Introduction: Obesity plays an important role in functional impairment, symptom severity and mortality in HFpEF. Prior studies suggest a protective effect of obesity on HFpEF outcomes up to a BMI of 35 kg/m2, above which clinical outcomes worsen. We investigated the effects of severe obesity (BMI > 35 kg/m2) on exercise performance and cardiorespiratory fitness (CRF) in HFpEF patients.
Methods: Thirty carefully screened, clinically stable HFpEF patients (12M,18F) were divided into 2 groups by BMI strata: LO (BMI < 35 kg/m2, n=16) and HI (BMI > 35 kg/m2, n=14). AV nodal blocking agents were held for 5 half-lives prior to exercise testing. Subjects performed a single 5 minute bout of sub-max exercise followed by incremental stages of treadmill exercise to peak VO2. Peak VO2, RER, Ve/VCO2 were measured using Douglas bags. Cardiac output (Qc) was measured by acetylene rebreathing methods.AVO2 difference was calculated from VO2 and Qc. Stroke volume (SV) reserve was defined as change in SV from rest to sub-max exercise.
Results: HFpEF patients in HI group were younger (67 vs 72 years; p=0.013) and heavier (108 vs 85 kg; p<0.001) compared to LO group. (Table) Both groups had similar degree of functional impairment (13.8 vs 12.7 ml/kg/min). CRF, assessed by absolute VO2, was higher in the HI group driven by larger peak Qc (14.6 vs 10.7 L/min; p<0.01). SV reserve was also significantly higher in the HI group (71 vs 48%; p<0.05). There was a trend towards lower Ve/VCO2, a measure of ventilatory inefficiency, in the HI group.
Conclusion: Despite higher body mass, HFpEF patients with severe obesity had similar functional capacity compared to patients with lower BMI. Absolute CRF was actually higher in severe obesity driven by larger Qc and SV reserve arguing against significant effect from obesity per se on cardiorespiratory dysfunction.