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

GE Austin, NB Ratliff, J Hollman, S Tabei… - Journal of the American …, 1985 - Elsevier
GE Austin, NB Ratliff, J Hollman, S Tabei, DF Phillips
Journal of the American College of Cardiology, 1985Elsevier
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 …
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.
Elsevier