JACC: Heart Failure
Post-Exercise Oxygen Uptake Recovery DelayA Novel Index of Impaired Cardiac Reserve Capacity in Heart Failure
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Author + information
- Cole S. Bailey, BAa,
- Luke T. Wooster, BSa,
- Mary Buswell, BSa,
- Sarvagna Patel, BSa,
- Paul P. Pappagianopoulos, MEdb,
- Kristian Bakken, NPb,
- Casey White, BSb,
- Melissa Tanguay, MS, CEPa,
- Jasmine B. Blodgett, MS, CEPa,
- Aaron L. Baggish, MDa,
- Rajeev Malhotra, MDa and
- Gregory D. Lewis, MDa,b,∗ (glewis{at}partners.org)
- aCardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- bPulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- ↵∗Address for correspondence:
Dr. Gregory D. Lewis, Cardiopulmonary Exercise Laboratory, Heart Failure/Cardiac Transplantation, Massachusetts General Hospital, Gray Bigelow 8th Floor, 55 Fruit Street, Boston, Massachusetts 02114.
Graphical abstract
Abstract
Objectives This study sought to characterize the functional and prognostic significance of oxygen uptake (VO2) kinetics following peak exercise in individuals with heart failure (HF).
Background It is unknown to what extent patterns of VO2 recovery following exercise reflect circulatory response during exercise in HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF).
Methods We investigated patients (30 HFpEF, 20 HFrEF, and 22 control subjects) who underwent cardiopulmonary exercise testing with invasive hemodynamic monitoring and a second distinct HF cohort (n = 106) who underwent noninvasive cardiopulmonary exercise testing with assessment of long-term outcomes. Fick cardiac output (CO) and cardiac filling pressures were measured at rest and throughout exercise in the initial cohort. A novel metric, VO2 recovery delay (VO2RD), defined as time until post-exercise VO2 falls permanently below peak VO2, was measured to characterize VO2 recovery kinetics.
Results VO2RD in patients with HFpEF (median 25 s [interquartile range (IQR): 9 to 39 s]) and HFrEF (28 s [IQR: 2 to 52 s]) was in excess of control subjects (5 s [IQR: 0 to 7 s]; p < 0.0001 and p = 0.003, respectively). VO2RD was inversely related to cardiac output augmentation during exercise in HFpEF (ρ = −0.70) and HFrEF (ρ = −0.73, both p < 0.001). In the second cohort, VO2RD predicted transplant-free survival in univariate and multivariable Cox regression analysis (Cox hazard ratios: 1.49 and 1.37 per 10-s increase in VO2RD, respectively; both p < 0.005).
Conclusions Post-exercise VO2RD is an easily recognizable, noninvasively derived pattern that signals impaired cardiac output augmentation during exercise and predicts outcomes in HF. The presence and duration of VO2RD may complement established exercise measurements for assessment of cardiac reserve capacity.
Footnotes
Support was obtained from the National Institutes of Health (5R01HL131029 to Dr. Lewis) (K08HL111210 to Dr. Malhotral), the American Heart Association (15GPSGC24800006 to Dr. Lewis), and the Hassenfeld Clinical Scholars Program (Mr. Bailey, Mr. Wooster, Dr. Malhotra, and Dr. Lewis). Dr. Malhotra is a consultant for MyoKardia and Third Pole; and received grant support from the National Heart, Lung, and Blood Institute. Dr. Lewis has received contractual funding support for cardiopulmonary exercise testing core laboratory services from the NHLBI, Abbott Vascular, Ironwood, and Stealth Therapeutics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Mr. Bailey and Wooster contributed equally to this paper and are joint first authors. Drs. Malhotra and Lewis contributed equally to this paper and are joint senior authors.
- Received December 17, 2017.
- Accepted January 4, 2018.
- 2018 American College of Cardiology Foundation
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