Clinical Trial: Clinical and Angiographic Outcomes With Hyperglycemic Control Post PCI
Study Status: Completed
Recruit Status: Completed
Study Type: Interventional
Official Title: Does Reduction of Hyperglycemia With Insulin Impact Restenosis and Improve Clinical Outcomes Following PCI?
Brief Summary:
Coronary artery disease is a process that results in “hardening of the arteries”. When the arteries that supply blood and oxygen to your heart muscle become clogged or narrowed, a heart attack may result, or you may feel chest discomfort (angina) – sometimes even while resting. One approach to treating this condition is a balloon procedure known as coronary angioplasty.
The major limitation of coronary angioplasty is renarrowing of the artery (restenosis) in the first six months following the procedure requiring either repeat angioplasty or referral for bypass surgery. Patients with diabetes have always been identified as having higher rates of restenosis and poor outcomes following angioplasty, despite some important scientific advances. We think that the level of blood sugar control at the time of angioplasty and in the following months may be related to the extent of restenosis.
We expect that a reduction in blood sugar with insulin may, in turn, reduce the restenosis process and improve your long-term outcome.
Detailed Summary:
Studies consistently show that diabetes (DM) is an independent predictor of angiographic restenosis as well as clinical outcomes after PCI. A common criticism of the early PCI trials is that stents were not routinely used. However, even when stents are used, the presence of DM is associated with a higher restenosis rate and lower event rate survival. In a series of 3,554 consecutive patients (715 DM patients) undergoing stenting procedures at a single centre the incidence of restenosis and total vessel occlusion by angiographic assessment was significantly higher in diabetes. Increased restenosis rates were consistently demonstrated across a broad range of lesion types.
The pathophysiology of restenosis is viewed as a complex temporal sequence of interactions involving several cellular and mechanical factors including elastic recoil, thrombosis, intimal hyperplasia, extra cellular matrix elaboration, apoptosis, oxidative stress and unfavorable arterial remodeling (“arterial shrinkage”). The exposure of subendothelial elements initiates platelet adhesion and activation. Activated platelets at the site of injury secrete growth factors that release smooth muscle cells from growth inhibition and induce their proliferation and subsequent migration from the media to the intima. Smooth muscle cell proliferation continues beyond the phase of platelet deposition. Extracellular matrix is produced and secreted by smooth muscle cells that have migrated into the injured intimal zone. This hypocellular matrix material forms the bulk of the intimal tissue. Although mechanical factors such as early vessel elastic recoil may play a major role following balloon angioplasty, this mechanism should not significantly affect the stented segments as the stent provides a rigid endovascular scaffold. Similarly, late arterial remodelling which has been postulated to be a significant fac
Sponsor: Hamilton Health Sciences Corporation
Current Primary Outcome: Volume of intimal hyperplasia in the stented segment by IVUS at 6 months following PCI
Original Primary Outcome: Same as current
Current Secondary Outcome: Late loss in minimal luminal diameter of stented site in coronary vessel evaluated by QCA at 6 months post-PCIb) Rate of clinical events at one year (hospital admission for unstable angina, CHF, MI, stroke, revascularization, and death)
Original Secondary Outcome: Same as current
Information By: McMaster University
Dates:
Date Received: December 13, 2006
Date Started: July 2002
Date Completion: September 2005
Last Updated: December 13, 2006
Last Verified: December 2006
