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Daily high-dose aspirin does not lower APRI in the Aspirin-Myocardial Infarction Study
Shilpa Tiwari-Heckler1, Z Gordon Jiang1, Yury Popov1
1Division of Gastroenterology and Hepatology, Department of Medicine.
Insights
Daily high-dose aspirin did not significantly reduce liver fibrosis (APRI) in myocardial infarction patients. Further clinical trials are needed to explore antiplatelet agents
Area of Science:
- Cardiology
- Hepatology
- Pharmacology
Background:
- Antiplatelet agents, like aspirin, may reduce liver fibrosis by inhibiting platelet activation and growth factor production.
- Previous studies suggested a link between aspirin use and reduced liver fibrosis, warranting further investigation.
- The Aspirin-Myocardial Infarction Study (AMIS) provides a unique dataset to explore this association in a rigorous trial setting.
Purpose of the Study:
- To investigate the effect of daily high-dose aspirin on liver fibrosis markers in patients with a history of myocardial infarction.
- To determine if aspirin use influences the aspartate aminotransferase (AST)-to-Platelet Ratio Index (APRI), a surrogate for liver fibrosis.
Main Methods:
- A multicenter, randomized, double-blind, placebo-controlled trial (AMIS) involving 4,524 participants.
- APRI was calculated at baseline and annually using platelet count and AST levels.
- Statistical analysis assessed the annual change in APRI associated with daily aspirin use.
Main Results:
- Daily aspirin use was associated with a slight, non-significant increase in APRI (0.007 per year).
- Aspirin did not significantly impact platelet counts.
- In a subgroup with probable significant fibrosis, aspirin showed a non-significant trend towards APRI reduction.
Conclusions:
- High-dose aspirin did not significantly affect APRI in patients with myocardial infarction.
- The findings do not support the use of daily high-dose aspirin for reducing liver fibrosis in this population.
- New clinical trials are necessary to evaluate other antiplatelet agents or aspirin regimens for potential antifibrotic effects.
Abstract:
Antiplatelet agents reduce liver fibrosis by inhibiting platelet activation and platelet-derived growth factor production. Previous cross-sectional epidemiological studies suggest that the use of aspirin is related to reduced liver fibrosis. The Aspirin-Myocardial Infarction Study (AMIS) aims to examine this relationship in a multicenter, randomized, double-blind and placebo-controlled trial. The existing clinical trial of aspirin was conducted to study the benefit of one gram aspirin daily among 4 524 individuals who had experienced at least one documented myocardial infarction. The aspartate aminotransferase (AST)-to-Platelet Ratio Index (APRI) was calculated at baseline and annually from the platelet count and AST levels. Participants in the AMIS trial had a mean baseline APRI of 0.34±0.36, and only 1% individuals had APRI scores higher than 1.0, a common cutoff for cirrhosis. The daily use of aspirin was associated with an increase, rather than a reduction of APRI, by 0.007 per year (95% CI 0.002-0.015, P=0.12). The use of aspirin did not significantly affect platelet counts. In a sensitivity analysis of individuals with probable significant fibrosis at baseline (APRI≥0.7), the aspirin group had a sustained reduction in APRI over time, although this change was not significant compared to that in the placebo group. In the AMIS trial, the daily use of high-dose aspirin did not significantly affect APRI, a surrogate index of liver fibrosis. This study highlights the need for de novo clinical trials to investigate the potential benefit of antiplatelet agents on liver fibrosis.
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