Abstract 18928: Post-Exercise Recovery VO2 Plateau Duration: A Novel Index of Impaired Hemodynamic Response to Exercise in Heart Failure
Introduction: Exercise intolerance, as quantified by degree of impairment in peak oxygen uptake (VO2), is a cardinal manifestation of heart failure (HF). HF patients are known to have delayed VO2 kinetics during recovery. However, it is unknown to what extent easily-discernible patterns of VO2 recovery kinetics reflect circulatory response during exercise.
Hypothesis: Delayed VO2 kinetics, as indicated by the duration of recovery VO2 plateau (RecVO2P), will indicate severity of impairment in cardiac output (CO) augmentation during exercise.
Methods: Recovery O2 kinetics were measured in 52 patients referred for cardiopulmonary exercise testing (CPET) with invasive hemodynamic monitoring (n=16 normal controls, n=18 HFpEF with resting pulmonary arterial wedge pressure, PAWP≥15, and n=18 HFrEF with LVEF <0.45 and NYHA Class II-IV). Delay in O2 recovery kinetics was calculated as time until O2 uptake fell permanently below peak VO2 (highest 30s median within final min of exercise, see Figure) as well as the time to reach 50% of peak VO2 during recovery (T1/2). Fick COs and cardiac filling pressures were measured at rest and during each minute of exercise (n=570 paired measurements).
Results: Patients with HFrEF and HFpEF demonstrated RecVO2P durations in excess of controls (Figure). In the combined HF groups, RecVO2P was inversely related to CO augmentation during exercise (r=-0.74, p<0.001) and this relationship persisted after adjustment for age, sex, BMI, and LVEF. RecVO2P was also related to excursions in PAWP and mean pulmonary arterial pressure indexed to CO during exercise (r=0.35, r=0.51, respectively, both p<0.04). RecVO2P>24sec signaled severe impairment in exercise hemodynamic response (Figure).
Conclusions: An easily recognizable non-invasively derived recovery VO2 plateau pattern is an indicator of impaired circulatory response to exercise in HF that may complement exercise gas exchange measurements for assessment of cardiac reserve capacity.
Author Disclosures: C. Bailey: None. L. Wooster: None. A.S. Eisman: None. C. White: None. A. Ryfa: None. P.P. Pappagianopoulos: None. K. Bakken: None. C. Hardin: None. R. Malhotra: None. G.D. Lewis: Other Research Support; Significant; Abbott Vascular, Novartis, Stealth, Shape Systems. Consultant/Advisory Board; Significant; Sonivie.
- © 2016 by American Heart Association, Inc.