2011
DOI: 10.1097/mol.0b013e32834ab106
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The effect of statins on high-risk atherosclerotic plaque associated with low endothelial shear stress

Abstract: The relationship between low ESS and statins has not been fully investigated, but the available data underscore the vasculoprotective effect of statins. Understanding the mechanisms whereby statins reduce the atherogenic and inflammatory phenotype resulting from a low ESS environment would provide new insights to design strategies to prevent regional formation of high-risk, inflamed plaques likely to rupture and cause an adverse clinical event.

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Cited by 6 publications
(3 citation statements)
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“…SS changes with the degree of stenosis, and the changed stress regulates the development of plaques into high risk plaques [ 173 ]. Locally increased SS using a developed flow divider indicates that SS reduces in-stent neointimal formation by 50% [ 174 , 175 ]. Attempts to increase SS to inhibit intimal hyperplasia are not applicable to atherosclerotic vulnerable plaque treatment [ 68 ] because HSS is the critical factor for high-risk coronary plaque formation.…”
Section: Discussionmentioning
confidence: 99%
“…SS changes with the degree of stenosis, and the changed stress regulates the development of plaques into high risk plaques [ 173 ]. Locally increased SS using a developed flow divider indicates that SS reduces in-stent neointimal formation by 50% [ 174 , 175 ]. Attempts to increase SS to inhibit intimal hyperplasia are not applicable to atherosclerotic vulnerable plaque treatment [ 68 ] because HSS is the critical factor for high-risk coronary plaque formation.…”
Section: Discussionmentioning
confidence: 99%
“…126 Statins upregulate atheroprotective transcriptional factors and hence they are likely to counterbalance the detrimental effects of low ESS. 127 Both aspirin and ticlopidine significantly inhibit platelet aggregation under high ESS conditions. 128 In an animal model of vulnerable plaque, metoprolol treatment restored ESS values and this was associated with a reduction in inflammatory cytokines, attenuation of expansive remodeling, reduced histopathological indices of vulnerability, and a trend toward reduced plaque size and rate of rupture.…”
Section: Effects Of Medications On Plaque Stability and Local Essmentioning
confidence: 96%
“…11 The reasons underlying this observation remain unknown. Although some studies suggest that plaque erosion and stable plaques may also lead to ACS, this review will predominantly focus on biomechanical factors influencing plaque rupture at sites of TCFA, which is the commonest finding in patients presenting with ACS.…”
mentioning
confidence: 99%