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These actions probably occur subsequent to inhibition of platelet COX-1-dependent thromboxane formation and its action as a multipotent autocrine and paracrine agent. This likely involves inhibition of thrombin formation as well as inhibition of secondary pro-inflammatory mediators, such as sphingosine-1-phosphate. Experimental and limited clinical data additionally suggest antiinflammatory effects of aspirin independent of its antiplatelet action. For example, aspirin at antiplatelet doses might acetylate COX-2 in vascular cells, directing the activity of the enzyme into a 15-lipoxygenase which by transcellular metabolism results in the formation of 15-epi-lipoxin (\u2018aspirin-triggered lipoxin\u2019), an antiinflammatory mediator. Furthermore, aspirin stimulates eNOS via lysine-acetylation, eventually resulting in induction of heme oxygenase (HO-1), which improves the antioxidative potential of vascular cells. All of these effects have been seen at antiplatelet doses of 100\u2013300 mg\/day, equivalent to peak plasma levels of 10\u201330 \u03bcM. Many more potentially antiinflammatory mechanisms of aspirin have been described, mostly salicy-late-related, at low to medium millimolar concentrations and, therefore, are of minor clinical interest. Altogether, there is a wealth of data supporting antiiflammatory effects of aspirin in ACS, but studies generating direct evidence for antiinflammatory effects in ACS remain to be done.<\/jats:p>","DOI":"10.1160\/th15-03-0191","type":"journal-article","created":{"date-parts":[[2015,6,18]],"date-time":"2015-06-18T06:41:11Z","timestamp":1434609671000},"page":"469-477","source":"Crossref","is-referenced-by-count":25,"title":["Antiinflammatory effects of aspirin in ACS: relevant to its cardio coronary actions?"],"prefix":"10.1160","volume":"114","author":[{"given":"Karsten","family":"Schr\u00f6r","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Hohlfeld","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"194","published-online":{"date-parts":[[2017,11,21]]},"reference":[{"key":"10.1160\/TH15-03-0191-1","doi-asserted-by":"crossref","unstructured":"Hohlfeld T, Schr\u00f6r K. 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