Abstract 5884: Cardiovascular Reserve Function in Heart Failure with Preserved Ejection Fraction: Systolic versus Diastolic Determinants
Background Patients with heart failure and preserved ejection fraction (HFpEF) display impaired heart rate and vascular reserve with exercise, but it remains unknown to what extent systolic, diastolic, and ventricular-arterial (VA) coupling responses contribute.
Objectives To compare ventricular-vascular function at rest and during matched submaximal and peak exercise in patients with HFpEF and hypertension (HTN).
Methods Age/gender matched subjects with HFpEF (n=19) and HTN (n=14) underwent metabolic exercise testing with simultaneous echo-Doppler hemodynamic assessment. Load-independent contractility was assessed by peak power index (PWR/EDV), single beat end systolic elastance (Ees), and preload recruitable stroke work (PRSW). Afterload was determined by arterial elastance (Ea), VA interaction by the coupling ratio (Ea/Ees), and diastolic function was examined by echo-Doppler and tissue Doppler echo.
Results Diastolic function (E/E′ ratio, A′) was abnormal at rest in HFpEF, while other hemodynamics were similar (Table⇓). Exercise capacity was markedly reduced in HFpEF (peak VO2 12.8±2.9 vs 18.3±3.9 ml/kg*min, p<0.0001). The increase in contractility with exercise was blunted in HFpEF, both at matched low level and peak workloads. HFpEF displayed less vasodilation and abnormal VA coupling with exercise. Diastolic reserve was similar in HFpEF and HTN, but heart rate responses were lower in HFpEF (45±17 vs 66±15 bpm, p<0.002). Exercise capacity was significantly associated with contractile reserve (r=0.75, p<0.001), but not diastolic reserve (p=NS). The combination of heart rate and VA coupling reserve explained 85% of the variability in peak VO2 (p<0.0001).
Conclusions While diastolic dysfunction is present at rest, exercise capacity is limited more by impaired contractile and heart rate responses and abnormal VA coupling. Systolic reserve dysfunction contributes to exercise intolerance in HFpEF, and may provide a novel therapeutic target.