The 2020 Scientific Sessions of the American Heart Association (AHA) featured 139 presentations of works related to COVID-19. While most of the studies were reporting epidemiologic and clinical data from diverse regions of the world, some investigators focused on understanding the mechanisms of the disease, especially thromboembolism and cardiovascular complications. Indeed, we and others have linked the systemic manifestations of the disease to a direct or indirect involvement of the endothelium. 2–4 Notably, endothelial cells express all the co-factors necessary for the internalization of SARS-CoV-2 in human host cells (Figure 1). Our group has shown that the microRNA cargo of extracellular vesicles released by endothelial cells could contribute to the pathogenesis of thromboembolic complications of COVID-19. 5 On these grounds, we have selected some AHA presentations from experts in bioengineering and nanomedicine who developed innovative tools to dissect endothelial dysfunction in COVID-19.

Jason Hinman et al. 6 at UCLA generated 3D printed models of the human middle cerebral artery, endothelialized with human endothelial cells. Endothelialized models were subjected to 3D rotational perfusional culture at variable pulsatile flow rates and biotinylated recombinant Sars-CoV-2 S protein was used to judge regional vessel binding of virus. ACE2 expression was modulated in a flowdependent manner. Pulsatile flow was able to drive ACE2 expression in these 3D endothelialized models and flow-mediated ACE2 expression was associated with binding of recombinant SARS-CoV-2 Spike protein to the vessel wall, thereby indicating a direct cerebrovascular susceptibility to SARS-CoV-2. 6