Reply

We would like to thank Roncati et al for their letter and comments related to our article. Approximately 1 year ago in the early stages of the coronavirus disease 2019 (COVID-19) pandemic, hospitals in New York City experienced some of the highest concentrations of cases in the United States. We cared for a great number of patients with arterial and/or venous thromboembolic complications related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Among these were many patients with COVID-19 and acute arterial ischemia requiring emergent surgical treatment.

In addition to the greater mortality, we found these patients had a higher body mass index, higher average in-hospital D-dimer levels, and lower rates of antiplatelet usage. This constellation suggested that a generalized hyperinflammatory, hypercoagulable state, as nicely outlined in detail by Roncati et al in their letter to the editor, was primarily responsible. Finally, we found an unusual preponderance of large vessel thromboses, including those in the aortoiliac distribution. During the past year, the hypercoagulability seen in patients with COVID-19 has been increasingly elucidated and will continue to be further characterized. Although this has been an extremely difficult time for healthcare workers around the world, the opportunity for cross-specialty and global collaboration, as is illustrated by their letter to the editor and our article in the Journal, has been rewarding and hopefully will help expedite the characterization of these processes at a more detailed cellular and molecular level.

As we continue to treat patients with SARS-CoV-2 infection, we expect to encounter new and challenging obstacles such as the arterial and venous complications described. For example, we have seen in recent weeks the characterization of an even newer phenomenon, a condition known as SARS-CoV-2 vaccine–induced immune thrombotic thrombocytopenia. As was recently demonstrated in a New England Journal article, the mechanism of this hypercoagulable disorder related to COVID-19 vaccination is closely related to that which leads to heparin-induced thrombocytopenia.¹ This requires treatment with non–heparin anticoagulant agents. It is important to differentiate hypercoagulable complications such as these in patients with SAR-CoV-2 infection because the treatment implications could differ. As vascular disease experts, it is inherent for us to understand the mechanisms underlying these complications whether or not they require surgical intervention.