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While histamine has been shown to play a crucial role in many physiological and pathological processes, its effects on neutrophil\u2010platelet interactions in thromboinflammatory complications of AMI remain elusive. In this study, we show a previously unknown mechanism by which neutrophil\u2010derived histamine protects the infarcted heart from excessive neutrophil\u2010platelet interactions and redundant arterial thrombosis. Using histamine\u2010deficient (histidine decarboxylase knockout, HDC<jats:sup>\u2212\/\u2212<\/jats:sup>) and wild\u2010type murine AMI models, we demonstrate that histamine deficiency increases the number of microthrombosis after AMI, in accordance with depressed cardiac function. Histamine\u2010producing myeloid cells, mainly Ly6G<jats:sup>+<\/jats:sup> neutrophils, directly participate in arteriole thrombosis. Histamine deficiency elevates platelet activation and aggregation by enhancing Akt phosphorylation and leads to dysfunctional characteristics in neutrophils which was confirmed by high levels of reactive oxygen species production and CD11b expression. Furthermore, HDC<jats:sup>\u2212\/\u2212<\/jats:sup> platelets were shown to elicit neutrophil extracellular nucleosomes release, provoke neutrophil\u2010platelet interactions and promote HDC\u2010expressing neutrophils recruitment in arteriole thrombosis in vivo. In conclusion, we provide evidence that histamine deficiency promotes coronary microthrombosis and deteriorates cardiac function post\u2010AMI, which is associated with the enhanced platelets\/neutrophils function and neutrophil\u2010platelet interactions.<\/jats:p>","DOI":"10.1111\/jcmm.15037","type":"journal-article","created":{"date-parts":[[2020,2,17]],"date-time":"2020-02-17T06:40:33Z","timestamp":1581921633000},"page":"3504-3520","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Histamine deficiency facilitates coronary microthrombosis after myocardial infarction by increasing neutrophil\u2010platelet interactions"],"prefix":"10.1111","volume":"24","author":[{"given":"Hui","family":"Li","sequence":"first","affiliation":[{"name":"Shanghai Institute of Cardiovascular Diseases Zhongshan Hospital Fudan University Shanghai China"},{"name":"Department of Cardiology Zhongshan Hospital Fudan University Shanghai 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