Objectives: We sought to elucidate the effects of 20- mg versus 5- mg atorvastatin on thoracic and abdominal aortic plaques. Background: Regression of thoracic aortic plaques by simvastatin was demonstrated using magn...Objectives: We sought to elucidate the effects of 20- mg versus 5- mg atorvastatin on thoracic and abdominal aortic plaques. Background: Regression of thoracic aortic plaques by simvastatin was demonstrated using magnetic resonance imaging(MRI). However, the effects of different doses of statin have not been assessed. Methods: Using MRI, we investigated the effects of 20- mg versus 5- mg atorvastatin on thoracic and abdominal aortic plaques in 40 hypercholesterolemic patients who were randomized to receive either dose. Treatment effects were evaluated as changes in vessel wall thickness(VWT) and vessel wall area(VWA) of atherosclerotic lesions from baseline to 12 months of treatment. Results: The 20- mg dose induced a greater low- density lipoprotein(LDL) cholesterol reduction than did the 5- mg dose(- 47% vs.- 34% , p< 0.001). Although 20 mg and 5 mg reduced C- reactive protein(CRP) levels(- 47% and- 28% ), the degree of CRP reduction did not differ between the two doses. The 20- mg dose reduced VWT and VWA of thoracic aortic plaques(- 12% and - 18% , p< 0.001), whereas 5 mg did not(+ 1% and + 4% ). Regarding abdominal aortic plaques, even 20 mg could not reduce VWT or VWA(- 1% and + 3% ), but instead progression was observed with 5mg treatment(+ 5% and + 12% , p< 0.01). Notably, the degree of plaque regression in thoracic aorta correlated with LDL cholesterol(r=0.64) and CRP(r=0.49) reductions. Although changes in abdominal aortic plaques only weakly correlated with LDL cholesterol reduction(r=0.34), they correlated with age(r=0.41). Conclusions: One- year 20- mg atorvastatin treatment induced regression of thoracic aortic plaques with marked LDL cholesterol reduction, whereas it resulted in only retardation of plaque progression in abdominal aorta. Thoracic and abdominal aortic plaques may have different susceptibilities to lipid lowering.展开更多
OBJECTIVES: The purpose of this study was to investigate the role of shear stress(SS) in plaque regression. BACKGROUND: A condition favorable to the development of atherosclerotic lesions is low oscillating SS. In the...OBJECTIVES: The purpose of this study was to investigate the role of shear stress(SS) in plaque regression. BACKGROUND: A condition favorable to the development of atherosclerotic lesions is low oscillating SS. In the descending thoracic aorta, the relationship between plaque distribution and SS has never been characterized. The regression of plaque as the result of lipid-lowering therapy is associated with reverse atherogenic mechanisms. Therefore, we investigated the role of SS in plaque regression. Magnetic resonance imaging(MRI) provides a unique opportunity to noninvasively study morphology and hemodynamics. METHODS: Cross-sectional images of atherosclerotic plaques in the descending thoracic aorta of 10 asymptomatic, hypercholesteremic patients were acquired at baseline and 24 months after starting lipid-lowering therapy by using a black-blood sequence on a 1.5-T clinical MRI system(5 mm×780 μm×780 μm). Average wall thickness(WT) was derived per quadrant. The aorta was subdivided in segments 2 cm in length starting 1 cm from the aortic arch. RESULTS: Average WT decreased with increasing distance from the arch(3.0±0.7 mm vs. 2.5±0.3 mm; p< 0.05) and showed a helical pattern from the proximal to distal segments. Phase-contrast MRI was performed in the thoracic aorta of eight healthy volunteers to derive typical average SS distribution. Shear stress predicted the location of WT(r2=0.29, p< 0.05) but did not predict plaque regression. The best predictor of plaque regression was baseline WT. CONCLUSIONS: Our data showing an association between WT and average low SS locations support the role of local hemodynamics in the development of atherosclerotic lesions in descending thoracic aorta. Furthermore, SS does not seem to be the major predictor for plaque regression by lipid-lowering interventions. Therefore, our data suggest that other mechanisms are involved in the lipid-reversal mechanism.展开更多
文摘Objectives: We sought to elucidate the effects of 20- mg versus 5- mg atorvastatin on thoracic and abdominal aortic plaques. Background: Regression of thoracic aortic plaques by simvastatin was demonstrated using magnetic resonance imaging(MRI). However, the effects of different doses of statin have not been assessed. Methods: Using MRI, we investigated the effects of 20- mg versus 5- mg atorvastatin on thoracic and abdominal aortic plaques in 40 hypercholesterolemic patients who were randomized to receive either dose. Treatment effects were evaluated as changes in vessel wall thickness(VWT) and vessel wall area(VWA) of atherosclerotic lesions from baseline to 12 months of treatment. Results: The 20- mg dose induced a greater low- density lipoprotein(LDL) cholesterol reduction than did the 5- mg dose(- 47% vs.- 34% , p< 0.001). Although 20 mg and 5 mg reduced C- reactive protein(CRP) levels(- 47% and- 28% ), the degree of CRP reduction did not differ between the two doses. The 20- mg dose reduced VWT and VWA of thoracic aortic plaques(- 12% and - 18% , p< 0.001), whereas 5 mg did not(+ 1% and + 4% ). Regarding abdominal aortic plaques, even 20 mg could not reduce VWT or VWA(- 1% and + 3% ), but instead progression was observed with 5mg treatment(+ 5% and + 12% , p< 0.01). Notably, the degree of plaque regression in thoracic aorta correlated with LDL cholesterol(r=0.64) and CRP(r=0.49) reductions. Although changes in abdominal aortic plaques only weakly correlated with LDL cholesterol reduction(r=0.34), they correlated with age(r=0.41). Conclusions: One- year 20- mg atorvastatin treatment induced regression of thoracic aortic plaques with marked LDL cholesterol reduction, whereas it resulted in only retardation of plaque progression in abdominal aorta. Thoracic and abdominal aortic plaques may have different susceptibilities to lipid lowering.
文摘OBJECTIVES: The purpose of this study was to investigate the role of shear stress(SS) in plaque regression. BACKGROUND: A condition favorable to the development of atherosclerotic lesions is low oscillating SS. In the descending thoracic aorta, the relationship between plaque distribution and SS has never been characterized. The regression of plaque as the result of lipid-lowering therapy is associated with reverse atherogenic mechanisms. Therefore, we investigated the role of SS in plaque regression. Magnetic resonance imaging(MRI) provides a unique opportunity to noninvasively study morphology and hemodynamics. METHODS: Cross-sectional images of atherosclerotic plaques in the descending thoracic aorta of 10 asymptomatic, hypercholesteremic patients were acquired at baseline and 24 months after starting lipid-lowering therapy by using a black-blood sequence on a 1.5-T clinical MRI system(5 mm×780 μm×780 μm). Average wall thickness(WT) was derived per quadrant. The aorta was subdivided in segments 2 cm in length starting 1 cm from the aortic arch. RESULTS: Average WT decreased with increasing distance from the arch(3.0±0.7 mm vs. 2.5±0.3 mm; p< 0.05) and showed a helical pattern from the proximal to distal segments. Phase-contrast MRI was performed in the thoracic aorta of eight healthy volunteers to derive typical average SS distribution. Shear stress predicted the location of WT(r2=0.29, p< 0.05) but did not predict plaque regression. The best predictor of plaque regression was baseline WT. CONCLUSIONS: Our data showing an association between WT and average low SS locations support the role of local hemodynamics in the development of atherosclerotic lesions in descending thoracic aorta. Furthermore, SS does not seem to be the major predictor for plaque regression by lipid-lowering interventions. Therefore, our data suggest that other mechanisms are involved in the lipid-reversal mechanism.