muscle deoxygenation (HHb) kinetics were assessed during moderate-intensity ULKE exercise. Peak exercise and reserve Vo(2)(p), Q, and systemic arterial-venous oxygen difference (a-vO(2diff)) were 23-52% lower (P < 0.05) in HTR. The reduced Q and a-vO(2diff) reserves were associated with lower HR and HHb reserves, respectively. The phase II Vo(2)(p) time delay was greater (HTR: 38 +/- 2 vs. CON: 25 +/- 1 s, P < 0.05), while time constants for phase II Vo(2)(p) (HTR: 54 +/- 8 vs. CON: 31 +/- 3 s), Q (HTR: 66 +/- 8 vs. CON: 28 +/- 4 s), and HHb (HTR: 27 +/- 5 vs. CON: 13 +/- 3 s) were significantly slower in HTR. The HR half-time was slower in HTR (113 +/- 21 s) vs. CON (21 +/- 2 s, P < 0.05); however, no significant difference was found between groups for SV kinetics (HTR: 39 +/- 8 s vs. CON 31 +/- 6 s). The lower peak Vo(2)(p) and prolonged Vo(2)(p) kinetics in HTR were secondary to impairments in both cardiovascular and skeletal muscle function that result in reduced oxygen delivery and utilization by the active muscles.

Impaired arterial compliance and aerobic endurance in kidney transplant recipients.

BACKGROUND: Cardiovascular disease is the leading cause of morbidity and mortality in kidney transplant recipients (KTR). Two risk factors for cardiovascular disease that have not been examined in this population are arterial compliance and aerobic capacity. The primary objective was to determine small and large artery compliance and aerobic endurance in KTR. A secondary objective was to explore the relationship between aging and arterial compliance and aerobic endurance in KTR. METHODS: Sixty-two clinically stable KTR were recruited from the University of Alberta Renal Transplant Clinic. Small and large artery compliance was assessed using computerized arterial pulse waveform analysis. Aerobic endurance was determined using the six-minute walk test. Age-matched normative data from healthy individuals was used for comparison. RESULTS: Small arterial compliance was lower in KTR (5.5+/-3 ml/mm Hg x 100) compared to age-matched healthy individuals' predicted values (7.9+/-0.9 ml/mm Hg x 100, P<0.0001). No difference was found for large artery compliance between KTR (16.0+/-6.6 ml/mm Hg x 10) and age-matched healthy predicted values (15.2+/-1.3 ml/mm Hg x 10, P=0.5). Small and large artery compliance were 35% (P=0.026) and 36% (P=0.005) higher in younger (<51 years) versus older (>51 years) KTR, respectively. The six-minute walk distance was 28% lower in KTR (495+/-92 m) compared to healthy age-predicted values (692+/-56 m P<0.0001). CONCLUSIONS: Compromised arterial compliance and poor aerobic endurance may partially explain the high incidence of cardiovascular disease in KTR. Interventions demonstrated to improve these parameters may afford substantial clinical benefit in this population.