Ignite Creation Date:
2024-05-05 @ 6:44 PM
Last Modification Date:
2024-10-26 @ 9:36 AM
Study NCT ID:
NCT00533039
Status:
COMPLETED
Last Update Posted:
2009-10-09
First Post:
2007-09-19
Brief Title:
sPLA2 Inhibition to Decrease Enzyme Release After PCI Trial
Sponsor:
University Health Network Toronto
Organization:
University Health Network Toronto
Study Overview
Official Title:
sPLA2 Inhibition to Decrease Enzyme Release After PCI SPIDER-PCI Trial
Status:
COMPLETED
Status Verified Date:
2008-06
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:
SPIDER-PCI
Brief Summary:
As evidence accumulates that atherogenesis or Coronary Artery Disease CAD may not be simply a disorder of lipid metabolism but an inflammatory disease the focus of treatment has shifted A-002 or Varespladib is an anti-inflammatory drug for treatment of chronic and acute diseases It acts by inhibiting secretory phospholipase A2 sPLA2 - one of a family of enzymes leading to inflammation - which may be important in 1 the development of atherosclerosis and 2 the increase in occurence of cardiovascular events after angioplasty Previous studies have demonstrated that sPLA2 1 facilitates the pro-atherogenic effects of low-density LDL or bad cholesterol and 2 increased levels post-angioplasty correlate with an increased risk of events at followup contact Therefore this study proposes to investigate the ability of A-002 to prevent or reduce myocardial damage after angioplasty by inhibiting the cascade of inflammatory mediators
Substudy - Subjects who agree will also have a vascular ultrasound 24h post-PCI to assess endothelial function
Substudy - Subjects who agree will also have a vascular ultrasound 24h post-PCI to assess endothelial function
Detailed Description:
Tissue injury after angioplasty is likely due to micro-emboli from mechanical trauma to a thrombotic lesion during angioplasty In response to the ischemia sPLA2 possibly localized within atherosclerotic vascular tissue as well as from macrophages and monocytes is released Following ischemia-induced release sPLA2 can bind to ischemically challenged cardiomyocytes and adversely affect their survival either directly through toxic effects on cardiomyocytes or indirectly by facilitating inflammation It may be possible through sPLA2 inhibition to salvage non-lethally jeopardized cells following an ischemic episode thereby reducing the infarcted area and amount of tissue damage Previous studies in patients with unstable angina support this hypothesis and conclude that sPLA2 levels can be used to predict clinical outcomes We hypothesize that sPLA2 inhibition with A-002 will reduce myocardial injury post-angioplasty
Substudy - Peripheral vascular ultrasound should be done prior to receiving study drug and 24h post-PCI Coronary endothelial function will be assessed at the time of PCI
Substudy - Peripheral vascular ultrasound should be done prior to receiving study drug and 24h post-PCI Coronary endothelial function will be assessed at the time of PCI
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
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| A Sub-study of SPIDER-PCI | None | None | None |