Key result
Statins may act as antithrombotic agents in acute coronary syndromes by targeting cellular pathways involved in acute inflammation and subsequent thrombosis.
Statins may provide broad beneficial effects beyond lipid lowering, potentially acting as antithrombotic agents in acute coronary syndromes by targeting cellular pathways involved in inflammation and thrombosis.
Does not yet support practice changes in ACS; leaves open confirmation of antithrombotic effects in prospective trials.
HMG CoA reductase inhibitors, or statins, are standard of care for preventing cardiovascular disease in at-risk populations. Statins are a well-established therapy proven to reduce long-term cardiovascular mortality and morbidity for prevention of secondary cardiovascular events and have become guidelinerecommended therapy following acute myocardial infarction. Emerging data from clinical trials over the last decade indicates that statin therapy may provide broad beneficial effects beyond their primary lipid lowering mechanisms. In coronary heart disease, statins have demonstrated a unique ability to target several cellular pathways, which appear to play an underappreciated role in acute inflammation and subsequent thrombosis. Herein, we review the potential mechanisms where statins may act as antithrombotic agents in the setting of acute coronary syndromes and discuss the clinical implications of these findings.
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Sexton et al. (2016) conducted a review in Acute Coronary Syndromes. Statins (HMG CoA reductase inhibitors) was evaluated. Statins may act as antithrombotic agents in acute coronary syndromes by targeting cellular pathways involved in acute inflammation and subsequent thrombosis.
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