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Am J Physiol Heart Circ Physiol 292: H1427-H1434, 2007. First published November 3, 2006; doi:10.1152/ajpheart.00567.2006
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Leg flow-mediated arterial dilation in elderly patients with heart failure and normal left ventricular ejection fraction

W. Gregory Hundley,1,2,4 Ersin Bayram,2 Craig A. Hamilton,2 Eric A. Hamilton,2 Timothy M. Morgan,3 Stephen N. Darty,1 Kathryn P. Stewart,1 Kerry M. Link,4 David M. Herrington,1,3 and Dalane W. Kitzman1

Departments of 1Internal Medicine (Cardiology Section), 2Biomedical Engineering, 4Radiology, and 3Public Health Sciences, The Wake Forest University School of Medicine, Winston-Salem, North Carolina

Submitted 1 June 2006 ; accepted in final form 23 October 2006

Background: flow-mediated arterial dilation (FMAD), an indicator of endothelial function, is reduced in patients with heart failure and reduced left ventricular ejection fraction (HFREF). Many elderly patients with heart failure exhibit a normal left ventricular ejection fraction (HFNEF). It is unknown whether FMAD is severely reduced in the elderly with HFNEF. Methods and Results: 30 participants >60 yr of age, 11 healthy, 9 with HFNEF, and 10 with HFREF, underwent a cardiovascular magnetic resonance (CMR) assessment of FMAD in the superficial femoral artery followed within 48 h by symptom-limited exercise with expired gas analysis. Elderly patients with HFREF and HFNEF had severely reduced peak oxygen consumption (VO2 peak; 12 ± 2 and 13 ± 1 ml·kg–1·min–1, respectively) vs. their healthy age-matched contemporaries (20 ± 3 ml·kg–1·min–1). FMAD was 3.8 ± 1.3% (0.85 ± 0.22 mm2) in patients with HFREF; it was 12.1 ± 3.6% (3.1 ± 1.2 mm2) and 13.7 ± 5.9% (3.9 ± 1.7 mm2), respectively, in patients with HFNEF and age-matched healthy older individuals. After adjustment for age and gender, the association of FMAD with VO2 was high in healthy and HFREF subjects (P = 0.05 and 0.02, respectively) but less so in HFNEF participants (P = 0.58). Conclusions: elderly patients with HFNEF do not exhibit marked reduction in leg FMAD. These data suggest that mechanisms other than impaired femoral arterial endothelial function contribute to the severe exercise intolerance experienced by these individuals.

endothelial function; magnetic resonance imaging



Address for reprint requests and other correspondence: W. G. Hundley, Section on Cardiology, Wake Forest Univ. School of Medicine (Bowman Gray Campus), Medical Center Blvd., Winston-Salem, NC 27157-1045 (e-mail: ghundley{at}wfubmc.edu)




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