Intimal proliferation of smooth muscle cells as an explanation for recurrent coronary artery stenosis after percutaneous transluminal coronary angioplasty

Abstract

The pathologic changes in the coronary arteries of three patients who died 5, 17 and 62 days, respectively, after percutaneous transluminal coronary angioplasty were studied. Changes in the vessel wall seen early after angioplasty included focal denudation of the endothelium, splits in the intima extending to and along the inner aspect of the media, focal intimal necrosis and adventitial hemorrhage. Extensive medial dissections were seen in the coronary arteries of the two patients who died 5 and 17 days after coronary angioplasty. Fibrin was deposited on the surface of the intima, within intimal cracks and in areas of intimal and medial necrosis. Focal proliferation of smooth muscle cells was prominent on neointimal surfaces of the coronary artery from the patient who died 17 days after angioplasty. The previously dilated coronary segment from the patient who died 62 days after angioplasty was stenosed by an extensive recent proliferation of smooth muscle cells that were distributed over the entire circumference of the intimal surface as well as within gaps in the old atherosclerotic plaques. This type of intimal proliferation would appear to be responsible for the recurrent coronary artery stenosis that develops in some patients after coronary angioplasty.

Uremic levels of oxalic acid suppress replication and migration of human endothelial cells.

“…Since in all experiments, regardless of the protocol used, oxalate caused significant inhibition of cellular replication, the results from all protocols have been combined in the data presented. 51 …”

“…For short-term experiments in which chromium release was studied, endothelial cells were incubated in medium containing 51 Cr (sodium chromate, 5 jiCi/ml; New England Nuclear, Boston, MA) for 3 hours and washed twice before use. For long-term experiments, cells were incubated with 51 Cr for 24 hours.…”

Novel Paradigms for Dialysis Vascular Access

“…Although this process differs in various pathologic conditions, the traditional paradigm for the pathogenesis of neointimal hyperplasia stresses the migration of smooth muscle cells from the media to the intima (42,43). Recent evidence, primarily from models of arterial injury (coronary angioplasty and saphenous vein bypass grafting), have supported a concept whereby the adventitial layer of the vessel plays an active role in neointima formation characterized by the following events (14,15,(44)(45)(46): (1) adventitial activation of fibroblasts in response to endothelial cell injury; (2) adventitial proliferation and migration of fibroblasts from the adventitia, through the media, and into the intima, where these cells transform into myofibroblasts and vascular smooth muscle cells controlled by matrix metalloproteinases and local cytokines and growth factors; and (3) further proliferation of myofibroblasts and vascular smooth muscle cells within the intima, and synthesis of new extracellular matrix to form the lesion of neointimal hyperplasia.…”

Radiation therapy to prevent coronary artery restenosis

“…The gradual development of the concept that restenosis was the end-result of an uncontrolled proliferation of tissue at the injury site laid the groundwork for radiation being tested in this area. 13,14,15,16 In vitro studies had demonstrated the inhibition of proliferation of arterial smooth muscle cells (SMC's) and fibroblasts as well as decreased collagen synthesis by fibroblasts. 17,18,19 The development of the porcine overstretch balloon injury model of restenosis has provided an excellent model in which to evaluate new therapies since as radiation.…”