Abstract 2372: Heart Failure With Preserved Ejection Fraction: Do Abnormalities in Oxygen Utilization Contribute to Exercise Intolerance?
Background: Peak oxygen uptake (peak VO2) is depressed in patients with heart failure with preserved ejection fraction (HFpEF) suggesting that cardiac reserve is impaired. To test this hypothesis, we assessed the hemodynamic response to exercise in patients with HFpEF.
Methods: Eleven highly screened, elderly patients with HFpEF and 13 healthy, elderly controls were enrolled. Cardiopulmonary stress testing was performed. Cardiac output (Qc) was measured using the acetylene rebreathing technique. The cardiac output response to exercise was determined from a linear regression of the Qc and VO2 at four points: steady state exercise at rest, ~30% of peak VO2, ~60% of peak VO2 and maximal exercise. Cardiac power output [CPO=Qc*MAP] and stroke work index [SWI=SV*MAP/BSA] were calculated. 31P magnetic resonance spectroscopy of the thigh muscle was performed on one HFpEF subject and one control using a 1.5T Siemens scanner. Beta blockers were generally held for testing.
Results: The groups were well matched for age and gender (HFpEF=73 +/− 7 yrs, 7F/4M vs. control=70 +/− 4 yrs, 6F/7M; p=0.212). Normalized peak VO2 was lower in HFpEF patients when compared to controls (HFpEF=13.7±3.4 vs. control=21.6±3.6 ml/kg/min; p<0.001). However, the peak cardiac power output (HFpEF±1790 +/− 509 vs. control=2701 +/− 1139 L*mmHg/min; p=0.164) and peak stroke work index (HFpEF=6762 +/− 767 vs. control=7071 +/− 1497 mL*mmHg/m^2; p=0.56) were similar between groups. Unexpectedly, the cardiac output response to exercise was abnormally elevated in HFpEF patients when compared to controls (HFpEF=11.2±3.6 vs. control=8.3±1.5 L/L; p=0.015). This pattern is seen in patients with abnormalities in oxidative phosphorylation. 31P-MRS supported this observation, as phosphocreatine recovery and ADP recovery time were impaired in the HFpEF subject.
Conclusions: Contrary to our hypothesis, cardiac reserve was not impaired in HFpEF. The combination of the depressed peak VO2 and abnormally elevated cardiac output response to exercise suggests that an abnormality in oxygen utilization is present in HFpEF which may contribute to the limitations in functional capacity associated with this condition. These findings were supported by 31P-MRS. Additional investigation is warranted.