Ignite Creation Date:
2024-05-06 @ 10:13 AM
Last Modification Date:
2024-10-26 @ 12:26 PM
Study NCT ID:
NCT03199131
Status:
COMPLETED
Last Update Posted:
2020-01-23
First Post:
2017-03-22
Brief Title:
The Right Ventricle in Chronic Pressure Overload Identifying Novel Molecular Targets for Functional Imaging
Sponsor:
Centre Chirurgical Marie Lannelongue
Organization:
Centre Chirurgical Marie Lannelongue
Study Overview
Official Title:
The Right Ventricle in Chronic Pressure Overload Identifying Novel Molecular Targets for Functional Imaging
Status:
COMPLETED
Status Verified Date:
2020-01
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:
MVD
Brief Summary:
Chronically elevated pulmonary pressures do not immediately result in right ventricular failure During the initial period of exposure the RV adapts to the increased afterload by altering its metabolism and morphology so as to meet the increased work requirement Several interconnected adaptive mechanisms have been proposed including myocyte hypertrophy a switch in the primary fuel used for ATP generation increased angiogenesis and decreased production of mitochondrial reactive oxygen species While adaptation is initially successful in many cases it is temporary and after an uncertain period of time the ventricle begins to fail This transition from a compensated to decompensated state is difficult to predict clinically and patients with different etiologies of CPOS progress to overt RV failure over significantly different time periods This variability hinders the implementation of treatments that are tailored to a specific disease stage
Detailed Description:
Chronically elevated pulmonary pressures do not immediately result in right ventricular failure During the initial period of exposure the RV adapts to the increased afterload by altering its metabolism and morphology so as to meet the increased work requirement Several interconnected adaptive mechanisms have been proposed including myocyte hypertrophy a switch in the primary fuel used for ATP generation increased angiogenesis and decreased production of mitochondrial reactive oxygen species While adaptation is initially successful in many cases it is temporary and after an uncertain period of time the ventricle begins to fail This transition from a compensated to decompensated state is difficult to predict clinically and patients with different etiologies of CPOS progress to overt RV failure over significantly different time periods This variability hinders the implementation of treatments that are tailored to a specific disease stage As right heart failure is the primary outcome determinant in patients with pulmonary hypertension understanding the major mediators of RV compensation failure and recovery is essential to improving patient survival Recently there have been significant advances in the ability to assess RV function in vivo using functional imaging techniques including positron emission tomography PET and cardiac MRI CMR CMR is an established and validated method of precisely defining cardiac structure and function and new PET protocols have been developed that measure glucose utilization oxygen consumption apoptosis and angiogenesis Importantly the in vivo nature of PET and CMR allow for the non-invasive collection of detailed structural metabolic and physiologic data on the performance of the RV5 When taken in combination with established echocardiographic evaluation these new platforms allow in-depth analysis of cardiac structure and function without the need for invasive procedures In order to maximize the potential of these techniques however a molecular imaging target needs to be identified so as to allow physicians to detect the transition from a compensated to decompensated state Such a marker has not yet been reported
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