Pathophysiology of atherosclerosis: Development, regression, restenosis

Abstract

There is now a very large number of patients with coronary artery disease who have also undergone percutaneous interventions such as coronary angioplasty. Atherosclerosis and restenosis are two distinct pathologic processes with different underlying pathophysiologic mechanisms, different natural histories, different clinical presentations, and treatment strategies. Management strategies to target both processes are currently poorly applied in clinical practice. The development of integrated management strategies to target atherosclerosis, as well as restenosis in the postprocedural period remains a priority.

Endothelial dysfunction and restenosis following percutaneous coronary intervention

“…Although a number of factors, such as diabetes and small reference vessel size, have been identified that influence its frequency its pathogenesis is not fully [3,13,14]. Even with the utilization of the best possible predictive model, the lowest risk group of patients undergoing coronary intervention (non-diabetic patients with vessel size greater than 3.5 mm and lesion length ≤15mm) may have a restenosis rate around 10% [13].…”

“…Endothelial cells also influence adhesion, aggregation and activation of platelets as well as migration of inflammatory cells following balloon injury [6,16]. Endothelial loss therefore leads to further stimulation of vascular smooth muscle cell growth via production of platelet derived growth factor, interluekin-1, interluekin-6, basic fibroblast growth factor and tumor necrosis factor-α amongst others [3,17]. Thus restoration of a normally functioning endothelial monolayer at the site of coronary intervention is critical in the return of normal vessel function.…”

“…The process of "in-stent" restenosis is likely precipitated by the endothelial disruption and intimal and medial vascular injury that occurs at the time of balloon inflation [3]. This vascular injury results in exposure of the thrombogenic subendothelium, platelet and vascular smooth muscle cell activation, thrombosis, and the release of a number of growth factors that mediate VSMC migration and proliferation and the production of abundant extracellular matrix [4,5].…”

Surface modification and direct plasma amination of L605 CoCr alloys: on the optimization of the oxide layer for application in cardiovascular implants

“…Atherosclerosis is a cardiovascular disease characterized by the formation of a plaque that narrows the arterial walls, leading to thrombus formation and ultimately heart attacks. 1 Once it has progressed to the late stages, this disease is surgically treated by the implantation of a stent which is a metallic wire mesh. This device is introduced with a catheter to the narrowed zone and is expanded up to 25% deformation to reopen the arterial ow, deploying the device whilst avoiding the collapse of the artery.…”