Low cardiorespiratory fitness (CRF) and obesity are significant risk factors for heart
failure (HF). However, given the inverse association between CRF and obesity, the
independent contributions of low CRF and adiposity toward HF risk are not well established.
We evaluated the association of CRF and measures of adiposity with left ventricular
(LV) peak systolic strain—a subclinical measure of LV dysfunction—among the Dallas
Heart Study phase II participants without cardiovascular disease who had CRF estimated
using a submaximal treadmill test and LV systolic circumferential strain assessment
by tissue-tagged cardiac magnetic resonance imaging. Peak midwall systolic circumferential
strain (Ecc) was determined by harmonic phase imaging. Associations of CRF and adiposity
measures with Ecc were determined using adjusted linear regression analysis. A total
of 1,617 participants were included in the analysis. After adjustment for baseline
risk factors, higher waist circumference (WC) and lower CRF were associated with higher
Ecc (WC: β = 0.07; p = 0.01; CRF: β = −0.17; p = < 0.0001), whereas % body fat and
body mass index were not associated with Ecc. The relationship between WC and Ecc
was attenuated completely after additional adjustment for CRF. In contrast, the association
between CRF and Ecc did not attenuate after additional adjustment for WC and other
measures of LV structure and function (β = −0.18; p = < 0.0001). Taken together, our
study findings suggest that lower CRF, but not measures of adiposity, is associated
with greater impairment in LV strain independent of LV mass and ejection fraction.
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Article Info
Publication History
Published online: July 25, 2017
Accepted:
July 10,
2017
Received:
December 8,
2016
Footnotes
Funding sources: Dr. Berry receives funding from (1) the Dedman Family Scholar in Clinical Care endowment at University of Texas Southwestern Medical Center , and (2) 14SFRN20740000 from the American Heart Association prevention network. Dr. Haykowsky is supported by the Moritz Chair in Geriatrics, College of Nursing and Health Innovation, University of Texas at Arlington , and the National Institute of Nursing Research of the National Institutes of Health R15NR016826 . Dr. Nelson is supported by 16SDG27260115 from the American Heart Association. IJN is supported by grant K23DK106520 from the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institute of Health and by the Dedman Family Scholarship in Clinical Care from UT Southwestern. The Dallas Heart Study was supported by a grant from the Reynolds Foundation and grant UL1TR001105 from the National Center for Advancing Translational Sciences of the National Institutes of Health .
See page 1409 for disclosure information.
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