Prolonged proliferative response of smooth muscle cells after experimental intravascular stenting

Abstract

The purpose of this experimental in vivo study was to determine the time course of smooth muscle cell proliferation early and late after intravascular stenting compared to conventional balloon angioplasty in normal vessels. A balloon expandable 2.0 mm tantalum Strecker stent was placed in the right carotid artery of 33 male New Zealand White rabbits after they had been fed a 0.5% cholesterol diet for 28 days. In addition, balloon angioplasty was performed in 27 of the animals; 19 contralateral vessels served as controls without treatment. The vessels were excised at 7, 14, 28, 42 or 90 days after treatment. During the final 18 h before the rabbits were killed, bromodeoxyuridine (BrdU) was applied and proliferating cells were detected by using a monoclonal antibody against BrdU. In histological cross sections the proportion of cells undergoing DNA synthesis was determined. Analysis was performed separately in the intimal and medial layers. Additionally, the area adjacent to the stent wire was compared with the intermediate area. Smooth muscle cells were identified by alpha-actin staining. Intimal wall thickness increased from 23 +/- 28 microns (control group without intervention) to 323 +/- 84 microns within 42 days after stenting (P < 0.01), and to 81 +/- 82 microns at day 42 after balloon angioplasty (P < 0.05). However, between 42 and 90 days following stent implantation a significant (P < 0.05) decrease in neointimal thickness was observed (90 days: 215 +/- 15 microns).(ABSTRACT TRUNCATED AT 250 WORDS)

Liver X Receptor Agonists Suppress Vascular Smooth Muscle Cell Proliferation and Inhibit Neointima Formation in Balloon-Injured Rat Carotid Arteries

“…42,43 To determine the effect of synthetic LXR ligands on mitogeninduced CASMC proliferation, quiescent cells were treated with T1317 or GW3965 and stimulated with PDGF (20 ng/mL) and insulin (1 mol/L) for 72 hours. Both LXR ligands inhibited PDGF/insulin-stimulated CASMC proliferation in a dose-dependent manner (84.2Ϯ4.6 inhibition at 5 mol/L T1317 and 100% inhibition at 3 mol/L GW3965, respectively; PϽ0.05; Figure 3A).…”

Coronary artery and myocardial inflammatory reaction induced by intracoronary stent

“…Coronary stent implantation seems to cause a more severe lesion [6,7] and a more intense inflammatory response inside the arterial wall than in other types of percutaneous interventions [8,9]. The arterial wall distension and the vascular lesion caused by the balloon in angioplasty and the placement of the stent, act as a potent stimulus for the proliferation of smooth muscle cells and neo-intimal hyperplasia [10,11].…”

Exercise-Induced Coronary Artery Vasodilation Is Not Impaired by Stent Placement

“…5 Stenting mechanically stabilizes the dilated segment, which might convert a formerly dynamic artery into a rigid tube. Furthermore, the implantation of a metallic prosthesis induces considerable injury to the arterial wall, with prolonged inflammatory, prothrombotic, and proliferative reactions 6,7 that are likely to extend beyond the stented segment. The purpose of the present study was, therefore, to evaluate coronary vasomotor response of the proximal and distal vessel segment several months after stenting using bicycle exercise as a physiological stress test.…”