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Atherosclerosis regression

A decrease in serum cholesterol levels results in a decrease not only in the lipid content but also in the size of experimentally induced atherosclerotic lesions. Evidence of this association in man has been demonstrated by coronary angiography. " Human femoral atherosclerosis regressed in response to diet and/or drug therapy (clofibrate, NA, or clofibrate in combination with neomycin). "> The degree of retardation of atherosclerosis was directly correlated with the decrease in serum cholesterol levels. " Regression in patients with Type IV hyperlipoproteinemia was also associated with the decrease in serum triglyceride levels however, no such correlation was found in another study. ... [Pg.199]

Tsimikas, S. et al. Increased plasma oxidized phospholipid apolipoprotein B-lOO ratio with concomitant depletion of oxidized phospholipids from atherosclerotic lesions after dietary lipid-lowering a potential biomarker of early atherosclerosis regression. Arterioscler. Thromb. Vase. Biol. 27 (2007) 175-81. [Pg.349]

Fewer progressing lesions (P<0.03), less new atheroma formation (P<0.03), more atherosclerosis regression (P=0.002)... [Pg.698]

Toth PP, Maid KC. A commentary on the implications of the ENHANCE (ezetimibe and simvastatin in hypercholesterolemia enhances atherosclerosis regression) trial should ezetimibe move to the back of the line as a therapy for dyslipidemia J Clin Lipidol 2008 2 313-7. [Pg.930]

Probucol. Probucol is an antioxidant that is effective in lowering LDL cholesterol. Whereas probucol was known to lower cholesterol after relatively simple clinical trials (160), its mechanism of action as an antioxidant in the treatment of atherosclerosis is quite novel. Probucol has been shown to have the abiUty to produce regression of atherosclerotic lesions in animal models (161). Probucol therefore represents a novel class of pharmaceutical agent for the treatment of atherosclerosis. This effect occurs mechanistically, in part, by preventing oxidation of LDL, a necessary step in foam cell formation. This antioxidant activity has been shown in laboratory experiments and its activity in lowering LDL cholesterol in human studies is well documented (162). [Pg.131]

Tangirala, RK, Pratico, D, FitzGerald, GA, Chun, S, Tsukamoto, K, Maugeais, C, Usher, DC, Pure, E, and Rader, DJ, 2001. Reduction of isoprostanes and regression of advanced atherosclerosis by apolipoprotein E. J Biol Chem 276, 261-266. [Pg.352]

Yoshii T, Iwai M, Li Z, Chen R, Ide A, Fnknnaga S, Oshita A, Mogi M, Higaki J, Horinchi M. (2006) Regression of atherosclerosis by amlodipine via anti-inflammatory and anti-oxidative stress actions. Hypertens Res 29 457 66. [Pg.221]

Nicholls SJ, Tuzcu EM, Sipahi 1, Grasso AW, Schoenhagen P, Hu T, Wolski K, Crowe T, Desai MY, Hazen SL, Kapadia SR, Nissen SE. (2007) Statins, high-density lipoprotein cholesterol, and regression of coronary atherosclerosis. J Amer Med Assn 297 499-508. [Pg.624]

A number of studies have investigated the use of PGE and PGI2 compounds in Raynaud s phenomenon and peripheral atherosclerosis. In the latter case, prolonged infusions have been used to permit remodeling of the vessel wall and to enhance regression of ischemic ulcers. [Pg.450]

Williams JK, Armstrong ML, Heistad DD. Vasa vasorum in atherosclerotic coronary arteries responses to vasoactive stimuli and regression of atherosclerosis. Circ Res 1988 62 515-523. [Pg.344]

The noninvasive demonstration that lowering plasma cholesterol sufficiently results in either regression or lack of progression of atherosclerosis in man (and the very large amount of evidence to support this from animal studies) leads one to expect that direct evidence can be obtained that choles-... [Pg.218]

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. Atherosclerosis 30(1), 27 -43. [Pg.332]

Kritchevsky, D., Tepper, S.A., Wright, S., Tso, P., Czarnecki, S.K. 2004. Conjugated linoleic acid isomer effects in atherosclerosis Growth and regression of lesions. Lipids. 39, 611-616. [Pg.131]

Toomey, S., Roche, H., Fitzgerald, D., Belton, O. 2003. Regression of pre-established atherosclerosis in the apoE(-/-) mouse by conjugated linoleic acid. Biochem. Soc. Trans. 31, 1075-1079. [Pg.135]

RA is a potent activator of PPARa and PPAR-y (Belury et al., 2002). Yu et al. (2002) found that inhibition of pro-inflammatory products by RA was associated with PPAR-y activation. Likewise, Toomey et al. (2003) showed that the regression of preestablished atherosclerosis in apo E- mice fed RA is associated with an increased expression of PPARy. [Pg.618]

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]

Kano H, Hayashi T, Sumi D, Esaki T, Asai Y, et al. 1999. A HMG-CoA reductase inhibitor improved regression of atherosclerosis in the rabbit aorta without affecting serum lipid levels possible relevance of up-regulation of endothelial NO synthase mRNA. Biochem. Biophys. Res. Commun. 259 414-19... [Pg.121]


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See also in sourсe #XX -- [ Pg.195 ]




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