Ignite Creation Date:
2024-05-06 @ 7:34 AM
Last Modification Date:
2024-10-26 @ 11:49 AM
Study NCT ID:
NCT02556450
Status:
COMPLETED
Last Update Posted:
2022-03-08
First Post:
2015-09-08
Brief Title:
Bioprofiling Response to Mineralocorticoid Receptor Antagonists for the Prevention of Heart Failure
Sponsor:
ACS Biomarker
Organization:
ACS Biomarker
Study Overview
Official Title:
Bioprofiling Response to Mineralocorticoid Receptor Antagonists for the Prevention of Heart Failure A Proof of Concept Clinical Trial Within the EU FP 7 European Union FP7 HOMAGE Programme Heart OMics in AGing
Status:
COMPLETED
Status Verified Date:
2022-03
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:
Homage
Brief Summary:
Despite advances in care prognosis remains poor once overt Heart Failure HF has developed Prevention is most efficient when directed toward patients at risk and when mechanistically targeted to patients most likely to respond An increase in myocardial and possibly vascular collagen content fibrosis may be a major determinant of the transition to HF In patients with hypertension and diabetes two important risk-factors for HF changes in blood markers of fibrosis occur before clinically overt HF develops These markers are also related to prognosis
In the general population Galectin-3 Gal-3 a potential marker of fibrosis is associated with cardiovascular CV risk factors and predicts development of HF In animal models Gal-3 is a key mediator of aldosterone-induced CV and renal fibrosis and dysfunction
The investigators hypothesize that the mineralocorticoid receptor antagonist MRA spironolactone may prevent HF by acting on extracellular matrix remodelling especially in patients with active fibrogenesis identified by high Gal-3 levels The benefitrisk ratio of spironolactone might be superior in patients with a higher compared to lower plasma concentrations of Gal-3
Main objective is to investigate whether spironolactone can favourably alter extra-cellular matrix remodelling assessed by changes in the fibrosis biomarker Procollagen Type III N-Terminal Peptide PIIINP in patients at increased risk of developing heart failure and whether this effect is greater in patients with increased plasma concentrations of Gal-3
In the general population Galectin-3 Gal-3 a potential marker of fibrosis is associated with cardiovascular CV risk factors and predicts development of HF In animal models Gal-3 is a key mediator of aldosterone-induced CV and renal fibrosis and dysfunction
The investigators hypothesize that the mineralocorticoid receptor antagonist MRA spironolactone may prevent HF by acting on extracellular matrix remodelling especially in patients with active fibrogenesis identified by high Gal-3 levels The benefitrisk ratio of spironolactone might be superior in patients with a higher compared to lower plasma concentrations of Gal-3
Main objective is to investigate whether spironolactone can favourably alter extra-cellular matrix remodelling assessed by changes in the fibrosis biomarker Procollagen Type III N-Terminal Peptide PIIINP in patients at increased risk of developing heart failure and whether this effect is greater in patients with increased plasma concentrations of Gal-3
Detailed Description:
The investigators hypothesize that the mineralocorticoid receptor antagonist MRA spironolactone may prevent HF by acting on extracellular matrix remodelling especially in patients with active fibrogenesis identified by high Gal-3 levels The benefitrisk ratio of spironolactone might be superior in patients with a higher compared to lower plasma concentrations of Gal-3
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None