Abstract 3961: Peripheral Vascular Endothelial Function Remains Impaired in Heart Transplant Recipients
Background and Rationale: Individuals with heart failure (HF) have severely reduced peak aerobic power (VO2peak) and abnormal peripheral vascular endothelial function. Previous investigations have shown that heart transplantation (HTX) is associated with an improvement in VO2peak. However, the effect of HTX on peripheral vascular endothelial function has not been well studied.
Hypothesis: We tested the hypothesis that HTX recipients would have improved VO2peak but similar brachial artery endothelial function compared to clinically stable individuals with HF.
Methods: Forty-two HF (NYHA functional class I to III; age (mean±SD): 62±12 years; 76% men) and 31 HTX patients (age: 58±11 years; 77% men) were recruited for this investigation. VO2peak, peak heart rate, systolic blood pressure and rate pressure product were obtained during a symptom-limited cycle exercise test. Age-predicted VO2peak was calculated from regression equations for healthy sedentary men and women. Brachial artery endothelial function was measured using the flow-mediated dilation procedure.
Results: HTX patients had increased VO2peak (HTX: 1.7±0.6 vs. HF: 1.4±0.5 L·min-1, p=0.019; HTX: 20.6 ± 7.5 vs. HF: 16.4±5.8 ml·kg-1·min-1, p=0.011), and percent of age-predicted VO2peak (HTX: 70±22 vs. HF: 60±20%, p=0.044) compared to HF patients. HTX recipients had increased peak heart rate (HTX: 144±22 vs. HF: 112±30 bpm, p<0.001), systolic blood pressure (HTX: 174±26 vs. HF: 150±30 mmHg, p=0.001) and rate pressure product (HTX: 25±6 vs. HF: 17±6 bpm·mmHg·103, p<0.001) compared to individuals with HF. Endothelium-dependent (HF: 3.9±4.9 vs. HTX: 3.8±4.7%, p=0.995) and endothelium-independent vasodilation (HF: 12.7±8.0 vs. HTX: 11.6±6.5%, p=0.568) of the brachial artery were not different between the groups.
Conclusions: VO2peak is increased in HTX recipients compared to HF patients but it remains 30% lower in comparison to healthy sedentary individuals. Reduced VO2peak in HTX recipients may be secondary to abnormal peripheral vascular endothelial function that remains impaired following HTX. Interventions that improve endothelial function may play an important role in improving the reduced VO2peak in HTX recipients.