Author + information
- Received August 1, 2016
- Revision received October 25, 2016
- Accepted November 2, 2016
- Published online April 24, 2017.
- Ambarish Pandey, MDa,
- Norrina B. Allen, PhDb,
- Colby Ayers, MSc,
- Jared P. Reis, PhDd,
- Henrique T. Moreira, MD, PhDe,
- Stephen Sidney, MD, MPHf,
- Jamal S. Rana, MD, PhDf,g,h,
- David R. Jacobs Jr., PhDi,
- Lisa S. Chow, MDj,
- James A. de Lemos, MDa,
- Mercedes Carnethon, PhDb and
- Jarett D. Berry, MD, MSa,b,∗ ()
- aDivision of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas
- bDepartment of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois
- cDepartment of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas
- dDivision of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, Maryland
- eCardiovascular Department, Johns Hopkins University School of Medicine, Baltimore, Maryland
- fDivision of Research, Kaiser Permanente Northern California, Oakland, California
- gDivision of Cardiology, Kaiser Permanente Northern California, Oakland
- hDepartment of Medicine, University of California, San Francisco, California
- iDivision of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota
- jDepartment of Medicine, Division of Diabetes, Endocrinology, and Metabolism, University of Minnesota, Minneapolis, Minnesota
- ↵∗Address for correspondence:
Dr. Jarett D. Berry, Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390.
Objectives This study sought to evaluate the association between early-life cardiorespiratory fitness (CRF) and measures of left ventricular (LV) structure and function in midlife.
Background Low CRF in midlife is associated with a higher risk of heart failure. However, the unique contributions of early-life CRF toward measures of LV structure and function in middle age are not known.
Methods CARDIA (Coronary Artery Risk Development in Young Adults) study participants with a baseline maximal treadmill test and an echocardiogram at year 25 were included. Associations among baseline CRF, CRF change, and echocardiographic LV parameters (global longitudinal strain [GLS] and global circumferential strain, E/e′) were assessed using multivariable linear regression.
Results The study included 3,433 participants. After adjustment for baseline demographic and clinical characteristics, lower baseline CRF was significantly associated with higher LV strain (standardized parameter estimate [Std β] = −0.06; p = 0.03 for GLS) and ratio of early transmitral flow velocity to early peak diastolic mitral annular velocity (E/e′) (Std β = −0.10; p = 0.0001 for lateral E/e′), findings suggesting impaired contractility and elevated diastolic filling pressure in midlife. After additional adjustment for cumulative cardiovascular risk factor burden observed over the follow-up period, the association of CRF with LV strain attenuated substantially (p = 0.36), whereas the association with diastolic filling pressure remained significant (Std β = −0.05; p = 0.02 for lateral E/e′). In a subgroup of participants with repeat CRF tests at year 20, greater decline in CRF was significantly associated with increased abnormalities in GLS (Std β = −0.05; p = 0.02) and higher diastolic filling pressure (Std β = −0.06; p = 0.006 for lateral E/e′) in middle age.
Conclusions CRF in young adulthood and CRF change were associated with measures of LV systolic function and diastolic filling pressure in middle age. Low CRF–associated abnormalities in systolic function were related to the associated higher cardiovascular risk factor burden. In contrast, the inverse association between CRF and LV diastolic filling pressure was independent of cardiovascular risk factor burden.
This project was funded by the Strategically Focused Research Network Grant for Prevention from the American Heart Association to University of Texas Southwestern Medical Center, Dallas and Northwestern University School of Medicine, Chicago. Dr. Berry has received funding from the Dedman Family Scholar in Clinical Care endowment at the University of Texas Southwestern Medical Center and from grant 14SFRN20740000 from the American Heart Association prevention network. Dr. Allen has received a research grant from Novartis. Dr. Rana has received a research grant from Regeneron/Sanofi. Dr. Chow has received research support from Eli Lilly. CARDIA (Coronary Artery Risk Development in Young Adults) is conducted and supported by the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with the University of Alabama at Birmingham (HHSN268201300025C and HHSN268201300026C), Northwestern University (HHSN268201300027C), University of Minnesota (HHSN268201300028C), Kaiser Foundation Research Institute (HHSN268201300029C), and Johns Hopkins University School of Medicine (HHSN268200900041C). CARDIA is also partially supported by the Intramural Research Program of the National Institute on Aging (NIA) and an intra-agency agreement between NIA and the NHLBI (AG0005). This manuscript has been reviewed by CARDIA for scientific content.
The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received August 1, 2016.
- Revision received October 25, 2016.
- Accepted November 2, 2016.