Importance of inflammation in arteriosclerotic plaque destabilization and rupture

Although Rudolf Virchow considered arteriosclerosis an inflammatory disease in his book Cellular Pathology publisched in 1858, the opinion that it was a degenerative arterial disease as a civilization disease prevailed. Nowadays, a great attention has been paid to the inflammatory process in the patogenesis of arteriosclerosis and particularly in the destabilization and rupture of plaque. To find out whether T and B lymphocytes, lipid macrophages, vascular smooth muscle and mast cells as well as plaque destabilization and rupture are present in ruptured arteriosclerotic plaque in the coronary arteries. Histochemical and immunochemical analyses of 68 ruptured arteriosclerotic plaques from the coronary arteries were performed. Microscopic examination revealed the presence of inflammation elements in all of them. The following histochemical and immunochemical methods were applied: Masson's trichrome, actins, vimentin, CD3, CD43, CD68, CD20, CD45 and chlorine acetyl esterase. The control group included 10 arteriosclerotic plaques from the coronary arteries with fibrous cap, but without inflammation cells. Rupture of the arteriosclerotic plaque fibrous cap, with thinned and torn collagen fibers, was found in all of the 68 arteriosclerotic plaques. In 57 out of 68 analysed plaques, the increased number of T-lymphocytes, lipid macrophages, vascular smooth muscle and mast cells particularly on the plaque rupture site were found. In the remaining 11 specimens, mast cells were present in a somewhat smaller number. In the control group with the stable plaque, inflammation cells were not observed. Our results pointed out that the inflammatory elements, which might exert an effect upon the arteriosclerotic plaque destabilization, and rupture had been present in the ruptured arteriosclerotic plaque.