Ultrastructure of intramural coronary arteries in pigs with hypertrophic cardiomyopathy Journal Article

Authors: Shyu, J. J.; Cheng, C. H.; Erlandson, R. A.; Lin, J. H.; Liu, S. K.
Article Title: Ultrastructure of intramural coronary arteries in pigs with hypertrophic cardiomyopathy
Abstract: Pigs with hypertrophic cardiomyopathy diagnosed by echocardiographic examination were selected for study from a genetic breeding herd. Under dissecting microscopic examination, intramural coronary arteries in the septum and left ventricular free wall of euthanized pigs were collected for ultrastructural study. The major lesions of wall thickening included degeneration or denudation of endothelium, subendothelial edema, proliferation of collagen fiber, and hyperplasia of smooth muscle cells. Smooth muscle cells proliferated and migrated through the internal elastic lamella into the intima, which caused the early lesion of wall thickening of the intramural coronary arteries. The extent of smooth muscle cell proliferation was related to the severity of endothelial damage. The smooth muscle cells in the intima were identified by immunohistochemical staining (i.e., smooth muscle actin [SMA] stain). Three major types of severe wall thickening with narrow lumen were observed in the intramural coronary arteries. Edema in the intima caused the major lesion of Type I wall thickening. The internal elastic lamella was broken into small interrupted fragments, and fine fragments of elastic fibers surrounded by the cellular processes of smooth muscle were observed in Type I lesions. Many smooth muscle cells proliferated in the intima and media, which constituted the major lesion of Type II wall thickening of the intramural coronary arteries. Many vacuolized, degenerated smooth muscle cells with fewer sarcoplasmic myofilaments could be clearly observed in the Type II lesions. In advanced cases, severe vacuolization and degeneration of smooth muscle cells with the presence of many bizarrely shaped smooth muscle cells in the walls of the intramural coronary arteries could be observed, which caused the major lesion of Type III wall thickening. Pigs with hypertrophic cardiomyopathy, characterized by spontaneously occurring lesions in intramural coronary arteries, may prove a valuable animal model for human disease. © 2002 Elsevier Science Inc. All rights reserved.
Keywords: immunohistochemistry; controlled study; nonhuman; cell proliferation; animals; animal tissue; smooth muscle fiber; edema; animal experiment; animal model; disease severity; endothelium, vascular; cell migration; echocardiography; actins; tissue injury; coronary artery; coronary vessels; swine; cell hyperplasia; heart ventricles; cell degeneration; artery wall; intima; tunica intima; muscle, smooth, vascular; cell vacuole; hypertrophic cardiomyopathy; cell ultrastructure; artery lesion; heart left ventricle; coronary artery obstruction; sarcoplasmic reticulum; priority journal; article; smooth muscle cells; intramural coronary artery; wall thickening; artery endothelium; elastic fiber; myofilament; cardiomyopathy, hypertrophic; swine diseases
Journal Title: Cardiovascular Pathology
Volume: 11
Issue: 2
ISSN: 1054-8807
Publisher: Elsevier Science, Inc.  
Date Published: 2002-03-01
Start Page: 104
End Page: 111
Language: English
DOI: 10.1016/s1054-8807(01)00101-6
PUBMED: 11934602
PROVIDER: scopus
Notes: Export Date: 14 November 2014 -- Source: Scopus
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