Contribution of Endothelin-1 to Exercise Intolerance in Heart Failure
NCT02124824 · Status: COMPLETED · Phase: EARLY_PHASE1 · Type: INTERVENTIONAL · Enrollment: 30
Last updated 2021-12-20
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.
Conditions
Interventions
- DRUG
-
BQ-123
Endothelin subtype A antagonist
Sponsors & Collaborators
- collaborator OTHER
-
VA Office of Research and Development
lead FED
Principal Investigators
-
David W. Wray, PhD · VA Salt Lake City Health Care System, Salt Lake City, UT
Study Design
- Allocation
- RANDOMIZED
- Purpose
- BASIC_SCIENCE
- Masking
- SINGLE
- Model
- PARALLEL
Eligibility
- Min Age
- 45 Years
- Max Age
- 75 Years
- Sex
- ALL
- Healthy Volunteers
- Yes
Timeline & Regulatory
- Start
- 2014-09-01
- Primary Completion
- 2019-03-31
- Completion
- 2019-03-31
- FDA Drug
- Yes
Countries
- United States
Study Locations
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