Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT03541213 |
| Other study ID # |
2017-A00904-49 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
N/A
|
| First received |
|
| Last updated |
|
| Start date |
January 23, 2019 |
| Est. completion date |
September 7, 2020 |
Study information
| Verified date |
July 2022 |
| Source |
University Hospital, Angers |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Interventional
|
Clinical Trial Summary
Iron is involved in essential functions of the body. It allows the transport of oxygen in the
blood, via hemoglobin, at the muscular level, via myoglobin, and it is also involved in
cellular metabolism in general, in particular for the production of ATP at the mitochondrial
level, within the cytochromes and iron-sulfur proteins of the respiratory chain.
Recently, iron deficiency has been identified as an important prognostic factor in heart
failure patients. Iron therapy improves symptoms and physical performances of heart failure
patients, even in the absence of anemia. As a result, the correction of iron deficiency is
now proposed as one of the therapies for heart failure. However, the pathophysiology of the
association between cardiac dysfunction and iron deficiency is still poorly understood.
The investigators previously developed a mouse model of iron deficiency without anemia, in
which the investigators observed impaired physical performances, a decrease of left
ventricular ejection fraction, and a decrease in mitochondrial complex I activity. These
abnormalities were normalized after iron injection. These animal data suggest that iron
deficiency is responsible for left ventricular dysfunction secondary to mitochondrial I
complex abnormalities, and that iron therapy corrects them.
Iron deficiency is very common in the preoperative period of cardiac surgery, affecting 40 to
50% of patients. During this surgery, it is possible to perform a myocardial biopsy without
risk to the patient.
The purpose of this study is to verify in patients requiring valvular heart surgery, if iron
deficiency is responsible for a decrease in mitochondrial complex I activity and a decrease
in cardiac function during the perioperative period, and to verify whether iron treatment
improves these abnormalities.
Description:
Iron is involved in essential functions of the body. It allows the transport of oxygen in the
blood, via hemoglobin, at the muscular level, via myoglobin, and it is also involved in
cellular metabolism in general, in particular for the production of ATP at the mitochondrial
level, within the cytochromes and iron-sulfur proteins of the respiratory chain.
Iron deficiency has been shown to be responsible for fatigue and muscle weakness, regardless
of the presence of an anemia. Recently, iron deficiency has been identified as an important
prognostic factor in heart failure patients, with a prevalence increasing with NYHA class
level, and association with mortality. Iron therapy improves the symptoms of heart failure
patients and the 6-minute walk test, even in the absence of anemia. The correction of iron
deficiency is now proposed as one of the therapies for heart failure. However, the
pathophysiology of the association between cardiac dysfunction and iron deficiency is still
poorly understood.
The investigators previously developed a mouse model of iron deficiency without anemia, in
which the investigators observed impaired physical performances, a decrease of left
ventricular ejection fraction, and a decrease in mitochondrial complex I activity. These
abnormalities were normalized after iron injection. These animal data suggest that iron
deficiency is responsible for left ventricular dysfunction secondary to mitochondrial I
complex abnormalities, and that iron therapy corrects them.
Iron deficiency is very common in the preoperative period of cardiac surgery, affecting 40 to
50% of patients. During this surgery, it is possible to perform a myocardial biopsy without
risk to the patient. There is therefore an opportunity to further explore the impact of iron
deficiency and its treatment on mitochondrial energy metabolism of cardiomyocytes. We
hypothesize that the activity of the mitochondrial complex I is decreased in the presence of
iron deficiency and that the iron treatment corrects this decrease.
The purpose of this study is to verify in patients requiring valvular heart surgery, if iron
deficiency is responsible for a decrease in mitochondrial complex I activity and a decrease
in cardiac function during the perioperative period, and to verify whether iron treatment
improves these abnormalities.
