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,
and
DF Phillips
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.
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J. M. Isner, M. Kearney, S. Bortman, and J. Passeri
Apoptosis in Human Atherosclerosis and Restenosis
Circulation,
June 1, 1995;
91(11):
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[Abstract]
[Full Text]
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A. E. Villa, L. A. Guzman, E. J. Poptic, V. Labhasetwar, S. D'Souza, C. L. Farrell, E. F. Plow, R. J. Levy, P. E. DiCorleto, and E. J. Topol
Effects of Antisense c-myb Oligonucleotides on Vascular Smooth Muscle Cell Proliferation and Response to Vessel Wall Injury
Circ. Res.,
April 1, 1995;
76(4):
505 - 513.
[Abstract]
[Full Text]
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L. Weir, D. Chen, C. Pastore, J. M. Isner, and K. Walsh
Expression of gax, a Growth Arrest Homeobox Gene, Is Rapidly Down-regulated in the Rat Carotid Artery during the Proliferative Response to Balloon Injury
J. Biol. Chem.,
March 10, 1995;
270(10):
5457 - 5461.
[Abstract]
[Full Text]
[PDF]
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M. R. Soma, E. Donetti, C. Parolini, C. R. Sirtori, R. Fumagalli, and G. Franceschini
Recombinant Apolipoprotein A-IMilano Dimer Inhibits Carotid Intimal Thickening Induced by Perivascular Manipulation in Rabbits
Circ. Res.,
March 1, 1995;
76(3):
405 - 411.
[Abstract]
[Full Text]
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S. O. Marx, T. Jayaraman, L. O. Go, and A. R. Marks
Rapamycin-FKBP Inhibits Cell Cycle Regulators of Proliferation in Vascular Smooth Muscle Cells
Circ. Res.,
March 1, 1995;
76(3):
412 - 417.
[Abstract]
[Full Text]
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I. Nyamekye, S. Anglin, J. McEwan, A. MacRobert, S. Bown, and C. Bishop
Photodynamic Therapy of Normal and Balloon-Injured Rat Carotid Arteries Using 5-Amino-Levulinic Acid
Circulation,
January 15, 1995;
91(2):
417 - 425.
[Abstract]
[Full Text]
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M. Simons, G. Leclerc, R. D. Safian, J. M. Isner, L. Weir, and D. S. Baim
Relation between Activated Smooth-Muscle Cells in Coronary-Artery Lesions and Restenosis after Atherectomy
N. Engl. J. Med.,
March 4, 1993;
328(9):
608 - 613.
[Abstract]
[Full Text]
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S. R. Johansson, L. Ekstrom, and H. Emanuelsson
Higher Recurrence Rate After Coronary Angioplasty in Unstable Angina Pectoris
Angiology,
April 1, 1991;
42(4):
273 - 280.
[Abstract]
[PDF]
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