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Plaque regression

That atherosclerotic plaques may regress has been amply demonstrated in experimental animals [65] and more recently in humans [66]. Similarly, both human cutaneous and tendinus xanthomas may undergo regression with specific treatment regimens [67], At least four mechanisms appear essential in plaque regression  [Pg.266]


Petronio AS, Amoroso G, Limbruno U, et al. Simvastatin does not inhibit intimal hyperplasia and restenosis but promotes plaque regression in normocholesterolemic patients undergoing coronary stenting a randomized study with intravascular ultrasound. Am Heart J 2005 149 520-526. [Pg.169]

Wissler RW, Vesselinovitch D. Can atherosclerotic plaques regress Anatomic and biochemical evidence from nonhuman animal models. Am J Cardiol 1990 65 33FM0F. [Pg.285]

Although treatment of hyperlipidemia can cause slow physical regression of plaques, the well-documented reduction in acute coronary events that follows vigorous lipid-lowering treatment is attributable chiefly to mitigation of the inflammatory activity of macrophages and is evident within 2-3 months after starting therapy. [Pg.777]

Malinow, M.R., McLaughlin, P., Naito, H.K., Lewis, L.A., and McNulty, W.P. 1978. Effect of alfalfa meal on shrinkage (regression) of atherosclerotic plaques during cholesterol feeding in monkeys. [Pg.200]

Administration of inorganic trivalent chromium compounds or extracts of brewers yeast resulted in decreased blood glucose levels and cholesterol levels and regression of atherosclerotic plaques (Pi-Sunyer and Offenbacher 1984). Improved insulin sensitivity also resulted in an increased incorporation of amino acids into proteins and cell transport of amino acid in rats receiving supplemental chromium (Roginski and Mertz 1969). [Pg.202]

Statins (see Section 5.15) are a group of medications that have proved popular for the treatment of atherosclerosis. They have few short- or long-term undesirable side-effects. Rosuvastatin is a statin shown to demonstrate regression of atherosclerotic plaque within the coronary arteries. The antioxidant effects of the statins may be partly responsible for their therapeutic success. [Pg.107]

Primary and secondary prevention diet and drug trials have been performed to determine whether lowering of cholesterol will prevent CHD Tables 21-15 and Tables 21-16 summarize these trials. A number of earher angiographic smdies demonstrated that cholesterol reduction leads to regression of atherosclerosis and plaque stabilization. Most of the primary and secondary smdies were double-blinded, randomized, and placebo-controlled, lasting for 5 years or... [Pg.446]

Small, D.M. 1988. Progression and regression of atherosclerotic lesions. Arteriosclerosis 8 103-129. Aikawa, M., Libby, P. 2004. The vulnerable atherosclerotic plaque pathogenesis and therapeutic approach. [Pg.604]

Llodra, J., Angeli, V., Liu, J., Trogan, E., Fisher, E.A., Randolph, G.J. 2004. Emigration of monocyte-derived cells from atherosclerotic lesions characterizes regressive, but not progressive, plaques. Proc. Natl. Acad. Sci. U.S.A. 101 11779-11784. [Pg.606]

Introduction - Atherosclerosis is defined by the WHO "as a variable combination of changes of the intima of arteries consisting of the focal accvimulation of lipids, complex carbohydrates, blood and blood products, fibrous tissue and calcium deposits and associated with medial changes." Once formed the advanced plaque seldom regresses, and consequently major research attention has concentrated on prevention of additional deposits or, in the longer view, on the primary prevention of all lesions. [Pg.150]


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