Dose-dependent effect of aspirin on carotid atherosclerosis.

Ranke, C; Hecker, Hartmut; Creutzig, A; Alexander, Klaus

doi:10.1161/01.cir.87.6.1873

Cited by 78 publications

(33 citation statements)

References 31 publications

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“…14 Although the authors as well as previous studies already highlighted that blocking platelet CD40L might reduce thrombus formation and stability, 1,15 the current report identifies-for the first time-that blocking platelet CD40L might preserve the natural T reg response, as a potential novel mechanism to explain the putative plaquegrowth-suppressing effects of antiplatelet drugs.…”

mentioning

confidence: 62%

Platelets suppress Treg recruitment

Moura

Tjwa²

2010

Blood

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mentioning

confidence: 62%

Platelets suppress Treg recruitment

Moura

Tjwa²

2010

Blood

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“…First, the pharmacokinetics of aspirin in mice could be different from that in humans; second, whereas humans get a once-daily administration, the animals in our study had a multiple daily dosing. Considering the existence of relatively little literature on the effect of this drug on atherosclerosis, 27,28 our observations suggest that a reevaluation of aspirin in atherosclerotic plaque progression and composition in humans is timely.…”

Section: Discussionmentioning

confidence: 94%

Effect of Low-Dose Aspirin on Vascular Inflammation, Plaque Stability, and Atherogenesis in Low-Density Lipoprotein Receptor–Deficient Mice

et al. 2002

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Background-Atherosclerosis is a complex vascular inflammatory disease. Low-dose aspirin is a mainstay in the prevention of vascular complications of atherosclerosis. We wished to determine the effect of low-dose aspirin on vascular inflammation, plaque composition, and atherogenesis in LDL receptor-deficient mice fed a high fat diet. Methods and Results-In LDL receptor-deficient mice fed a high fat diet compared with control mice, low-dose aspirin induced a significant decrease in circulating levels and vascular formation of soluble intercellular molecule-1, monocyte chemoattractant protein-1, tumor necrosis factor-␣, interleukin-12p 40, without affecting lipid levels. This was associated with significant reduction of the nuclear factor B activity in the aorta. Low-dose aspirin also significantly reduced the extent of atherosclerosis. Finally, aortic vascular lesions of the aspirin-treated animals showed 57% reduction (PϽ0.05) in the amount of macrophage cells, 77% increase in smooth muscle cells (PϽ0.05), and 23% increase in collagen (PϽ0.05). Conclusions-Our results suggest that in murine atherosclerosis, low-dose aspirin suppresses vascular inflammation and increases the stability of atherosclerotic plaques, both of which, together with its antiplatelet activity, contribute to its antiatherogenic effect. We conclude that low-dose aspirin might be rationally evaluated in the progression and evolution of human atherosclerotic plaque.

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“…32 Indeed, some clinical treatment studies already exist that show a causal role for platelet activity and progression of IMT of the carotid artery. Ranke et al 33 showed that aspirin treatment slowed carotid plaque growth in a dose-dependent manner, with a dose of 900 mg daily more efficient than 50 mg daily. Kodama et al 34 evaluated the effectiveness of long-term antiplatelet therapy in attenuating progression of IMT of the carotid artery of subjects with type 2 diabetes.…”

Section: Discussionmentioning

confidence: 99%

Platelet Degranulation Is Associated With Progression of Intima-Media Thickness of the Common Carotid Artery in Patients With Diabetes Mellitus Type 2

Fateh-Moghadam

Ersel

et al. 2005

ATVB

100

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Background-Platelets play a key role in atherogenesis and thromboembolic complications in patients with type 2 diabetes. Methods and Results-We prospectively examined the relationship between systemic platelet activation and progression of carotid wall thickness within 1 year in 105 patients with type 2 diabetes. The intima-media thickness (IMT) of the common carotid artery was measured bilaterally at study entry and after 1 year. Platelet activation was assessed with the use of immunologic markers of platelet activation (CD62P, CD63, and CD40L) and flow cytometry.

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Dose-dependent effect of aspirin on carotid atherosclerosis.

Abstract: The results of our study indicate that aspirin treatment slows carotid plaque growth in a dose-dependent fashion, with a dose of 900 mg daily more efficient than 50 mg daily.

Cited by 78 publications

References 31 publications

Platelets suppress Treg recruitment

Platelets suppress Treg recruitment

Effect of Low-Dose Aspirin on Vascular Inflammation, Plaque Stability, and Atherogenesis in Low-Density Lipoprotein Receptor–Deficient Mice

Platelet Degranulation Is Associated With Progression of Intima-Media Thickness of the Common Carotid Artery in Patients With Diabetes Mellitus Type 2

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