key: cord-0852941-2zgctph5 authors: Ong, Emily; Castro‐Dominguez, Yulanka; Brennan, Joseph; Oen‐Hsiao, Joyce title: COVID‐19 complicated by ST‐segment elevation myocardial infarction in a 29‐year‐old patient date: 2020-07-16 journal: Catheter Cardiovasc Interv DOI: 10.1002/ccd.29102 sha: 373d66fbee841cc0e2c1e54aa6eb3d3bbd692068 doc_id: 852941 cord_uid: 2zgctph5 We describe a case in which a 29‐year‐old male with no medical history presented with ST‐segment elevation myocardial infarction as his presentation of coronavirus disease. During cardiac catheterization, he was found to have total occlusion of his left anterior descending artery by thrombus. Laboratory testing revealed markedly elevated inflammatory markers as well as evidence of a hypercoagulable state in the setting of severe acute respiratory syndrome coronavirus 2 infection, which was suspected to be the inciting factor for his acute coronary event. COVID-19 also appears to be associated with a marked systemic inflammatory response particularly in severe cases. C-reactive protein, erythrocyte sedimentation rate, and ferritin are elevated, and those with more fulminant cases of the disease have significantly higher elevations of these markers compared to those with milder cases. 5 In severe COVID-19, cytokine storm with a profile suggestive of secondary hemophagocytic lymphohistiocytosis has also been observed, with elevated increased interleukin (IL)-2, IL-7, granulocyte colonystimulating factor, interferon-γ inducible protein 10, monocyte chemoattractant protein 1, macrophage inflammatory protein 1-α, and tumor necrosis factor-α. 6 Cardiac injury from this inflammatory response, as well as from a subsequent hypercoagulability, has been proposed as a mechanism of the cardiovascular complications that Microvascular injury and thrombosis were described in a case series in which skin and lung tissues from five patients with severe COVID-19 were examined. Inflammatory capillary injury with complement deposition was noted in both lung tissue and in skin lesions. Complementmediated endothelial injury and fibrin deposition and subsequent thrombosis were observed. 8 A separate case series also describes endothelial inflammation across the vascular beds of multiple organs, including the lungs, heart, kidneys, and intestines, of COVID-19 patients. A predominantly lymphocytic endotheliitis is described in this series. 9 The endothelial dysfunction observed in many cases can be expected to be the precipitant of a hypercoagulable state. The overall picture is one of hypercoagulability and a predisposi- We would like to thank Eric Brandt, MD, and Yanting Wang, MD, for their participation in the care of this patient and for their contribution to the manuscript. The authors declare no conflicts of interest. WHO. Coronavirus disease 2019 (COVID-19) situation report-134 Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study The executive group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) task force for the universal definition of myocardial infarction. Fourth universal definition of myocardial infarction Coronavirus fulminant myocarditis saved with glucocorticoid and human immunoglobulin Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China COVID-19: consider cytokine storm syndromes and immunosuppression Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: a report of five cases Endothelial cell infection and endotheliitis in COVID-19 COVID-19 complicated by STsegment elevation myocardial infarction in a 29-year-old patient