Contribution of Endothelin-1 to Exercise Intolerance in Heart Failure
Status:
Completed
Trial end date:
2019-03-31
Target enrollment:
Participant gender:
Summary
Heart disease is the leading cause of death in the United States, accounting for one in every
four deaths in 2010 and costing over $300 billion annually in health care, medication, and
lost productivity. Heart failure (HF), a clinical syndrome that develops as a consequence of
heart disease, is characterized by the worsening of symptoms, such as dyspnea and fatigue,
upon exertion, collectively defined as "exercise intolerance". Surprisingly, exercise
intolerance does not correlate with the degree of cardiac contractile (ventricular)
dysfunction, suggesting that changes in the peripheral circulation may be to blame for
exercise intolerance in this cohort. Though there are a host of factors that may contribute
to this impairment, disease-related increases in circulating endothelin-1 (ET-1) may be a
significant factor in the sequelae of exercise intolerance in HF. Thus, the overall purpose
of this Small Projects in Rehabilitation Research (SPiRE) proposal is to explore the
contribution of ET-1 to chronic vasoconstriction in HF patients, and to examine whether
inhibition of this pathway could improve vasodilatory ability, and thus exercise tolerance,
in Veterans with HF.