Ignite Creation Date:
2024-05-06 @ 11:32 AM
Last Modification Date:
2024-10-26 @ 12:46 PM
Study NCT ID:
NCT03541213
Status:
COMPLETED
Last Update Posted:
2022-07-29
First Post:
2018-05-17
Brief Title:
Impact of Iron Deficiency and Its Correction on Mitochondrial Metabolism of the Cardiomyocyte MitoCardioFer
Sponsor:
University Hospital Angers
Organization:
University Hospital Angers
Study Overview
Official Title:
Impact de la Carence Martiale et de Son Traitement Sur le métabolisme Mitochondrial du Cardiomyocyte MitoCardioFer
Status:
COMPLETED
Status Verified Date:
2022-07
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
MitoCardioFer
Brief 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
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
Detailed 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
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
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None