Key result
Acetylsalicylic acid normalized the neutrophil-lymphocyte ratio, passive aortic wall stiffness, and cardiac remodeling in a mouse model of advanced atherosclerosis, but did not affect survival.
Why the study?
Although acetylsalicylic acid is widely used for secondary prevention due to antithrombotic effects, whether it prevents vessel wall remodelling, atherosclerosis, and cardiovascular complications remained uninvestigated.
Does acetylsalicylic acid prevent the progression of vessel wall remodelling, atherosclerosis, and cardiovascular complications in mouse models of advanced atherosclerosis?
RCT (n=69)
Randomly divided
Does acetylsalicylic acid prevent the progression of vessel wall remodelling, atherosclerosis, and cardiovascular complications in mouse models of advanced atherosclerosis?
In a mouse model of advanced atherosclerosis, low-dose aspirin reduced aortic wall stiffness and adverse cardiac remodeling without affecting plaque progression or survival.
ASA may reduce aortic stiffness and cardiac remodelling in advanced atherosclerosis models; leaves open translation to human CV prevention beyond antithrombosis.
Acetylsalicylic acid (ASA) is widely used in secondary prevention of cardiovascular (CV) disease, mainly because of its antithrombotic effects. Here, we investigated whether ASA can prevent the progression of vessel wall remodelling, atherosclerosis, and CV complications in apolipoprotein E deficient (ApoE−/−) mice, a model of stable atherosclerosis, and in ApoE−/− mice with a mutation in the fibrillin-1 gene (Fbn1C1039G+/−), which is a model of elastic fibre fragmentation, accompanied by exacerbated unstable atherosclerosis. Female ApoE−/− and ApoE−/−Fbn1C1039G+/− mice were fed a Western diet (WD). At 10 weeks of WD, the mice were randomly divided into four groups, receiving either ASA 5 mg/kg/day in the drinking water (ApoE−/− (n = 14), ApoE−/−Fbn1C1039G+/− (n = 19)) or plain drinking water (ApoE−/− (n = 15), ApoE−/−Fbn1C1039G+/− (n = 21)) for 15 weeks. ApoE−/−Fbn1C1039G+/− mice showed an increased neutrophil–lymphocyte ratio (NLR) compared to ApoE−/− mice, and this effect was normalised by ASA. In the proximal ascending aorta wall, ASA-treated ApoE−/−Fbn1C1039G+/− mice showed less p-SMAD2/3 positive nuclei, a lower collagen percentage and an increased elastin/collagen ratio, consistent with the values measured in ApoE−/− mice. ASA did not affect plaque progression, incidence of myocardial infarction and survival of ApoE−/−Fbn1C1039G+/− mice, but systolic blood pressure, cardiac fibrosis and hypertrophy were reduced. In conclusion, ASA normalises the NLR, passive wall stiffness and cardiac remodelling in ApoE−/−Fbn1C1039G+/− mice to levels observed in ApoE−/− mice, indicating additional therapeutic benefits of ASA beyond its classical use.
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Roth et al. (2021) conducted an RCT in Advanced atherosclerosis (n=69). Acetylsalicylic acid (ASA) vs. Plain drinking water was evaluated on Neutrophil-lymphocyte ratio, passive aortic wall stiffness, and cardiovascular remodelling. Acetylsalicylic acid normalized the neutrophil-lymphocyte ratio, passive aortic wall stiffness, and cardiac remodeling in a mouse model of advanced atherosclerosis, but did not affect survival.
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