Early antithrombotic therapy and COVID-19: a better clinical course? New evidences from real-life cases

Abstract

Recentní onemocnění COVID-19 přináší možné rizikové faktory žilního tromboembolismu a horší klinický průběh u některých pacientů má spojitost s trombózou. Zatímco nízkomolekulární hepariny jsou zkoumány s ohledem na vhodnou dávku, ostatní elementy mohou být užitečné. Sdílíme naši zkušenost týkající se dvou pacientů s neočekávaným klinickým průběhem.

Post‑infectious acute myocardial infarction following COVID‑19 infection in a young patient

“…Moreover, the cytokines release, as interleukin-6, exerts proatherogenic effects, causing vascular smooth muscle proliferation, endothelial cell activation, and platelet activation. 9,10 Myocardial ischaemia can also be caused by microvascular dysfunction due to endothelial impairment. 3 Endothelial dysfunction in COVID-19 patients is caused primarily by the downregulation of angiotensin-converting enzyme-2 (ACE-2) receptors, triggering the kallikrein-bradykinin system and resulting in increased vascular permeability.…”

An "ordinary" case of COVID-19 pneumonia: when symptoms hide serious complications

“…7 However, while a full anticoagulant dose of LMWH is currently not recommended for each patient, an early antithrombotic strategy to prevent thromboembolism could improve clinical course in some patients. 9,10 In concomitance chest CT has quickly become a cornerstone both in early diagnosis and during follow-up. 11 While before the pandemic there was a general consensus on extensive use of bedside echocardiography as a fi rst line tool both for assessment of left and right ventricle, 12,13 to date this point of view is reversed.…”