Restenosis following coronary angioplasty

Abstract

Summary:Restenosis is the most important problem limiting the success of coronary angioplasty. Clinically, restenosis is seen in approximately one-third of patients undergoing percutaneous transluminal coronary angioplasty. Several clinical and angiographic risk factors have been identified which may contribute to the development of restenosis. Histopathologic studies indicate that restenosis is characterized by intimal proliferation of smooth muscle cells in a loose connective tissue matrix. These intimal lesions are associated predominantly with the nonatheromatous portion of the vessel wall. Thinning of the media of the plaque-free wall and marked fragmentation of the internal elustic lamina are also seen. Traumatic injury of the vessel wall during angioplasty probably triggers a series of cellular und subcellular events which may ultimately lead to niyointimal proliferation and restenosis. Although the exact mechanism by which this occurs is unknown, several factors may enhance smooth muscle cell growth and therefore may play a role in the development of restenosis. These include platelet deposition, mechanical stretching of the medi,a, inflammation of the vessel wall, the activity of growth factors, and alterations in vessel geometry. These possible mechanisms of restenosis suggest several potential ways to limit the proliferative response to vascular injury.Anticoagulants and platelet antagonists, direct inhibitors of smooth inuscle proliferation, anti-inflammatory agents, growth factor inhibitors, and new devices which improve final vessel geometry are currently being tested as methods to curb restenosis. Unfortunately, no treatment has yet been shown to reduce significantly the rate of restenosis following angioplasty. The problem of restenosis will most likely be solved by better understanding of the basic molecular and biologic phenomena involved in vascular injury and repair.

Serum Prostaglandin D Synthase Level after Coronary Angioplasty May Predict Occurrence of Restenosis

“…It is well known that PTCA produces platelet activation, which may lead to abrupt or threatened coronary closure or late restenosis (13,15). The flowcytometric analysis in the present study demonstrated the increased expression of the platelet membrane surface glycoprotein, P-selectin (CD62P) on the surface of platelets immediately after PTCA, which we have already described also in another report (20).…”

“…Percutaneous transluminal coronary angioplasty (PTCA) produces traumatic vessel wall injury and inflammation at the intervention site, which may act as the pathophysiologic trigger of acute-stage thrombotic complication or late-stage restenosis (12,13). In this process, activation of platelets, leukocytes, and vascular endothelial cells and cellular interaction among these cells mediated by their adhesion molecules appear to play important roles (13)(14)(15). This study was designed to investigate the kinetics of serum L-PGDS level after PTCA and to establish clinical significance of the level as a predictor of late restenosis.…”

Primary Everolimus-Eluting Stenting Versus Balloon Angioplasty With Bailout Bare Metal Stenting of Long Infrapopliteal Lesions for Treatment of Critical Limb Ischemia

“…In addition, primary stenting may reduce vessel wall traumatic injury following balloon dilation, which has been implicated in both increased local inflammation and late restenosis. 18,25 A number of clinical trials have shown that primary coronary stenting has a superior initial success rate and a lower incidence of restenosis compared to conventional balloon angioplasty. 23,26…”

The effects of coronary angioplasty on the global and regional left ventricular function in patients with angina pectoris after anterior myocardial infarction

“…Successful PTCA was defined as the reduction of the lesion severity to less than 50% [12]. Restenosis was defined as more than 50% diameter stenosis at the follow-up period [13]. The clinical characteristics of the patients (functional capacity and severity of angina pectoris according to NYHA) [14] and medications were recorded before and after PTCA during the follow-up period.…”