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BMI, Nutrition, Inflammation and Heart Failure Outcomes
Terry Lennie, Ph.D.,
Principal Investigator;
Debra Moser, D.N.Sc.,
Mary Kay Rayens, Ph.D.,
Thomas Whayne, M.D., Ph.D.,
John Novak, B.D.S., L.D.S., Ph.D.
Co-investigators
Funded by the National
Institute of Nursing Research
(2005-2008)
Abstract
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Cardiac cachexia is an independent risk factor for morbidity
and mortality in patients with heart failure (HF). In
contrast, obesity was recently reported to be associated
with decreased risk of morbidity and mortality. The finding
that overweight and obese patients with HF have surprisingly
better outcomes is in contrast to our current understanding
of the relationships between obesity and HF and conflicts
with the recommendation that these individuals should lose
weight. The biobehavioral mechanisms underlying the
differences in outcomes between these groups of patients are
not well understood. Nutritional intake is a major
contributor to body weight and may also play a crucial role
in influencing HF outcomes. Proinflammatory cytokines
released as part of the systemic inflammatory response to
both obesity and HF affect appetite, food intake, body
composition, myocardial function, and vascular epithelium
and are predictors of patient outcomes.
The purpose of the proposed research is to examine the
relationships among body fat content, nutritional intake,
inflammation, and patient outcomes in 300 patients with HF
of ischemic origin that are equally distributed among four
groups: underweight, normal weight, overweight, and obese.
The primary aim of this prospective study is to determine
the relationship between body fat mass and twelve-month
patient morbidity and mortality outcomes (composite
end-point of rehospitalization or death) and twelve-month
patient quality-of-life outcomes. Secondary aims are to
examine how differences in body fat mass and distribution
alter the effect of nutritional deficiencies (four-day food
diaries) and proinflammatory cytokine activity (tumor
necrosis factor-α [TNFα], soluble TNFα receptors,
interleukin-6, interleukin-1 receptor antagonist, and
interleukin-10) on patient outcomes.
Examination of the interactions among body fat content,
nutritional intake, and proinflammatory cytokine activity
will provide an understanding of the biobehavioral
mechanisms underlying the improved patient outcomes observed
in overweight and obese patients with HF. This will assist
with developing new nutrition and body weight guidelines for
patients with HF who are overweight and obese. An
understanding of the underlying mechanisms may also allow
application of these findings to underweight patients
resulting in improved outcomes for these patients.
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