Cardiac Mitochondrial Function in Explanted Human Hearts
NCT04500938 · Status: UNKNOWN · Type: OBSERVATIONAL · Enrollment: 24
Last updated 2020-08-06
Summary
Background:
Treatment of heart failure has improved considerably in the past decades. Despite this improvement, the disease may progress into an end-stage ultimately leaving the physicians with no other treatment option than heart transplantation (HTx). There are multiple etiologies underlying heart failure. Cardiomyopathy is the leading cause for HTx in any age-group with coronary artery disease being the second most common cause in adult patients.
Alterations in the mitochondrial function have been recognized as key factors in heart failure.
During the transplant procedure the diseased heart is removed, providing a unique opportunity to collect samples eligible for thorough mitochondrial examination.
Hopefully, the knowledge gained from this investigation will contribute with important insights in the diseased myocardial energy metabolism. Such knowledge may pave the way for development of treatments targeting both energy substrate supply for adenosine-triphosphate generation produced by the mitochondria as well as mitochondrial function in the failing heart.
Hypothesis:
The pathological myocardial function seen in heart failure is related to dysfunctional cardiac mitochondria
Objective:
To examine if cardiac mitochondrial function in end-stage heart failure of multiple etiologies is inferior to mitochondrial function in transplanted hearts with no signs of rejection or vasculopathy.
Design:
Myocardial mitochondrial function analyzed from 24 explanted hearts will be compared to endomyocardial biopsies from 20 HTx patients at scheduled biopsies (1 or 2 years after implantation).
Conditions
- End-stage Heart Failure
Sponsors & Collaborators
-
University of Aarhus
lead OTHER
Principal Investigators
-
Hans Eiskjær, MD, DMSc · University of Aarhus
Eligibility
- Min Age
- 18 Years
- Sex
- ALL
- Healthy Volunteers
- No
Timeline & Regulatory
- Start
- 2020-08-30
- Primary Completion
- 2024-02-28
- Completion
- 2024-02-28
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