Author + information
- Received February 9, 2017
- Revision received October 6, 2017
- Accepted October 12, 2017
- Published online February 14, 2018.
- Julian W. Sacre, PhDa,∗ (, )
- Chiew Wong, MD, PhDb,c,
- Yih-Kai Chan, PhDd,
- Melinda J. Carrington, PhDa,d,
- Simon Stewart, PhDa,d and
- Bronwyn A. Kingwell, PhDa
- aBaker Heart & Diabetes Institute, Melbourne, Australia
- bUniversity of Melbourne (Western Clinical School), Melbourne, Australia
- cDepartment of Cardiology—Western Health, The University of Melbourne, Melbourne, Australia
- dMary MacKillop Institute for Health Research, Australian Catholic University, Melbourne, Australia
- ↵∗Address for correspondence:
Dr. Julian W. Sacre, Baker Heart and Diabetes Institute, Level 4, 99 Commercial Road, Melbourne VIC 3004, Australia.
Objectives This study aimed to determine the association of stage B heart failure (SBHF) and its constituent left ventricular (LV) abnormalities with trajectory of exercise capacity over time, and assess whether this association is modified by reversion of these LV abnormalities to normal.
Background The LV abnormalities of SBHF may coincide with a reduction in exercise capacity that precedes the overt exercise intolerance of clinical heart failure (HF). Determining the predictive capacity of established and novel SBHF criteria for exercise capacity decline may improve HF risk stratification.
Methods LV structure/function (echocardiography) and exercise capacity (6-minute walk distance [6MWD]) were assessed at baseline and 3-year follow-up in 268 patients from the NIL-CHF (Nurse-led Intervention for Less Chronic Heart Failure) study (all stage A [SAHF] or SBHF). Changes (Δ) in 6MWD were compared between SAHF and SBHF and across each of 4 constituent components of SBHF: LV hypertrophy, regional wall motion abnormality(ies) (RWMA), left ventricular systolic dysfunction (LVSD) (ejection fraction <45%) and elevated early diastolic filling/annular velocity ratio (E/e’ ≥ 15).
Results Δ6MWD was similar in those with SAHF (n = 141) and SBHF (n = 127; –5 m [95% confidence interval (CI): −21 to +11 m]; covariate-adjusted). However, within the setting of SBHF there was substantive heterogeneity; that is, reductions in 6MWD were observed with persistent elevated E/e’ (−34 m [95% CI: −62 to −6 m]) and persistent LVSD (−41 m [95% CI: −74 to −8 m]), but not with LV hypertrophy (+17 m [95% CI: −15 to +49 m) or RWMA (+5 m [−27 to +36 m]), nor in patients whose elevated E/e’ or LVSD reverted to normal by 3 years (p > 0.10).
Conclusions Elevated E/e’ is associated with a similar degree of exercise capacity decline to LVSD, supporting that both LV functional criteria be considered in distinguishing SBHF from SAHF. That reversion of either manifestation of LV dysfunction was associated with preserved exercise capacity advocates targeting of these factors by HF preventive interventions.
The NIL-CHF study was supported by a National Health and Medical Research Council (NHMRC) Project Grant (#472662). The study was also supported in part by the Victorian Government’s Operational Infrastructure Support Program. Drs. Sacre, Stewart, and Kingwell are all supported by NHMRC Fellowships. Dr. Carrington is supported by a Future Leader Fellowship (Award Reference 100802) from the National Heart Foundation of Australia and previously throughout the duration of the NIL-CHF project, a NHMRC Fellowship. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received February 9, 2017.
- Revision received October 6, 2017.
- Accepted October 12, 2017.
- 2018 American College of Cardiology Foundation
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