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  • Editorial: In Vitro Evidence for the Role of Cytokine Storm in the Generation of Stent Thrombosis in COVID-19 Patients

    COVID-19 is a prothrombotic disease that enhances the risk for adverse complications, including stent thrombosis and mortality, in patients with acute coronary syndrome (ACS) [1][2][3][4]. COVID-19 is characterized by markedly elevated systemic levels of inflammatory cytokines [interleukin (IL-6 and tumor necrosis factor (TNF)-α)], fibrinogen, and d-dimer and a resultant hypercoagulable state [5][6]. Thus, ACS, a prothrombotic disease, is further aggravated by COVID-19. Several studies, including case reports, demonstrated higher rates of stent thrombosis and hospital mortality in patients with COVID-19 who were stented for ST-segment elevation myocardial infarction (STEMI) compared to patients with STEMI without COVID-19 [2][3][4][7]. Moreover, a higher incidence of multiple thrombotic culprit lesions, higher thrombus grade, and a lower rate of procedural success of primary percutaneous intervention were also reported in patients with COVID-19 and STEMI compared to patients with STEMI alone [3][8]. Elevated levels of d-dimer were also associated with high thrombus burden and low myocardial blush grade among these patients [3]. These important findings support the concept that patients with COVID-19 and STEMI ideally should be treated with the least thrombogenic stent(s).

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