ACCUMULATION OF MACROPHAGES IN THE ARTERIAL VESSEL WALL FOLLOWING EXPERIMENTAL BALLOON ANGIOPLASTY

Smooth muscle cell (SMC) proliferation is a key event in the development of restenosis after balloon angioplasty, and it is thought that macrophages play an important role in the complex process of activation ofSMCs after vascular injury induced by balloon angioplasty.The study was designed to determine the time course of the accumulation of macrophages in the intimal layer following experimental balloon angioplasty.To determine the extent and time course of the accumulation of macrophages after experimental balloon angioplasty, an intimal atheroma was produced by repeated weak electrical stimulation of the right carotid artery of 45 male New Zealand White rabbits. Additionally, the animals received an 0.5% cholesterol diet during the 28 days of plaque development. Transluminal balloon angioplasty was subsequently performed. At 3, 7, 14, 21, 28 and 42 days after balloon treatment the vessels from at least five animals from each group were excised and analysed for the presence of macrophages using immunocytochemical techniques. In one group of five animals plaque development occurred without subsequent balloon angioplasty; the animals were killed after 21 days (sham group). SMCs were identified by immunohistological staining of α-actin.Intimal thickening increased after dilatation from 137 ±62 μm (control group without balloon treatment) to 244 ± 47 μm in the 42 days after angioplasty (P<0.05). The percentage of macrophages in the intimal layer displayed a significant increase (P<0.01) at 14 days after angioplasty (9.1 ± 4.3% vs 2.0 ±1.7% in the control group). This increase persisted up to 21 days after intervention (8.0 ± 3.3%) and was significantly increased in comparison to the sham group with 3.1 ± 0.8% (P<0.05). Twenty-eight days after balloon dilatation the amount of macrophages in the intima had decreased (1.6 ± 1.6%), and was comparable to the pre-interventional control group.These results demonstrate that the occurrence of macrophages within the area of tissue injury is a delayed phenomenon and contributes to the vascular response to injury. © 1994 The European Society of Cardiology.