Ignite Creation Date:
2024-05-05 @ 11:59 AM
Last Modification Date:
2024-10-26 @ 9:17 AM
Study NCT ID:
NCT00190099
Status:
COMPLETED
Last Update Posted:
2005-11-18
First Post:
2005-09-11
Brief Title:
Dexamethasone-Eluting Stent in Acute Coronary Syndrome to Prevent Restenosis
Sponsor:
Far Eastern Memorial Hospital
Organization:
Far Eastern Memorial Hospital
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2004-12
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:
None
Brief Summary:
The major obstacle of the long- termed success of percutaneous coronary intervention PCI is the restenosis Restenosis results from complex pathophysiological response of the vascular tissue to the balloon injury In the pre-stent era 80 of it was attributed to vascular recoil However by way of the mechanical support of metallic stent recoil is no more the major reason of restenosis About 80 of In-stent restenosis resulted from intimal hyperplasia
The mechanism of the Intra-stent restenosis included 4 stages First stage comprised the first 3 days after balloon injury when the inflammatory reaction is most severe throughout the course At that time anti-inflammatory drug as steroid wuold be helpful to prevent the course of restenosis Until the end of the third week smooth muscle cells migrate and then proliferate in the second and the third stage and the key effort to prevent restenosis right now is inhibition of cell cycle Intravascular radiotherapy so called Brachytherapy and stent-based drug elution target upon them Among them rapamycin and paclitaxel proved to be effective both in animal and human experience The last stage is re-epithelization estrogen could promote the process and was considered to be effective in this stage
Stent-based elution of corticosteroid despite of its feasibility and safety was not as effective as other anti-proliferation agent eg Rapamycin etc The major reason might be the patient group with coronary artery disease is a heterogenous one
We believe if we applied corticosteroid over the patient with elevated inflammatory parameters ie acute coronary syndrome ACS the effect of anti-restenosis would be obvious
In this study by a special-designed phosphorylcholine-coated stent dexamethasone could be readily absorbed and then gradually released locally even 4 weeks after deployment
We expected a reduction of In-stent restenosis in ACS patient by the method with no or few systemic adverse effect of steroid and angiographic follow-up as well as intra-vascular ultrasound assessment would be performed according to pur protocol
The mechanism of the Intra-stent restenosis included 4 stages First stage comprised the first 3 days after balloon injury when the inflammatory reaction is most severe throughout the course At that time anti-inflammatory drug as steroid wuold be helpful to prevent the course of restenosis Until the end of the third week smooth muscle cells migrate and then proliferate in the second and the third stage and the key effort to prevent restenosis right now is inhibition of cell cycle Intravascular radiotherapy so called Brachytherapy and stent-based drug elution target upon them Among them rapamycin and paclitaxel proved to be effective both in animal and human experience The last stage is re-epithelization estrogen could promote the process and was considered to be effective in this stage
Stent-based elution of corticosteroid despite of its feasibility and safety was not as effective as other anti-proliferation agent eg Rapamycin etc The major reason might be the patient group with coronary artery disease is a heterogenous one
We believe if we applied corticosteroid over the patient with elevated inflammatory parameters ie acute coronary syndrome ACS the effect of anti-restenosis would be obvious
In this study by a special-designed phosphorylcholine-coated stent dexamethasone could be readily absorbed and then gradually released locally even 4 weeks after deployment
We expected a reduction of In-stent restenosis in ACS patient by the method with no or few systemic adverse effect of steroid and angiographic follow-up as well as intra-vascular ultrasound assessment would be performed according to pur protocol
Detailed Description:
The major obstacle of the long- termed success of percutaneous coronary intervention PCI is the restenosis Restenosis results from complex pathopysiological response of the vascular tissue to the balloon injury In the pre-stent era 80 of it was attributed to vascular recoil However by way of the mechanical support of metallic stent recoil is no more the major reason of restenosis About 80 of In-stent restenosis resulted from intimal hyperplasia
The mechanism of the Intra-stent restenosis included 4 stages First stage comprised the first 3 days after balloon injury when the inflammatory reaction is most severe throughout the course At that time anti-inflammatory drug as steroid would be helpful to prevent the course of restenosis Until the end of the third week smooth muscle cells migrate and then proliferate in the second and the third stage and the key effort to prevent restenosis right now is inhibition of cell cycle Intravascular radiotherapy so called Brachytherapy and stent-based drug elution target upon them Among them rapamycin and paclitaxel proved to be effective both in animal and human experience The last stage is re-epithelization estrogen could promote the process and was considered to be effective in this stage
Stent-based elution of corticosteroid despite of its feasibility and safety was not as effective as other anti-proliferation agent eg Rapamycin etc The major reason might be the patient group with coronary artery disease is a heterogenous one
We believe if we applied corticosteroid over the patient with elevated inflammatory parameters ie acute coronary syndrome ACS the effect of anti-restenosis would be obvious
In this study by a special-designed phosphorylcholine-coated stent dexamethasone could be readily absorbed and then gradually released locally even 4 weeks after deployment
We expected a reduction of In-stent restenosis in ACS patient by the method with no or few systemic adverse effect of steroid and angiographic follow-up as well as intra-vascular ultrasound assessment would be performed according to pur protocol
The mechanism of the Intra-stent restenosis included 4 stages First stage comprised the first 3 days after balloon injury when the inflammatory reaction is most severe throughout the course At that time anti-inflammatory drug as steroid would be helpful to prevent the course of restenosis Until the end of the third week smooth muscle cells migrate and then proliferate in the second and the third stage and the key effort to prevent restenosis right now is inhibition of cell cycle Intravascular radiotherapy so called Brachytherapy and stent-based drug elution target upon them Among them rapamycin and paclitaxel proved to be effective both in animal and human experience The last stage is re-epithelization estrogen could promote the process and was considered to be effective in this stage
Stent-based elution of corticosteroid despite of its feasibility and safety was not as effective as other anti-proliferation agent eg Rapamycin etc The major reason might be the patient group with coronary artery disease is a heterogenous one
We believe if we applied corticosteroid over the patient with elevated inflammatory parameters ie acute coronary syndrome ACS the effect of anti-restenosis would be obvious
In this study by a special-designed phosphorylcholine-coated stent dexamethasone could be readily absorbed and then gradually released locally even 4 weeks after deployment
We expected a reduction of In-stent restenosis in ACS patient by the method with no or few systemic adverse effect of steroid and angiographic follow-up as well as intra-vascular ultrasound assessment would be performed according to pur protocol
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